Protective Efficacy of Vitamin E Against Triazine-Induced Hepatic Damage in Freshwater Fish Channa punctatus (Bloch.)

Abstract

The widespread use of triazine herbicides in modern agriculture has resulted in increasing contamination of aquatic ecosystems, posing significant risks to non-target aquatic organisms, particularly fish. The present study was undertaken to evaluate the hepatotoxic effects of triazine herbicide exposure on the freshwater fish Channa punctatus (Bloch.) and to investigate the protective efficacy of Vitamin E against pesticide-induced liver damage. Healthy fish were exposed to a sublethal concentration of triazine herbicide for 30 days, while a separate treatment group received dietary supplementation of Vitamin E in addition to triazine exposure. Hepatic toxicity was assessed through biochemical analyses of liver function biomarkers, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), acid phosphatase (ACP), lactate dehydrogenase (LDH), total protein, albumin, globulin, and bilirubin. Histopathological examination of liver tissues was also performed to evaluate structural alterations. The results revealed significant increases in ALT, AST, ALP, ACP, LDH, and bilirubin levels in triazine-exposed fish compared with the control group, indicating severe hepatocellular damage and impaired liver function. Conversely, total protein, albumin, and globulin concentrations were significantly reduced, reflecting disruption of hepatic synthetic activity. Histological observations further confirmed liver injury, characterized by hepatocellular degeneration, cytoplasmic vacuolation, nuclear pyknosis, sinusoidal dilation, congestion, and disorganization of hepatic cords. These findings demonstrate that triazine exposure induces substantial biochemical and structural alterations in the liver of Channa punctatus. Vitamin E supplementation markedly ameliorated the toxic effects of triazine by restoring altered biochemical parameters toward normal levels and reducing the severity of histopathological lesions. The antioxidant properties of Vitamin E likely contributed to the stabilization of cellular membranes, inhibition of lipid peroxidation, and reduction of oxidative stress-induced tissue damage. Improved hepatic architecture and recovery of liver function biomarkers in the Vitamin E-treated group further confirmed its hepatoprotective potential. triazine herbicide causes significant hepatotoxicity in Channa punctatus, whereas Vitamin E provides effective protection against pesticide-induced liver damage. The study highlights the importance of antioxidant-based interventions in mitigating environmental toxicant-induced stress and provides valuable insights into the management of pesticide contamination in aquatic ecosystems.