PCO:0000001population of organismsCHEBI:16991deoxyribonucleic acidPCO:0000008population growth rate2decreased7functional changeIonizing Radiation<p>Ionizing radiation can vary in energy, dose, charge, and in the spatial distributions of energy transferred to other matter (linear energy transfer per unit length or LET) (ICRU 1970). At the same dose, low and high LET both generate energy deposition events, including many higher energy events (Goodhead and Nikjoo 1989). However, they differ in the spatial distribution and upper range of intensity of energy deposited. Lower LET such as gamma rays sparsely deposit many individual excitations or small clusters of excitations of low energy (Goodhead 1988). In contrast, high LET such as alpha particles have fewer tracks but readily transfer their energy to matter and therefore deposit their energy over a much smaller area (Goodhead 1994). Consequently, alpha and other high LET particles penetrate less deeply into tissue, interactions are densely focused on a narrow track, and individual energy depositions can be large (Goodhead 1988). These different energy deposition patterns can lead to differences in radiation effects including the pattern of DNA damage.</p>
<p>Exposure to ionizing radiation can come from natural and industrial sources. Space and terrestrial radiation includes a range of LET particles, while diagnostic radiation methods such as X-ray imaging, mammography and CT scans use low LET X-rays. Radiation therapy can use an external beam to direct radiation on a focused tissue area, or deposit solid or liquid radioactive materials in the body that release (mostly gamma) radiation internally. External radiotherapy typically uses X-rays but is moving towards higher LET charged particles such as protons and heavy ions (Durante, Orecchia et al. 2017).</p>
2019-05-03T12:36:362019-05-07T12:12:13Ultraviolet B radiation2017-04-15T16:04:522017-04-15T16:04:52Gamma radiation2017-04-15T16:04:312017-04-15T16:04:31Estrogen2019-05-08T11:40:272019-05-08T11:40:27WikiUser_22all speciesWCS_9606human10116rat10090mouse6239nematodeWCS_7955zebrafish3702thale-cress3349Scotch pineWCS_35525Daphnia magna3055Chlamydomonas reinhardtiiWCS_6396common brandling wormWCS_4472Lemna minor8030Salmo salarIncrease, Programmed cell deathIncrease, Programmed cell deathCellular2021-04-11T09:05:192021-04-12T02:17:32Decrease, ReproductionDecrease, ReproductionIndividual2021-04-11T08:21:372021-04-11T17:38:35Decrease, Population growth rateDecrease, Population growth ratePopulation<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">A population can be defined as a group of interbreeding organisms, all of the same species, occupying a specific space during a specific time (Vandermeer and Goldberg 2003, Gotelli 2008). As the population is the biological level of organization that is often the focus of ecological risk</span> <span style="color:black">assessments, population growth rate (and hence population size over time) is important to consider within the context of applied conservation practices.</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">If N is the size of the population and t is time, then the population growth rate (dN/dt) is proportional to the instantaneous rate of increase, r, which measures the per capita rate of population increase over a short time interval. Therefore, r, is a difference between the instantaneous birth rate (number of births per individual per unit of time; b) and the instantaneous death rate (number of deaths per individual per unit of time; d) [Equation 1]. Because r is an instantaneous rate, its units can be changed via division. For example, as there are 24 hours in a day, an r of 24 individuals/(individual x day) is equal to an r of 1 individual/(individual/hour) (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020). </span></span></span></span></p>
<p style="margin-left:144px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Equation 1: r = b - d</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">This key event refers to scenarios where r < 0 (instantaneous death rate exceeds instantaneous birth rate).</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Examining r in the context of population growth rate:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A population will decrease to extinction when the instantaneous death rate exceeds the instantaneous birth rate (r < 0). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black"> ● The smaller the value of r below 1, the faster the population will decrease to zero. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A population will increase when resources are available and the instantaneous birth rate exceeds the instantaneous death rate (r > 0)</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black"> ● The larger the value that r exceeds 1, the faster the population can increase over time </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A population will neither increase or decrease when the population growth rate equals 0 (either due to N = 0, or if the per capita birth and death rates are exactly balanced). For example, the per capita birth and death rates could become exactly balanced due to density dependence and/or to the effect of a stressor that reduces survival and/or reproduction (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Effects incurred on a population from a chemical or non-chemical stressor could have an impact directly upon birth rate (reproduction) and/or death rate (survival), thereby causing a decline in population growth rate. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● Example of direct effect on r: Exposure to 17b-trenbolone reduced reproduction (i.e., reduced b) in the fathead minnow over 21 days at water concentrations ranging from 0.0015 to about 41 mg/L (Ankley et al. 2001; Miller and Ankley 2004). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Alternatively, a stressor could indirectly impact survival and/or reproduction. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● Example of indirect effect on r: Exposure of non-sexually differentiated early life stage fathead minnow to the fungicide prochloraz has been shown to produce male-biased sex ratios based on gonad differentiation, and resulted in projected change in population growth rate (decrease in reproduction due to a decrease in females and thus recruitment) using a population model. (Holbech et al., 2012; Miller et al. 2022)</span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Density dependence can be an important consideration:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● The effect of density dependence depends upon the quantity of resources present within a landscape. A change in available resources could increase or decrease the effect of density dependence and therefore cause a change in population growth rate via indirectly impacting survival and/or reproduction. