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The deficit of GSH may result in a type of cell death called ferroptosis. The application of an iron chelator almost completely reverses ferroptosis which can be explained by the prevention of intralysosomal iron accumulation and leads to the suppression of induced oxidative stress permeabilization of lysosomal membranes ( In this work, we showed that intraperitoneal administration of exogenous glutathione restored mitochondrial redox status and improved the function of the cardiovascular system of old rats

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