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Mitochondrial glutathione (mGSH) is the critical mitochondrial pool of the antioxidant tripeptide glutathione, acting as the primary line of defense against mitochondrial oxidative stress and maintaining the mitochondrial redox environment[1][2][4][6]. mGSH supports detoxification of hydrogen peroxide and lipid hydroperoxides via enzymes such as glutathione peroxidases and glutathione-S-transferases, regulates protein redox states, and is key in mitochondrial energy production, cell death regulation, and iron–sulfur cluster biogenesis[1][2][6]. Impaired mGSH levels or altered redox status are implicated in multiple diseases, including metabolic, hepatic, neurodegenerative, and cardiovascular disorders, making the measurement of mitochondrial glutathione status a useful biomarker in research and potential therapeutic interventions[4][5][6].
Antioxidant supplementation increases reduced GSH pool (e.g., glutathione, N-acetylcysteine); Prevention of ROS-induced mitochondrial dysfunction; Ferroptosis inhibition (by maintaining GSH levels)
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