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Based on their findings, Kannan and colleagues hypothesized that the Na + -dependent GSH transporter may be operational for uphill transport of GSH while the Na + -independent GSH transporter may be operational bidirectionally and involved in GSH efflux [37]

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This process is particularly relevant in the context of diabetic patients, where clinical studies have demonstrated that elevated mitochondrial ROS levels can inactivate Nrf2 (24), thereby disrupting spindle assembly