Scholarlink

<p>Reno-cardiac syndrome or toxicity, a significant global health concern, involves underlying factors like inflammation, programmed cell death, and oxidative stress. Arsenic, a pervasive environmental contaminant, poses significant health risks to vertebrates due to its widespread distribution. Acute exposure has been associated with cardiovascular disorders and, more recently, renal dysfunction, contributing to increased morbidity and mortality. This study is designed to evaluate whether low-dose vitamin E (α-tocopherol) supplementation mitigates arsenic-induced reno-cardiac toxicity and elucidate the molecular mechanisms underlying its protective effects. Thirty-five adult male Wistar rats were randomly assigned into five groups of seven animals each and orally administered vitamin E (25 and 50&#xa0;mg/kg) for 7 days prior to concurrent co-administration of sodium arsenite (10&#xa0;mg/kg) and vitamin E for a further 7 consecutive days. Animals challenged with sodium arsenite exhibited marked increases in serum creatinine, lactate dehydrogenase, and urea, as well as elevated cardiac biomarkers, including creatine kinase-MB, alkaline phosphatase, antioxidant enzyme activities, and glutathione levels, reducing oxidative stress and inhibiting apoptosis. Notably, vitamin E shifted the Bax/Bcl-2 ratio towards Bcl-2, thereby favouring cell survival. Overall, these findings indicate that vitamin E not only counteracts arsenic-induced oxidative and redox disturbances in renal and cardiac tissues but also modulates the intrinsic apoptotic pathway to confer protective effects.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Low-dose vitamin E (α-tocopherol) modulates acute sodium arsenite-induced renocardiac toxicity by inhibiting oxidative stress and apoptosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月16日

查看全文
  • Omorede Ikponmwosa-Eweka,
  • Ikenna C. Maduako

摘要

Reno-cardiac syndrome or toxicity, a significant global health concern, involves underlying factors like inflammation, programmed cell death, and oxidative stress. Arsenic, a pervasive environmental contaminant, poses significant health risks to vertebrates due to its widespread distribution. Acute exposure has been associated with cardiovascular disorders and, more recently, renal dysfunction, contributing to increased morbidity and mortality. This study is designed to evaluate whether low-dose vitamin E (α-tocopherol) supplementation mitigates arsenic-induced reno-cardiac toxicity and elucidate the molecular mechanisms underlying its protective effects. Thirty-five adult male Wistar rats were randomly assigned into five groups of seven animals each and orally administered vitamin E (25 and 50 mg/kg) for 7 days prior to concurrent co-administration of sodium arsenite (10 mg/kg) and vitamin E for a further 7 consecutive days. Animals challenged with sodium arsenite exhibited marked increases in serum creatinine, lactate dehydrogenase, and urea, as well as elevated cardiac biomarkers, including creatine kinase-MB, alkaline phosphatase, antioxidant enzyme activities, and glutathione levels, reducing oxidative stress and inhibiting apoptosis. Notably, vitamin E shifted the Bax/Bcl-2 ratio towards Bcl-2, thereby favouring cell survival. Overall, these findings indicate that vitamin E not only counteracts arsenic-induced oxidative and redox disturbances in renal and cardiac tissues but also modulates the intrinsic apoptotic pathway to confer protective effects.