Hepatotoxic Effects of Atrazine on Clarias gariepinus (Burchell, 1822): Biochemical and Histopathological Studies.

The hepatotoxic effects of sub-lethal concentrations of atrazine (2.5, 25, 250, and 500 μg L-1) on Clarias gariepinus juveniles were assessed for 28 days in a quality-controlled laboratory procedure. The study was designed to determine the effects of atrazine on selected liver function biomarkers: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), albumin (ALB) and total protein (TP), and to analyze the liver tissues of the fish using a quantitative and qualitative histology-based health assessment protocol. The levels of ALB and TP in exposed specimens were observed to decrease with increasing concentrations of atrazine. However, the activities of ALT, AST, and ALP showed significant (p < 0.05) increase with increasing concentrations of atrazine. Hepatic assessment of the liver tissues revealed marked histopathological alterations, including structural changes (necrotic/apoptotic liver tissue, poor hepatic cord structure, and loss of normal architecture) in 52.2% of the liver tissues in the treatment groups; plasma alterations (vacuolation or fat inclusions, 22.9%) of hepatocytes; hypertrophied hepatocyte (55.2%); nuclear alterations (52.1%); focal necrosis (16.7%); complete degeneration of hepatocytes (60.45%); sinusoids congested with red blood cells or vascular congestion (70.8%); and karyolysis of the nucleus (18.8%). Findings from this study suggest that atrazine interferes with liver function markers and disrupts the normal architectural and structural components of the liver resulting in noninfectious liver injury. This condition resulted in repeated cycles, cell deaths, and inflammation, which could result in the eventual death of the exposed fish if exposure duration was prolonged.