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● This concept could be thought of in terms of community level interactions whereby one species is not impacted but a competitor species is impacted by a chemical stressor resulting in a greater availability of resources for the unimpacted species. In this scenario, the impacted species would experience a decline in population growth rate. The unimpacted species would experience an increase in population growth rate (due to a smaller density dependent effect upon population growth rate for that species). </span> </span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Closed versus open systems:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● The above discussion relates to closed systems (there is no movement of individuals between population sites) and thus a declining population growth rate cannot be augmented by immigration. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● When individuals depart (emigrate out of a population) the loss will diminish population growth rate. </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Population growth rate applies to all organisms, both sexes, and all life stages.</span></span></span></span></p>
<p> </p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Population growth rate (instantaneous growth rate) can be measured by sampling a population over an interval of time (i.e. from time t = 0 to time t = 1). The interval of time should be selected to correspond to the life history of the species of interest (i.e. will be different for rapidly growing versus slow growing populations). The population growth rate, r, can be determined by taking the difference (subtracting) between the initial population size, N</span><sub><span style="font-size:9pt"><span style="color:black">t=0 </span></span></sub><span style="color:black">(population size at time t=0), and the population size at the end of the interval, N</span><sub><span style="font-size:9pt"><span style="color:black">t=1 </span></span></sub><span style="color:black">(population size at time t = 1), and then subsequently dividing by the initial population size. </span></span></span></span></p>
<p style="margin-left:96px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Equation 2: r = (N</span><sub><span style="font-size:9pt"><span style="color:black">t=1 </span></span></sub><span style="color:black">- N</span><sub><span style="font-size:9pt"><span style="color:black">t=0</span></span></sub><span style="color:black">) / N</span><sub><span style="font-size:9pt"><span style="color:black">t=0</span></span></sub></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">The diversity of forms, sizes, and life histories among species has led to the development of a vast number of field techniques for estimation of population size and thus population growth over time (Bookhout 1994, McComb et al. 2021). </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● For stationary species an observational strategy may involve dividing a habitat into units. After setting up the units, samples are performed throughout the habitat at a select number of units (determined using a statistical sampling design) over a time interval (at time t = 0 and again at time t = 1), and the total number of organisms within each unit are counted. The numbers recorded are assumed to be representative for the habitat overall, and can be used to estimate the population growth rate within the entire habitat over the time interval. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● For species that are mobile throughout a large range, a strategy such as using a mark-recapture method may be employed (i.e. tags, bands, transmitters) to determine a count over a time interval (at time = 0 and again at time =1). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Population growth rate can also be estimated using mathematical model constructs (for example, ranging from simple differential equations to complex age or stage structured matrix projection models and individual based modeling approaches), and may assume a linear or nonlinear population increase over time (Caswell 2001, Vandermeer and Goldberg 2003, Gotelli 2008, Murray and Sandercock 2020). The AOP framework can be used to support the translation of pathway-specific mechanistic data into responses relevant to population models and output from the population models, such as changing (declining) population growth rate, can be used to assess and manage risks of chemicals (Kramer et al. 2011). As such, this translational capability can increase the capacity and efficiency of safety assessments both for single chemicals and chemical mixtures (Kramer et al. 2011). </span></span></span></span></p>
<p style="text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">Some examples of modeling constructs used to investigate population growth rate:</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A modeling construct could be based upon laboratory toxicity tests to determine effect(s) that are then linked to the population model and used to estimate decline in population growth rate. Miller et al. (2007) used concentration–response data from short term reproductive assays with fathead minnow (<em>Pimephales promelas</em>) exposed to endocrine disrupting chemicals in combination with a population model to examine projected alterations in population growth rate. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A model construct could be based upon a combination of effects-based monitoring at field sites (informed by an AOP) and a population model. Miller et al. (2015) applied a population model informed by an AOP to project declines in population growth rate for white suckers (Catostomus commersoni) using observed changes in sex steroid synthesis in fish exposed to a complex pulp and paper mill effluent in Jackfish Bay, Ontario, Canada. Furthermore, a model construct could be comprised of a series of quantitative models using KERs that culminates in the estimation of change (decline) in population growth rate. </span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● A quantitative adverse outcome pathway (qAOP) has been defined as a mathematical construct that models the dose–response or response–response relationships of all KERs described in an AOP (Conolly et al. 2017, Perkins et al. 2019). Conolly et al. (2017) developed a qAOP using data generated with the aromatase inhibitor fadrozole as a stressor and then used it to predict potential population‐level impacts (including decline in population growth rate). The qAOP modeled aromatase inhibition (the molecular initiating event) leading to reproductive dysfunction in fathead minnow (Pimephales promelas) using 3 computational models: a hypothalamus–pituitary–gonadal axis model (based on ordinary differential equations) of aromatase inhibition leading to decreased vitellogenin production (Cheng et al. 2016), a stochastic model of oocyte growth dynamics relating vitellogenin levels to clutch size and spawning intervals (Watanabe et al. 2016), and a population model (Miller et al. 2007).</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● Dynamic energy budget (DEB) models offer a methodology that reverse engineers stressor effects on growth, reproduction, and/or survival into modular characterizations related to the acquisition and processing of energy resources (Nisbet et al. 2000, Nisbet et al. 2011). Murphy et al. (2018) developed a conceptual model to link DEB and AOP models by interpreting AOP key events as measures of damage-inducing processes affecting DEB variables and rates.</span></span></span></span></p>
