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The disruption of cardiovascular and renal function by environmental toxicants remains a major concern in toxicological research, particularly when such agents interfere with biochemical markers essential for assessing organ integrity. Among these toxic agents, exposure to sodium
arsenite poses a serious threat due to its ability to induce acute myocardial injury and impair renal filtration processes. This study evaluated the potential of vitamin E to counteract these toxic effects in male Wistar rats, focusing exclusively on validated clinical biomarkers of cardiac
and renal injury. Rats exposed to sodium arsenite (Group C) showed a pronounced rise in cardiac troponin (59.24 ± 3.8 pg/mL) and CK-MB (62.30 ± 2.1 U/L), indicating significant myocardial cell damage relative to the control group. The nephrotoxic impact was equally evident, as reflected by elevated serum urea (24.49 ± 1.8 mg/dL) and creatinine (1.98 ± 0.1 mg/dL), demonstrating impaired glomerular filtration and reduced renal functional capacity. Administration of vitamin E showed a clear dose-dependent protective effect. Rats receiving 25 mg/kg (Group D) and 50 mg/kg (Group E) of vitamin E along with sodium arsenite experienced significant reductions in cardiac troponin (48.65 ± 2.2 and 40.04 ± 2.9 pg/mL) and CK-MB
(41.17 ± 2.9 and 31.02 ± 1.2 U/L), indicating decreased myocardial damage. Renal biomarkers also improved, with urea decreasing to 16.08 ± 1.6 and 10.20 ± 1.7 mg/dL, and creatinine dropping to 1.08 ± 0.1 and 0.88 ± 0.1 mg/dL in Groups D and E, respectively. These results highlight vitamin E’s ability to protect both cardiac and renal functions despite ongoing toxic exposure. Overall, this study shows that vitamin E provides significant cardioprotective and
nephroprotective effects, mainly by normalizing key biomarkers of myocardial and renal dysfunction in rats exposed to sodium arsenite.
arsenite poses a serious threat due to its ability to induce acute myocardial injury and impair renal filtration processes. This study evaluated the potential of vitamin E to counteract these toxic effects in male Wistar rats, focusing exclusively on validated clinical biomarkers of cardiac
and renal injury. Rats exposed to sodium arsenite (Group C) showed a pronounced rise in cardiac troponin (59.24 ± 3.8 pg/mL) and CK-MB (62.30 ± 2.1 U/L), indicating significant myocardial cell damage relative to the control group. The nephrotoxic impact was equally evident, as reflected by elevated serum urea (24.49 ± 1.8 mg/dL) and creatinine (1.98 ± 0.1 mg/dL), demonstrating impaired glomerular filtration and reduced renal functional capacity. Administration of vitamin E showed a clear dose-dependent protective effect. Rats receiving 25 mg/kg (Group D) and 50 mg/kg (Group E) of vitamin E along with sodium arsenite experienced significant reductions in cardiac troponin (48.65 ± 2.2 and 40.04 ± 2.9 pg/mL) and CK-MB
(41.17 ± 2.9 and 31.02 ± 1.2 U/L), indicating decreased myocardial damage. Renal biomarkers also improved, with urea decreasing to 16.08 ± 1.6 and 10.20 ± 1.7 mg/dL, and creatinine dropping to 1.08 ± 0.1 and 0.88 ± 0.1 mg/dL in Groups D and E, respectively. These results highlight vitamin E’s ability to protect both cardiac and renal functions despite ongoing toxic exposure. Overall, this study shows that vitamin E provides significant cardioprotective and
nephroprotective effects, mainly by normalizing key biomarkers of myocardial and renal dysfunction in rats exposed to sodium arsenite.
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