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Role of oxidative stress in pathophysiology of nonalcoholic fatty liver disease

It is possible that the recovery of glutathione levels may enhance the survival of affected neurons, either by increasing synthesis of GSH or by slowing its degradation [25]

GSH, the most abundant antioxidant in the heart, plays a fundamental role in normalizing a redox homeostatic mechanism that was shifted toward oxidative or reductive stress

In addition, the time of shift from receptor blockade to supersensitivity coincides rather closely with the shift from increased to decreased DA synthesis [164]

This observation means that xCT blockage induces the accumulation of glutamate that is converted into -ketoglutarate instead of being used in glutamate-cysteine exchange and consequently that is why cysteine does not enter the cell and give rise to glutathione

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