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Consequently, chronic alcohol consumption is a major contributor to oxidative stress, which not only promotes ROS production but also disrupts the redox system homeostasis of the body
EAAC1 -/- (KO) mice were descendants of the strain established by Peghini et al
Among these, selenium-dependent glutathione peroxidase 4 (GPX4) is crucial for preventing ferroptosis by detoxifying phospholipid hydroperoxide into the corresponding phospholipid alcohol at the expense of glutathione (GSH) [12,13,14,15]
