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Oxidative stress and free radicals, inflammation, and mitochondrial dysfunction have recently been shown to play key roles in the development of OCD [4, 5]

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226 unfortunately, however, AOAA was shown to also inhibit CSE activity

Glutathione might inhibit the effects of cerebral infarction and enhance antiapoptotic signaling after ischemic stroke, suggesting that GSH may be a potent therapeutic antioxidant that can attenuate severe pathologies after ischemic stroke, and stimulating GSH synthesis through administration of GSH precursors and micronutrients like selenium can optimize GSH and GSH peroxidase for optimal antioxidant defense in cerebral ischemia (155, 156)