Abstract
Most optic nerve injuries are axonal. Neurotrophin deprivation induces death of retinal ganglion cells (RGCs) in such cases, but this is probably not the only mechanism that causes their death. Various fluorophores and agents that block mitochondrial electron transport have been used to show that superoxide generated in the mitochondrial electron transport chain could act, in addition to neurotrophin deprivation, to signal cell death after axonal injury. More specifically, sulphydryls--probably on proteins--are downstream regulators of this signalling pathway, as shown by the neuroprotective effects of inhibition of sulphydryl oxidation by tris(2-carboxyethyl)phosphine in in vivo rat models. Other tools used to study early events in RGC death include novel reducing agents, inducible superoxide dismutase, and differentiation of the RGC-5 cell line.
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