Therapeutic potential of branched-chain amino acids against carbon tetrachloride-induced cardiopulmonary injuries in Wistar rats

Background: Carbon tetrachloride (CCl4) is a xenobiotic hepatotoxic agent that causes pathophysiological disorders in tissues and the liver. CCl4-induced cardiopulmonary toxicity is attributed to free radical-induced dyslipidemia and oxidative damage. Branched-chain amino acids (BCAAs) stimulate systemic defense against oxidative stress, which is probably caused by CCl4, through an improvement in the antioxidant system. Aim: This study aimed to explore the therapeutic benefits of BCAAs against CCl4-induced cardiopulmonary pathologies. Methods: A total of 28 inclusive Wistar rats stand under control was standard; group 2 comprised CCl4-received rats, whereas groups 3 and 4 comprised CCl4-rats supplemented with two varying levels of BCAAs. Results: Biochemical findings indicated that CCl4 provoked a rise in glucose and cholesterol levels compared with the control. The oxidative profile suggested increased malondialdehyde level and decreased superoxide dismutase activity in the CCl4-intoxicated heart. Supplemented BCAAs downregulated dyslipidemia and restored atrial changes in antioxidant components to be close to normal. Histopathological investigations using hematoxylin-eosin stain revealed damage to the inflamed heart-lung parenchyma of CCl4-intoxicated rats. An increase in fibrosis expression was detectable, simultaneously with a deprivation of protein content in cardiopulmonary sections, as shown by Masson trichrome and bromophenol blue techniques. Co-treated BCAAs intensified cardiopulmonary integrity, inducing scarce histological fibrosis with abundant protein. Accordingly, BCAA supplementation in CCl4-treated rats mitigated complications by reducing serum toxicity, enhancing antioxidant capacity, restoring protein expression, and improving organ health. Conclusion: The findings support the protective role of BCAAs with antioxidant benefits against CCl4-induced damage, suggesting their potential as a therapeutic agent for cardiopulmonary pathology. [Open Vet. J. 2025; 15(12.000): 6644-6659]