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Objective <p>Cobalt is an essential nutrient for humans and animals due to its presence and involvement in the synthesis of vitamin B<sub>12</sub> (cobalamin). However, toxicity could arise from chronic exposure or high dosages, thereby impacting negatively on organ functions such as heart and kidney. This study aimed to ascertain if rutin and vitamin E could reverse cobalt chloride-induced cardiorenal toxicity.</p> Methods <p>Thirty-five (35) male Wistar rats were divided randomly into five groups of seven rats each as follows: Group A-Control (clean water only), Group B-Cobalt chloride (300&#xa0;ppm) (CoCl<sub>2</sub>) only in drinking water, Group C-Rutin (100&#xa0;mg/kg) and cobalt chloride (300&#xa0;ppm) (R<sub>1</sub> + CoCl<sub>2</sub>), Group D-Rutin (200&#xa0;mg/kg) and cobalt chloride (300&#xa0;ppm) (R<sub>2</sub> + CoCl<sub>2</sub>), and Group E-Vitamin E (50&#xa0;mg/kg) and cobalt chloride (300&#xa0;ppm) (Vit. E + CoCl<sub>2</sub>); all for 7&#xa0;days. At the end of the experiment, blood pressure parameters were taken, cardiac and renal biomarkers of oxidative stress and antioxidant, histology, and immunohistochemistry were determined.</p> Results <p>Elevated blood pressure in Cobalt Chloride (CoCl<sub>2</sub>) group reduced significantly in dose dependency in treated CoCl<sub>2</sub> groups with vitamin E and Rutin. At the end of the experiment, administration of CoCl<sub>2</sub> to rats showed a significant increase in the blood pressure parameters when compared to the control, respectively. Also, CoCl<sub>2</sub> administration altered the activity and concentration of cardiac, and renal antioxidant markers, and serum levels of nitric oxide, hydrogen peroxide and malondialdehyde while rutin and vitamin E ameliorated this effect in a dose-dependent manner. Little or no visible lesion was observed in groups treated with rutin and vitamin E following histopathological assessment of the heart and kidney tissue. The immunopositivity of cardiac troponin, renal mineralocorticoid receptor and nuclear factor kappa beta was low in groups exposed to rutin and Vitamin E.</p> Conclusion <p>Cobalt chloride has been shown to induce cardio and renal toxicity and this study was able to show the ameliorative effect of rutin and vitamin E in a dose-dependent manner.</p>

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Rutin and vitamin E restore cobalt chloride-induced cardiorenal toxicity

  • 期刊论文

  • 发表日期：

    2025年10月23日

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  • Ebunoluwa Racheal Asenuga,
  • Omolola Victoria Awoyomi,
  • Temitayo Olabisi Ajibade,
  • Oluwaseun Olanrewaju Esan,
  • Moses Olusola Adetona,
  • Taiwo Olaide Oyagbemi,
  • Adewumi Victoria Adeogun,
  • Olumayowa Olawumi Igado,
  • Ebenezer Oyedele Ajiboye,
  • Ademola Adetokunbo Oyagbemi,
  • Temidayo Olutayo Omobowale,
  • Olufunke Eunice Ola-Davies,
  • Adebowale Benard Saba,
  • Adeolu Alex Adedapo,
  • Sanah Malomile Nkadimeng,
  • Evaristus Nwulia,
  • Oluwafemi Omoniyi Oguntibeju,
  • Momoh Audu Yakubu

摘要

Objective

Cobalt is an essential nutrient for humans and animals due to its presence and involvement in the synthesis of vitamin B12 (cobalamin). However, toxicity could arise from chronic exposure or high dosages, thereby impacting negatively on organ functions such as heart and kidney. This study aimed to ascertain if rutin and vitamin E could reverse cobalt chloride-induced cardiorenal toxicity.

Methods

Thirty-five (35) male Wistar rats were divided randomly into five groups of seven rats each as follows: Group A-Control (clean water only), Group B-Cobalt chloride (300 ppm) (CoCl2) only in drinking water, Group C-Rutin (100 mg/kg) and cobalt chloride (300 ppm) (R1 + CoCl2), Group D-Rutin (200 mg/kg) and cobalt chloride (300 ppm) (R2 + CoCl2), and Group E-Vitamin E (50 mg/kg) and cobalt chloride (300 ppm) (Vit. E + CoCl2); all for 7 days. At the end of the experiment, blood pressure parameters were taken, cardiac and renal biomarkers of oxidative stress and antioxidant, histology, and immunohistochemistry were determined.

Results

Elevated blood pressure in Cobalt Chloride (CoCl2) group reduced significantly in dose dependency in treated CoCl2 groups with vitamin E and Rutin. At the end of the experiment, administration of CoCl2 to rats showed a significant increase in the blood pressure parameters when compared to the control, respectively. Also, CoCl2 administration altered the activity and concentration of cardiac, and renal antioxidant markers, and serum levels of nitric oxide, hydrogen peroxide and malondialdehyde while rutin and vitamin E ameliorated this effect in a dose-dependent manner. Little or no visible lesion was observed in groups treated with rutin and vitamin E following histopathological assessment of the heart and kidney tissue. The immunopositivity of cardiac troponin, renal mineralocorticoid receptor and nuclear factor kappa beta was low in groups exposed to rutin and Vitamin E.

Conclusion

Cobalt chloride has been shown to induce cardio and renal toxicity and this study was able to show the ameliorative effect of rutin and vitamin E in a dose-dependent manner.