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This overload of ROS directly causes lipid peroxidation of the mitochondrial membranes, leading to the persistent opening of the inner membrane permeability transition pores and resulting in a decline in adenosine triphosphate (ATP) synthesis efficiency ( 2+ , resulting in the viability of nucleus pulposus cells recovering from 41% to 78% ( Mitochondrial dysfunction constitutes a core mechanism of energy metabolism imbalance, characterised by decreased activity of mitochondrial complexes I and III and increased electron leakage ( Dysregulation of epigenetic regulation exacerbates oxidative stress, as evidenced by increased methylation of the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter, resulting in reduced Nrf2 expression

The obesogen tributyltin induces abnormal ovarian adipogenesis in adult female rats

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ISC binding cysteine residues mutation results in nuclease activity and ATPase function defects in DNA2

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