<p style="margin-left:48px; text-align:start"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><span style="color:black">● Endogenous Lifecycle Models (ELMs), capture the endogenous lifecycle processes of growth, development, survival, and reproduction and integrate these to estimate and predict expected fitness (Etterson and Ankley, 2021). AOPs can be used to inform ELMs of effects of chemical stressors on the vital rates that determine fitness, and to decide what hierarchical models of endogenous systems should be included within an ELM (Etterson and Ankley, 2021).</span></span></span></span></p>
<p> </p>
<p>Consideration of population size and changes in population size over time is potentially relevant to all living organisms.</p>
Not SpecifiedUnspecificNot SpecifiedAll life stagesHigh<ul>
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</ul>
2016-11-29T18:41:242023-01-03T09:09:06Deposition of EnergyEnergy DepositionMolecular<p><span style="color:#0000ff"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">Deposition of energy refers to events where subatomic particles or electromagnetic radiation deposit energy in the media through which they transverse. The energy may either be sufficient (e.g. ionizing radiation) or insufficient (e.g. non-ionizing radiation) to ionize atoms or molecules (Beir, et al. 1999). </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">Ionizing radiation can cause the ejection of electrons from atoms and molecules, thereby </span></span></span><span style="color:#e74c3c"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">resulting in their ionization and the breakage of chemical bonds</span></span></span><span style="color:#0000ff"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">. The energy of these subatomic particles or electromagnetic waves ranges from 124 KeV to 5.4 MeV, and is dependent on the source and type of radiation (Zyla et al., 2020). Not all electromagnetic radiation is ionizing; as the incident radiation must have sufficient energy to free electrons from the atom or molecule’s electron orbitals. The energy can induce direct and indirect ionization events and </span></span></span><span style="color:#e74c3c"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">can be via internal (injections, inhalation, injection) or external exposure</span></span></span><span style="color:#0000ff"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">. Direct ionization is the principal path where charged particles interact with DNA to cause a biological damage. Photons, which are electromagnetic waves can also cause direct ionization. Indirect ionization produces free radicals of other molecules, specifically water, which can transform to damage critical targets such as DNA (Beir, et al. 1999; </span></span></span><span style="color:#e74c3c"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">Balagamwala et al., 2013</span></span></span><span style="color:#0000ff"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">). Given the fundamental nature of energy deposition by nuclei, nucleons or elementary particles in material, this process is universal to all biological contexts.</span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">Energy deposition is influenced by the linear energy transfer (LET) (Hall and Giaccia, 2018 UNSCEAR, 2020). High LET refers to energy above 10 keV μm-1 which produces more complex, dense structural damage than low LET radiation (below 10 keV μm-1). Low-LET particles produce sparse ionization events such as photons (X- and gamma rays), as well as high-energy protons. Low LET radiation travels farther into tissue but deposits smaller amounts of energy, whereas high LET radiation, which includes heavy ions, alpha particles and high-energy neutrons, does not travel as far but deposits larger amounts of energy into tissue at the same absorbed dose. The biological effect of the deposition of energy can be modulated by varying dose and dose rate of exposure, such as acute, chronic, or fractionated exposures (Hall and Giaccia, 2018). </span></span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px"><span style="color:#e74c3c">Non-ionizing radiation is a type of electromagnetic radiation that lacks the energy to ionize atoms or molecules. Examples of non-ionizing radiation include radio waves (wavelength: 100 km-1m), microwaves (wavelength: 1m-1mm), infrared radiation (wavelength: 1mm- 1 um), visible light (wavelengths: 400-700 nm), and ultraviolet radiation of longer wavelengths such as UVB (wavelengths: 315-400nm) and UVA (wavelengths: 280-315 nm). UVC radiation (X-X nm) is, in contrast to UVB and UVA, considered to be a type of ionizing radiation. Exposure to non-ionizing radiation occurs either from natural or anthropogenic sources, and include radio waves used for communication (broadcasting and cell phones), microwaves used in cooking food and in radar systems, infrared radiation emitted by warm objects or used in remote controls, thermal imaging and medical treatments. Visible light is the range of electromagnetic radiation that we can see and that is commonly used in photosynthesis in primary producers. UV radiation has key functions in melanisation (tanning) of a number of species, and exhibit key signalling roles in navigation and communication (e.g insects, aquatic invertebrates and fish), locomotory and predatory behavior (e.g. reptiles, birds and crustaceans) and growth and development (e.g. plants). UV radiation is also used in some medical treatments such as skin diseases (e.g. psoriasis, eczema, vitiligo and skin cancers). </span></span></span></p>
<table border="1" bordercolor="#ccc" cellpadding="5" cellspacing="0" style="border-collapse:collapse">
<tbody>
<tr>
<td style="background-color:#eeeeee; text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Radiation type</strong></span></span></td>
<td style="background-color:#eeeeee; text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Assay Name</strong></span></span></p>
</td>
<td style="background-color:#eeeeee; text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>References</strong></span></span></p>
</td>
