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The most significant finding with respect to GSH status was that rPT cells from one-month diabetic rats exhibited adaptive increases in cellular concentrations of GSH that were accompanied by increases in both mitochondrial GSH transport and mitochondrial respiration

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Another effect was cellular oxidative stress, since its exposure imbalanced the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase, and the phase II detoxifying enzyme glutathione S- transferase (GST) [1]