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Key Event Title
|Level of Biological Organization|
Key Event Components
|neuron death in response to oxidative stress||increased|
Key Event Overview
AOPs Including This Key Event
Key Event Description
How It Is Measured or Detected
Methods that have been previously reviewed and approved by a recognized authority should be included in the Overview section above. All other methods, including those well established in the published literature, should be described here. Consider the following criteria when describing each method: 1. Is the assay fit for purpose? 2. Is the assay directly or indirectly (i.e. a surrogate) related to a key event relevant to the final adverse effect in question? 3. Is the assay repeatable? 4. Is the assay reproducible?
It is possible to use several markers of neuronal cytoskeleton (e.g. : neurofimanent proteins, NF-L, -M, -H), synapses (e.g.: synaptophysin), neurotransmitters or enzymes involved in neurotransmitter synthesis (e.g.: thyrosine hydroxylase) and look for changes at the mRNA level with quantitative RT-PCR and at the protein level, with immunoblotting (ex. thyrosine hydroxylase, NF-L,-M,-H), immunocytochemistry followed by a quantification, or by enzymatic assays (e.g.: choline acetyltransferase, glutamic acid decarboxylase). Genomic, proteomic and metabolomic approaches are also suitable for a non targeted approach. All these techniques are widely used, but for a recent description in the context of neurotoxicology and neuroinflammation, see Sandström et al., 2014, von Tobel et al., 2014, Monnet-Tschudi et al., 2000).
Domain of Applicability
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