<td style="background-color:#eeeeee; text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Description</strong></span></span></p>
</td>
<td style="background-color:#eeeeee; text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>OECD Approved Assay</strong></span></span></p>
</td>
</tr>
<tr>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Ionizing radiation</span></span></td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Monte Carlo Simulations (Geant4)</span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Douglass et al., 2013; Douglass et al. 2012; <span style="color:#e74c3c">Zyla et al., 2020</span></span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Monte Carlo simulations are based on a computational algorithm that mathematically models the deposition of energy into materials.</span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">No</span></span></p>
</td>
</tr>
<tr>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Ionizing radiation</span></span></td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Fluorescent Nuclear Track Detector (FNTD)</span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Sawakuchi, 2016; Niklas, 2013; Koaira & Konishi, 2015</span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">FNTDs are biocompatible chips with crystals of aluminium oxide doped with carbon and magnesium; used in conjuction with fluorescent microscopy, these FNTDs allow for the visualization and the linear energy transfer (LET) quantification of tracks produced by the deposition of energy into a material.</span></span></p>
</td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">No</span></span></p>
</td>
</tr>
<tr>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Ionizing radiation</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Tissue equivalent proportional counter (TEPC)</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Straume et al, 2015</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Measure the LET spectrum and calculate the dose equivalent.</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">No</span></span></td>
</tr>
<tr>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Ionizing radiation</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">alanine dosimeters/NanoDots</span></span></td>
<td style="text-align:center">
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Lind et al. 2019; Xie et al., 2022</span></span></p>
</td>
<td style="text-align:center"> </td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">No</span></span></td>
</tr>
<tr>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Non-ionizing radiation</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">UV meters or radiameters</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Xie et at., 2020</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">UVA/UVB (irradiance intensity), UV dosimeters (accumulated irradiance over time), Spectrophoto meter (absorption of UV by a substance or material)</span></span></td>
<td style="text-align:center"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">No</span></span></td>
</tr>
</tbody>
</table>
<p> </p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Energy can be deposited into any substrate, both living and non-living; it is independent of age, taxa, sex, or life-stage. </span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Taxonomic applicability: </strong>This MIE is not taxonomically specific. </span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Life stage applicability: </strong>This MIE is not life stage specific. </span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><strong>Sex applicability: </strong>This MIE is not sex specific. </span></span></span></p>
LowUnspecificHighAll life stagesModerateModerateModerateHighHighHighModerateHighModerateModerateHighLow<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Balagamwala, E. H. et al. (2013), “Introduction to radiotherapy and standard teletherapy techniques”,<em> Dev Ophthalmol,</em> Vol. 52, Karger, Basel, https://doi.org/10.1159/000351045 </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Beir, V. et al. (1999), “The Mechanistic Basis of Radon-Induced Lung Cancer”, in <em>Health Risks of Exposure to Radon: BEIR V</em>I, National Academy Press, Washington, D.C., https://doi.org/10.17226/5499 </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Douglass, M. et al. (2013), “Monte Carlo investigation of the increased radiation deposition due to gold nanoparticles using kilovoltage and megavoltage photons in a 3D randomized cell model”<em>, Medical Physics</em>, Vol. 40/7, American Institute of Physics, College Park, https://doi.org/10.1118/1.4808150 </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Douglass, M. et al. (2012), “Development of a randomized 3D cell model for Monte Carlo microdosimetry simulations.”, <em>Medical Physics</em>, Vol. 39/6, American Institute of Physics, College Park, https://doi.org/10.1118/1.4719963 </span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Hall, E. J. and Giaccia, A.J. (2018), <em>Radiobiology for the Radiologist</em>, 8th edition, Wolters Kluwer, Philadelphia. </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Kodaira, S. and Konishi, T. (2015), “Co-visualization of DNA damage and ion traversals in live mammalian cells using a fluorescent nuclear track detector.”, <em>Journal of Radiation Research</em>, Vol. 56/2, Oxford University Press, Oxford, https://doi.org/10.1093/jrr/rru091 </span></span></span></p>
<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Lind, O.C., D.H. Oughton and Salbu B. (2019), "The NMBU FIGARO low dose irradiation facility", <em>International Journal of Radiation Biology</em>, Vol. 95/1, Taylor & Francis, London, https://doi.org/10.1080/09553002.2018.1516906.</span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Sawakuchi, G.O. and Akselrod, M.S. (2016), “Nanoscale measurements of proton tracks using fluorescent nuclear track detectors.”,<em> Medical Physics</em>, Vol. 43/5, American Institute of Physics, College Park, https://doi.org/10.1118/1.4947128 </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Straume, T. et al. (2015), “Compact Tissue-equivalent Proportional Counter for Deep Space Human Missions.”,<em> Health physics,</em> Vol. 109/4, Lippincott Williams & Wilkins, Philadelphia, https://doi.org/10.1097/HP.0000000000000334 </span></span></span></p>
<p><span style="color:#0000ff"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Niklas, M. et al. (2013), “Engineering cell-fluorescent ion track hybrid detectors.”, <em>Radiation Oncology</em>, Vol. 8/104, BioMed Central, London, https://doi.org/10.1186/1748-717X-8-141 </span></span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">UNSCEAR (2020), <em>Sources, effects and risks of ionizing radiation</em>, United Nations. </span></span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">Xie, Li. et al. (2022), "Ultraviolet B Modulates Gamma Radiation-Induced Stress Responses in Lemna Minor at Multiple Levels of Biological Organisation", <em>SSRN</em>, Elsevier, Amsterdam, http://dx.doi.org/10.2139/ssrn.4081705 .</span></span></p>
