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Insulin binding causes autophosphorylation of its receptor, resulting in activation and subsequent tyrosine phosphorylation of insulin receptor substrates and binding of the p85 regulatory subunit of phosphatidyl inositol kinase-3 (PI3K)

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Studies have shown that there is a close relationship between the survival of the mitochondrial GSH pool (mGSH) and that of the cells due to the central role of mitochondria in programmed cell death (apoptosis) as well as important involvement of ROS produced at 90% in mitochondria [17]