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In mammalian tissues, they also serve as scavengers of oxygen free radicals, effectively preventing oxidative stress-induced mitochondrial damage and mitochondria-dependent apoptosis in a variety of cell types 32,33,34
The idea is supported by maintenance of functional GSH/GSSG levels by Sp in BSO and neurotoxin treated cells as compared to untreated ones which showed a significant decline in the antioxidant ratio probably, due to enhanced formation of glutathionequinones 43
[1] [2] Baseline patient characteristics significantly affect side effect duration and severity
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Oxidative stress can induce the misfolding and oligomerization of alpha-synuclein, contributing to its accumulation and the formation of toxic aggregates [162]