<p><span style="color:#e74c3c"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Zyla, P.A. et al. (2020)<em>, Review of particle physics: Progress of Theoretical and Experimental Physics,</em> 2020 Edition, Oxford University Press, Oxford. </span></span></span></p>
<p> </p>
<p> </p>
2019-08-22T09:44:232023-04-28T08:40:04Increase, DNA damageIncrease, DNA DamageMolecular<p>DNA nucleotide damage, single, and double strand breaks occur in the course of cellular operations such as DNA repair and replication and can be induced directly and in neighboring “bystander” cells by internal or external stressors like reactive oxygen species, chemicals, and radiation. Ionizing radiation and RONS such as hydroxyl radicals or peroxide can create a range of lesions (a change in molecular structure) in the base of the nucleotide, with guanine particularly vulnerable because of its low redox potential (David, O'Shea et al. 2007). The same stressors can also break the sugar (deoxyribose)-phosphate backbone creating a single strand break. Simultaneous proximal breaks in both strands of DNA form double strand breaks, which are considered to be more destructive and mutagenic than lesions or single strand breaks. Double strand breaks can generate chromosomal abnormalities including changes in chromosomal number, breaks and gaps, translocations, inversions, and deletions (Yang, Craise et al. 1992; Haag, Hsu et al. 1996; Ponnaiya, Cornforth et al. 1997; Yang, Georgy et al. 1997; Unger, Wienberg et al. 2010; Behjati, Gundem et al. 2016; Morishita, Muramatsu et al. 2016).</p>
<p>However, DNA lesions and single strand breaks can also be destructive and mutagenic. Lesions can lead to point mutations (David, O'Shea et al. 2007) or single strand breaks (Regulus, Duroux et al. 2007). Lesions and single strand breaks can also promote the formation of double strand breaks: replication fork collapse and double strand breaks sometimes occur during mitosis when the replisome encounters an unrepaired single strand break (Kuzminov 2001), and clustered lesions and closely opposed single strand breaks can also form double strand breaks (Chaudhry and Weinfeld 1997; Vispe and Satoh 2000; Shiraishi, Shikazono et al. 2017). Complex damage consists of any combination of closely opposed DNA lesions, abasic sites, crosslinks, single, or double strand breaks in proximity. While classically induced by ionizing radiation, there is also evidence that it can be induced by oxidative activity (Sharma, Collins et al. 2016) or even by a single oxidizing particle (Ravanat, Breton et al. 2014). Complex damage is more difficult to repair (Kuhne, Rothkamm et al. 2000; Stenerlow, Hoglund et al. 2000; Pinto, Prise et al. 2005; Rydberg, Cooper et al. 2005).</p>
<p>DNA damage and resulting repair activity can trigger a halt in the cell cycle, cell death (apoptosis), and cause permanent changes to DNA including deletions, translocations, and sequence changes. DNA damage is also associated with an increase in genomic instability - the new appearance of DNA damage including double strand breaks, mutations, and chromosomal damage following repair of initial damage in affected cells or in clonal descendants or neighbors of DNA damaged cells. The mechanism behind this long term DNA damage is not clear, but telomere erosion appears to play a major role (Murnane 2012; Sishc, Nelson et al. 2015). Genomic instability is more common and longer lasting following complex damage (Ponnaiya, Cornforth et al. 1997), and is influenced by multiple factors including variants in DNA repair genes (Ponnaiya, Cornforth et al. 1997; Yu, Okayasu et al. 2001; Yin, Menendez et al. 2012), RONS (Dayal, Martin et al. 2008), estrogen (Kutanzi and Kovalchuk 2013), caspases (Liu, He et al. 2015), and telomeres (Sishc, Nelson et al. 2015).</p>
<p>DNA damage can be studied in isolated DNA, fixed cells, or living cells. Types of damage that can be detected include single and double strand breaks, nucleotide damage, complex damage, and chromosomal or telomere damage. The OECD test guideline for DNA synthesis Test No. 486 (OECD 1997) detects nucleotide excision repair, so it will reflect the formation of bulky DNA adducts but not the majority of oxidative damage to nucleotides, which is typically repaired via the Base Excision Repair pathway. The OECD test guideline alkaline comet assay Test No. 489 (OECD 2016) detects single and double strand breaks, including those arising from repair as well as some (alkali sensitive) nucleotide lesions including some lesions from oxidative damage. OECD tests for chromosomal damage and micronuclei Test No. 473, 475, 483, and 487 measure longer term effects of DNA damage but these tests require the damaged cell to subsequently undergo replication (OECD 2016; OECD 2016; OECD 2016; OECD 2016). They can therefore reflect a wider range of sources of DNA damage including changes in mitosis. Finally, tests for mutations reveal past DNA damage that resulted in a heritable change, and these are described in the key event ‘Increase in Mutation’.</p>
<p>Many other (non-test guideline) techniques have been used to examine specific forms of DNA damage (Table 1). Double strand breaks are commonly reported because of the significant risk attributed to breaks and the relative ease of detecting and quantifying them. Historically, single and double strand breaks were measured using gel electrophoresis, but are now commonly visualized microscopically using fluorescent or other labeled probes for double and single strand break repair such as H2AX and XRCC2. Base lesions can also be detected using labeled probes for base excision repair enzymes, or by chemical methods such as mass spectroscopy. Refinements on these methods can be used to characterize complex or clustered damage, in which various forms of damage occur in close proximity on a DNA molecule (Lorat, Timm et al. 2016; Nikitaki, Nikolov et al. 2016).</p>
<p>Certain challenges are common to all methods of detecting DNA damage. In the time required to initiate the detection method, some DNA may already be repaired, leading to undercounting of damage. On the other hand, apoptotic DSBs may be incorrectly included in a measurement of direct (non-apoptotic) induction of DSB damage unless controlled. All methods have difficulty distinguishing individual components of clustered lesions, and microscopic methods may undercount disparate breaks that are processed together in repair centers (Barnard, Bouffler et al. 2013). Methods that use isolated DNA (gel electrophoresis, analytical chemistry) are vulnerable to artifacts and must ensure that the DNA sample is protected from oxidative damage during extraction (Pernot, Hall et al. 2012; Barnard, Bouffler et al. 2013; Ravanat, Breton et al. 2014).</p>
