Organ-specific and time-dependent oxidative damage induced by chronic copper exposure: modulation by vitamin E.

Chronic exposure to copper ions, Cu(II), induces organ-specific oxidative damage and mitochondrial dysfunction, with distinct temporal and biochemical profiles across tissues. This study evaluated the protective effects of vitamin E (α-tocopherol) against Cu(II)-induced phospholipid and protein oxidation, redox imbalance, and bioenergetic disruption in rats. Cu(II) treatment led to early lipid peroxidation in the brain, heart, and lung, followed by delayed oxidative damage in the liver and kidney. Vitamin E effectively prevented phospholipid oxidation in all organs, but its protection against protein oxidation and mitochondrial respiratory impairment was organ-specific and time-dependent. Mitochondrial respiration declined in brain and heart tissues, with partial recovery in the heart after prolonged vitamin E supplementation. Electron transport chain activity was altered by Cu(II), notably with increased complex I activity in the liver and decreased complex I and II activity in the lung and kidney. Vitamin E failed to prevent these changes in most tissues. Glutathione modulation revealed adaptive redox responses in the lung and oxidative depletion in kidney. These findings highlight the complexity of Cu(II)-induced oxidative damage and the limited but significant protective role of vitamin E, emphasizing the need for targeted antioxidant strategies to preserve mitochondrial integrity and cellular function under metal-induced stress.