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These oxidized phosphatidylcholines contribute to ferroptosis by disturbing mitochondrial function and suppressing GPX4 activity, shown in cardiomyocytes during ischemia-reperfusion injury [54]

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Indeed, inhibition of enzymatic antioxidants and accumulation of excess levels of ROS generate OS in the ovary that directly affects oocyte quality and thereby reproductive outcome[10,14,64,65]