<p>Table 1. Common methods of detecting DNA damage</p>
<table border="1" cellpadding="0" cellspacing="0">
<tbody>
<tr>
<td style="height:22px; width:127px">
<p><strong>Target</strong></p>
</td>
<td style="height:22px; width:167px">
<p><strong>Name</strong></p>
</td>
<td style="height:22px; width:133px">
<p><strong>Method</strong></p>
</td>
<td style="height:22px; width:211px">
<p><strong>Strengths/Weaknesses</strong></p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Nucleotide damage</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Single cell gel electrophoresis (comet assay) with restriction enzymes (Collins 2004)</p>
</td>
<td style="height:22px; width:133px">
<p>Gel electrophoresis</p>
<p> </p>
</td>
<td style="height:22px; width:211px">
<p>A variant of the comet assay in which restriction enzymes allow the identification of different types of nucleotide damage.</p>
<p>The comet assay is more sensitive than PFGE, detecting damage from 0.1 Gy ionizing radiation (Pernot, Hall et al. 2012). A reproducible high-throughput application of the assay is available (Ge, Prasongtanakij et al. 2014; Sykora, Witt et al. 2018), and the test requires only a small (single cell) sample. Requires destruction of the cell.</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Nucleotide damage</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Labeled probes including Biotrin OxyDNA and anti- 8-oxoguanine-DNA glycosylase (OGG1) for oxidative damage and AP</p>
<p>endonuclease (APE1) for Base Excision Repair of less bulky lesions such as oxidative damage.</p>
</td>
<td style="height:22px; width:133px">
<p>Microscopy, FACS</p>
</td>
<td style="height:22px; width:211px">
<p>Most useful with FACS or other measures of average or relative intensity, as locations and numbers of damaged nucleotides can be difficult to distinguish using fluorescence microscopy. (Ogawa, Kobayashi et al. 2003; Nikitaki, Nikolov et al. 2016).</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Nucleotide damage</strong></p>
</td>
<td style="height:22px; width:167px">
<p>High performance liquid chromatography (HPLC), tandem mass spectrometry (MS/MS)</p>
</td>
<td style="height:22px; width:133px">
<p>Analytical chemistry</p>
</td>
<td style="height:22px; width:211px">
<p>Capable of quantifying low levels of specific nucleotide lesions (Madugundu, Cadet et al. 2014; Ravanat, Breton et al. 2014). Requires destruction of the cell.</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Nucleotide damage</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Unscheduled DNA synthesis test OECD Test Guideline 486 (OECD 1997)</p>
</td>
<td style="height:22px; width:133px">
<p>Autoradiography</p>
</td>
<td style="height:22px; width:211px">
<p>Measures DNA damage that is repaired using Nucleotide Excision Repair - mostly bulky adducts (OECD (Organisation for Economic Co-operation and Development) 2016).</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Non-specific DNA strand breaks</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Single cell gel electrophoresis (comet assay), alkali conditions</p>
<p>OECD Test Guideline 489 (OECD 2016)</p>
</td>
<td style="height:22px; width:133px">
<p>Gel electrophoresis</p>
</td>
<td style="height:22px; width:211px">
<p>When used in alkali conditions, the comet assay reveals single and double strand breaks and alkali-sensitive nucleotide lesions. See single cell gel electrophoresis (comet assay) with restriction enzymes above for further comments. </p>
<p> </p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Single strand breaks</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Labeled probe pXRCC1 (Lorat, Brunner et al. 2015)</p>
</td>
<td style="height:22px; width:133px">
<p>Microscopy</p>
</td>
<td style="height:22px; width:211px">
<p>Fluorescent probes can label single strand breaks in cells, while immunogold labeling is able to distinguish multiple single strand breaks in clusters (Lorat, Timm et al. 2016; Nikitaki, Nikolov et al. 2016).</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Double strand breaks</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Single cell gel electrophoresis (comet assay), neutral conditions</p>
</td>
<td style="height:22px; width:133px">
<p>Gel electrophoresis</p>
</td>
<td style="height:22px; width:211px">
<p>Neutral conditions help minimize the release of single strand breaks coiled DNA and alkali lesions, allowing the measurement of double strand breaks. Since single strand breaks can still appear, assay is not very sensitive or specific to double strand breaks (Pernot, Hall et al. 2012). See single cell gel electrophoresis (comet assay) with restriction enzymes above for further comments.</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Double strand breaks</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Pulsed field gel electrophoresis (PFGE)</p>
</td>
<td style="height:22px; width:133px">
<p>Gel electrophoresis</p>
</td>
<td style="height:22px; width:211px">
<p>Permits the quantitative measurement of double strand breaks, and can be combined with immunoblotting to detect DNA-associated proteins (Lobrich, Rydberg et al. 1995; Kawashima, Yamaguchi et al. 2017). Considered less sensitive than comet assay, but detected damage from 0.25 Gy ionizing radiation (Gradzka and Iwanenko 2005). Requires destruction of the cell.</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Double strand breaks</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Labeled probes including phosphorylated H2AX, 53BP1, Ku70, ATM (Lorat, Brunner et al. 2015)</p>
</td>
<td style="height:22px; width:133px">
<p>Microscopy</p>
</td>
<td style="height:22px; width:211px">
<p>Fluorescent probes can label individual double breaks in cells allowing for quantification, with immunogold labeling resolving breaks in clusters (Lorat, Timm et al. 2016; Nikitaki, Nikolov et al. 2016). Sensitive: detects damage from 0.001 Gy ionizing radiation (Rothkamm and Lobrich 2003; Ojima, Ban et al. 2008).</p>
</td>
</tr>
<tr>
<td style="height:22px; width:127px">
<p><strong>Chromosomal damage</strong></p>
</td>
<td style="height:22px; width:167px">
<p>Chromosomal aberrations and micronuclei</p>
<p>OECD Test Guidelines 473, 475, 483, and 487 (OECD 2016; OECD 2016; OECD 2016; OECD 2016)</p>
</td>
<td style="height:22px; width:133px">
<p>Microscopy</p>
</td>
<td style="height:22px; width:211px">
<p>Detects major DNA damage resulting from large breaks and rearrangements, or mitotic failures. Damage does not appear until DNA undergoes mitosis, so slower and limited to damage in replicating cells. Insensitive tosmall deletions and substitutions.</p>
</td>
</tr>
</tbody>
</table>
CL:0000255eukaryotic cell<p><a name="_ENREF_1">Barnard, S., S. Bouffler, et al. (2013). "The shape of the radiation dose response for DNA double-strand break induction and repair." Genome integrity 4(1): 1.</a></p>
