Taurine mitigates sodium arsenite–induced cardiorenal dysfunction in cockerel chicks: from toxicological, biochemical, and immunohistochemical stand‑points

Abstract

The Heart and kidney are adversely affected by arsenic toxicity, a highly toxic environmental pollutant. The aim of this study was to evaluate cardio-renal protective effects of taurine against sodium arsenite–induced toxicity. Taurine (2-amino ethane sulphonic acid; TAU) is a major free intracellular amino acid in many mammalian tissues including the liver. Taurine supplementation has been documented to mitigate steatosis and hepatotoxicity in several animal models. Sixty cockerel chicks (1-day old) of uniform weight were randomly assigned into six groups of ten cockerel chicks: Group A, Control; Group B, Sodium arsenite (SA) 75 mg/kg body weight; Group C, SA + 100 mg/kg taurine; Group D, SA + 200 mg/kg taurine; Group E, 100 mg/kg taurine and Group F, 200 mg/kg taurine. At the end of the experiment, blood pressure, electrocardiogram, electrolytes, and kidney function tests together with immunohistochemistry of cardiac troponin, gelatinase-associated lipocalin (NGAL), and podocin were assessed. Our findings revealed significant (P < 0.05) increases in blood pressure parameters, pulse rate, serum electrolytes (sodium, potassium, chloride, and bicarbonate) and markers of oxidative stress, prolonged QTc and PR interval with concurrent significant decrease in antioxidant status of cockerels intoxicated with SA. Immunohistochemistry revealed higher expressions of cardiac troponin, renal NGAL, and podocin in SA-intoxicated chicks relative to control and taurine-treated chicks. Our study shows that taurine supplementation improved the electrolytes and electrocardiographic changes, attenuated oxidative stress biomarkers, high blood pressure, and lowered cardiac troponin, renal NGAL and podocin immuno-reactivity.