This study investigates the role of vitamin E in mitigating the oxidative stress induced by tramadol in male rabbits, as measured by thiobarbituric acid-reactive substances (TBARS) levels in blood, brain, and testes tissues. TBARS levels serve as a reliable indicator of lipid peroxidation and oxidative damage. Tramadol administration significantly increased blood TBARS levels from 2.60 ± 0.017 nmol/ml in the control group to 3.128 ± 0.095 nmol/ml (p < 0.05), reflecting heightened oxidative stress. Vitamin E treatment reduced TBARS levels to 1.69 ± 0.043 nmol/ml, demonstrating its potent antioxidant capacity. In the tramadol + vitamin E group, TBARS levels were moderately reduced to 2.75 ± 0.036 nmol/ml, indicating partial mitigation of oxidative stress. Tramadol treatment elevated brain TBARS levels from 43.8 ± 1.01 nmol/gT in the control group to 48.6 ± 2.02 nmol/gT, indicating oxidative damage to brain lipids. Vitamin E alone reduced TBARS to 39.7 ± 0.71 nmol/gT, showing neuroprotective effects. The tramadol + vitamin E group showed intermediate TBARS levels of 44.38 ± 1.42 nmol/gT, reflecting partial oxidative stress alleviation. Tramadol significantly increased TBARS levels in testes tissue from 13.8 ± 0.69 nmol/gT in controls to 24.0 ± 1.17 nmol/gT (p < 0.05), indicating testicular oxidative stress. Vitamin E treatment reduced TBARS to 11.2 ± 0.23 nmol/gT, while the tramadol + vitamin E group exhibited moderate levels of 14.3 ± 1.70 nmol/gT, suggesting protective effects on reproductive tissue. Tramadol induces significant oxidative stress across all studied tissues, as evidenced by elevated TBARS levels. Vitamin E effectively reduces lipid peroxidation and oxidative damage, highlighting its potential as a therapeutic antioxidant. While the combination of tramadol and vitamin E ameliorates oxidative stress, it does not fully restore TBARS levels to normal. These findings underscore the value of vitamin E in managing oxidative stress associated with tramadol use.
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