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<p><a name="_ENREF_8">Gradzka, I. and T. Iwanenko (2005). "A non-radioactive, PFGE-based assay for low levels of DNA double-strand breaks in mammalian cells." DNA repair 4(10): 1129-1139.</a></p>
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<p><a name="_ENREF_10">Kawashima, Y., N. Yamaguchi, et al. (2017). "Detection of DNA double-strand breaks by pulsed-field gel electrophoresis." Genes to cells : devoted to molecular & cellular mechanisms 22(1): 84-93.</a></p>
<p><a name="_ENREF_11">Kuhne, M., K. Rothkamm, et al. (2000). "No dose-dependence of DNA double-strand break misrejoining following alpha-particle irradiation." International journal of radiation biology 76(7): 891-900.</a></p>
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<p><a name="_ENREF_13">Kuzminov, A. (2001). "Single-strand interruptions in replicating chromosomes cause double-strand breaks." Proceedings of the National Academy of Sciences of the United States of America 98(15): 8241-8246.</a></p>
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<p><a name="_ENREF_15">Lobrich, M., B. Rydberg, et al. (1995). "Repair of x-ray-induced DNA double-strand breaks in specific Not I restriction fragments in human fibroblasts: joining of correct and incorrect ends." Proceedings of the National Academy of Sciences of the United States of America 92(26): 12050-12054.</a></p>
<p><a name="_ENREF_16">Lorat, Y., C. U. Brunner, et al. (2015). "Nanoscale analysis of clustered DNA damage after high-LET irradiation by quantitative electron microscopy--the heavy burden to repair." DNA repair 28: 93-106.</a></p>
<p><a name="_ENREF_17">Lorat, Y., S. Timm, et al. (2016). "Clustered double-strand breaks in heterochromatin perturb DNA repair after high linear energy transfer irradiation." Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology 121(1): 154-161.</a></p>
<p><a name="_ENREF_18">Madugundu, G. S., J. Cadet, et al. (2014). "Hydroxyl-radical-induced oxidation of 5-methylcytosine in isolated and cellular DNA." Nucleic acids research 42(11): 7450-7460.</a></p>
<p><a name="_ENREF_19">Morishita, M., T. Muramatsu, et al. (2016). "Chromothripsis-like chromosomal rearrangements induced by ionizing radiation using proton microbeam irradiation system." Oncotarget 7(9): 10182-10192.</a></p>
<p><a name="_ENREF_20">Murnane, J. P. (2012). "Telomere dysfunction and chromosome instability." Mutation research 730(1-2): 28-36.</a></p>
<p><a name="_ENREF_21">Nikitaki, Z., V. Nikolov, et al. (2016). "Measurement of complex DNA damage induction and repair in human cellular systems after exposure to ionizing radiations of varying linear energy transfer (LET)." Free radical research 50(sup1): S64-S78.</a></p>
<p><a name="_ENREF_22">OECD (1997). Test No. 486: Unscheduled DNA Synthesis (UDS) Test with Mammalian Liver Cells in vivo.</a></p>
<p><a name="_ENREF_23">OECD (2016). Test No. 473: In Vitro Mammalian Chromosomal Aberration Test.</a></p>
<p><a name="_ENREF_24">OECD (2016). Test No. 475: Mammalian Bone Marrow Chromosomal Aberration Test.</a></p>
<p><a name="_ENREF_25">OECD (2016). Test No. 483: Mammalian Spermatogonial Chromosomal Aberration Test.</a></p>
<p><a name="_ENREF_26">OECD (2016). Test No. 487: In Vitro Mammalian Cell Micronucleus Test.</a></p>
<p><a name="_ENREF_27">OECD (2016). Test No. 489: In Vivo Mammalian Alkaline Comet Assay.</a></p>
<p><a name="_ENREF_28">OECD (Organisation for Economic Co-operation and Development) (2016). Overview of the set of OECD Genetic Toxicology Test Guidelines and updates performed in 2014–2015. No. 238.</a></p>
<p><a name="_ENREF_29">Ogawa, Y., T. Kobayashi, et al. (2003). "Radiation-induced oxidative DNA damage, 8-oxoguanine, in human peripheral T cells." International journal of molecular medicine 11(1): 27-32.</a></p>
<p><a name="_ENREF_30">Ojima, M., N. Ban, et al. (2008). "DNA double-strand breaks induced by very low X-ray doses are largely due to bystander effects." Radiation research 170(3): 365-371.</a></p>
<p><a name="_ENREF_31">Pernot, E., J. Hall, et al. (2012). "Ionizing radiation biomarkers for potential use in epidemiological studies." Mutation research 751(2): 258-286.</a></p>
<p><a name="_ENREF_32">Pinto, M., K. M. Prise, et al. (2005). "Evidence for complexity at the nanometer scale of radiation-induced DNA DSBs as a determinant of rejoining kinetics." Radiation research 164(1): 73-85.</a></p>
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<p><a name="_ENREF_35">Ravanat, J. L., J. Breton, et al. (2014). "Radiation-mediated formation of complex damage to DNA: a chemical aspect overview." Br J Radiol 87(1035): 20130715.</a></p>
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<p><a name="_ENREF_37">Rothkamm, K. and M. Lobrich (2003). "Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses." Proceedings of the National Academy of Sciences of the United States of America 100(9): 5057-5062.</a></p>
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2016-11-29T18:41:302019-05-08T12:28:464afa2700-ec07-4ec7-b177-1b1a965661b25f1212e4-be79-4c30-8e33-0fbca81a900f2022-01-21T07:18:452022-01-21T07:18:455f1212e4-be79-4c30-8e33-0fbca81a900f2e3a71a2-9d58-43fa-bc55-12847cf714932021-04-11T09:21:032021-04-11T09:21:032e3a71a2-9d58-43fa-bc55-12847cf71493c4fd2694-ca67-4c5b-bfd1-d273b55f99422022-01-21T07:19:532022-01-21T07:19:53c4fd2694-ca67-4c5b-bfd1-d273b55f994240e48d7c-874d-425f-adf8-e832d62f84b72021-04-11T08:26:552021-04-11T08:26:55Deposition of ionising energy leading to population decline via programmed cell deathDNA damage leading to population decline via programmed cell death<h3 style="text-align:justify"><span style="font-size:11pt"><span style="background-color:white"><span style="font-family:"等线 Light""><span style="color:#4472c4"><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black">Li Xie<sup>1,3</sup>, You Song<sup>1</sup> and Knut Erik </span></span></span><a href="https://www.google.no/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0ahUKEwju4ty69sXMAhWEVywKHQHMAVEQFggcMAA&url=http%3A%2F%2Fwww.niva.no%2Fse-ansatt%3Fnavn%3DKnut-Erik%2520Tollefsen&usg=AFQjCNEcD7iL_TI4IPB7RrXApxFvdea9ZA&sig2=W3HomTsh5RonGjOyuROqOQ"><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black">Tollefsen</span></span></span></a><sup><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"><span style="color:black">1,2,3</span></span></span></sup></span></span></span></span></h3>
<p><span style="font-size:11pt"><span style="font-family:等线"><sup><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif">1</span></span></sup><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"> Norwegian Institute for Water Research (NIVA), Section of Ecotoxicology and Risk Assessment, Gaustadalléen 21, N-0349 Oslo, Norway</span></span></span></span></p>
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:等线"><sup><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif">2</span></span></sup><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif"> Norwegian University of Life Sciences (NMBU), Faculty of Environmental Sciences and Natural Resource Management (MINA), P.O. Box 5003, N-1432 Ås, Norway</span></span></span></span></p>
<p><span style="font-size:11pt"><span style="font-family:等线"><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif">3. </span></span><span style="font-size:12.0pt"><span style="font-family:"Times New Roman",serif">Centre for Environmental Radioactivity, Norwegian University of Life Sciences (NMBU), Post box 5003, N-1432 Ås, Norway</span></span></span></span></p>
Under development: Not open for comment. Do not cite<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:10.5pt">Ionising and non-ionizing radiation </span></span><span style="font-size:10.5pt"> can induce DNA damage (strand breaks, abatic sites, oxidized bases, and DNA-proteincross-links</span>) <span style="font-size:10.5pt">in cells of primary producers. Excessive DNA strand breaks can trigger programmed cell death leading to reduction in development (size and weight) and/or reproduction (number of organisms and/or leaves) to reduce the overall population.</span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">It is well documented that ionizing radiation( (eg. X-rays, gamma, photons, alpha, beta, neutrons, heavy ions) leads to energy deposition on the atoms and molecules of the substrate. Many studies, have demonstrated that the type of radiation and distance from source has an impact on the pattern of energy deposition (Alloni, et al. 2014). High linear energy transfer (LET) radiation has been associated with higher-energy deposits (Liamsuwan et al., 2014) that are more densely-packed and cause more complex effects within the particle track (Hada and Georgakilas, 2008; Okayasu, 2012ab; Lorat et al., 2015; Nikitaki et al., 2016) in comparison to low LET radiation. Parameters such as mean lineal energy, dose mean lineal energy, frequency mean specific energy and dose mean specific energy can impact track structure of the traversed energy into a medium (Friedland et al., 2017)</span></span><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:12px">. The detection of energy deposition by ionizing radiation can be demonstrated with the use of fluorescent nuclear track detectors (FNTDs). FNTDs used in conjunction with fluorescent microscopy, are able to visualize radiation tracks produced by ionizing radiation (Niklas et al., 2013; Kodaira et al., 2015; Sawakuchi and Akselrod, 2016). In addition, these FNTD chips can quantify the LET of primary and secondary radiation tracks up to 0.47 keV/um (Sawakuchi and Akselrod, 2016). This co-visualization of the radiation tracks and the cell markers enable the mapping of the radiation trajectory to specific cellular compartments, and the identification of accrued damage (Niklas et al., 2013; Kodaira et al., 2015). There are no known chemical initiators or prototypes that can mimic the MIE.</span></span></p>
<p>Maintenance of sustainable fish and wildlife populations (i.e., adequate to ensure long-term delivery of valued ecosystem services) is a widely accepted regulatory goal upon which risk assessments and risk management decisions are based.</p>
adjacentHighHighadjacentHighHighadjacentHighHighadjacentHighHigh<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:14px">The essentiality of all key events was considered as Moderate to High. Essentiality evaluations were mainly based on specifically designed studies demonstrating the expected effect pattern predicted by the AOP to occur after exposure to Cobalt-60 external radiation (ionising radiation) and Ultraviolet B radiation (UVB) .</span></span></p>
HighUnspecificLowHermaphroditeNot SpecifiedAll life stagesHighAdult, reproductively matureHigh<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:14px"><span style="background-color:#ffffff">The evidence for the MIE, KE and AO were considered Moderate to High for all Key Events and Key Event Relationships. The overall assessment of the AOP were considered Moderate. </span></span></span></p>
<p><span style="font-size:14px"><strong><span style="background-color:#ffffff">Taxonomic: </span></strong><span style="background-color:#ffffff">all primary producers</span><strong><span style="background-color:#ffffff"> </span></strong></span></p>
<p><span style="font-size:14px"><span style="background-color:#ffffff"><strong>Life stage</strong>: all stage<strong>s</strong></span></span></p>
<p><span style="font-size:14px"><span style="background-color:#ffffff"><strong>Sex:</strong> both genders (</span></span>dioecious plants) and not relevant (hermaphrodites)</p>
<p><span style="font-size:14px"><span style="background-color:#ffffff"><strong>Stressors</strong>: Ionizing radiation, Ultraviolet B radiation (UVB)</span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:14px">The essentiality of all key events was considered as Moderate to High. Essentiality evaluations were mainly based on specifically designed studies demonstrating the expected effect pattern predicted by the AOP to occur after exposure to Cobalt-60 external radiation (ionising radiation) and Ultraviolet B radiation (UVB) .</span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:14px"><strong>Biological Plausibility: </strong></span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:11pt"><strong><span style="font-size:10.5pt"><span style="background-color:white"><span style="color:#212529">Empirical Evidence:</span></span></span></strong></span></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><strong><span style="font-size:14px">Overall confidence in the AOP: </span></strong></span></p>
<p><span style="font-family:Arial,Helvetica,sans-serif"><span style="font-size:14px">Quantitative data were generated in studies with <em>Lemna minor</em> and the freshwater algae <em>Chlamydomonas reinhardtii</em> exposed to external gamma radiation from a Cobalt-60 source (ionizing radiation) and artificial UVB (non-ionizing radiation). The quantitative understanding of the AOP was therefore considered to be Moderate for these species.</span></span></p>
HighHighHigh<p><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif">Xie, L., Solhaug, K. A., Song, Y., Brede, D. A., Lind, O. C., Salbu, B., & Tollefsen, K. E. (2019). Modes of action and adverse effects of gamma radiation in an aquatic macrophyte Lemna minor. <em>Science of the Total Environment</em>, <em>680</em>, 23-34.</span></span></p>
<p style="text-align:justify"><span style="font-size:12px"><span style="font-family:Arial,Helvetica,sans-serif"><span style="background-color:white"><span style="color:#222222">Xie, L., Solhaug, K. A., Song, Y., Johnsen, B., Olsen, J. E., & Tollefsen, K. E. (2020). Effects of artificial ultraviolet B radiation on the macrophyte Lemna minor: a conceptual study for toxicity pathway characterization. </span></span><em>Planta</em>, <em>252</em>(5), 1-18.</span></span></p>
2021-04-11T08:57:582023-04-29T13:02:19