Acute toxic effects of endosulfan on cellular Stress, genotoxicity, and histopathological alterations in Milkfish (Chanos chanos) under freshwater conditions.

BACKGROUND

The present study aimed to evaluate the acute toxicity of endosulfan (99% purity; α:β ratio of 7:3) in milkfish (Chanos chanos) under freshwater acclimated conditions over a 96-hour exposure period. Milkfish (C. chanos) is a commercially important tropical species widely cultured across freshwater, brackish, marine, and hypersaline environments.

METHOD: An experiment was conducted in Milkfish (C. chanos) acclimated under freshwater condition to determine the lethal concentration (LC50) of endosulfan at 96 hrs using probit analysis. The fish were exposed to graded concentrations of endosulfan (25.5, 26.5, 27.5, 28.5, and 29.5 µg L-¹) for 96 hours. Toxicological effects were evaluated through a suite of biochemical, immunological, neurophysiological, cytogenetic, and histopathological biomarkers. Antioxidative enzyme activities, including superoxide dismutase, glutathione-S-transferase, and catalase, were assessed alongside immunological parameters such as blood glucose, phagocytic activity (measured via nitroblue tetrazolium reduction), and serum cortisol levels. Neurotoxicity was evaluated through acetylcholinesterase activity, while chromosomal aberrations and histopathological alterations in the liver and gills were examined to determine cellular and tissue-level damage.

RESULTS

The 96-hour LC50 value (95% confidence limits) for C. chanos (mean body weight: 110 g) was estimated at 27.47 µg L-¹. A significant dose and time dependent alteration was observed across all assessed parameters, including antioxidative enzymes, immune responses, neurotransmitter activity, metabolic functions, and cytogenetic integrity. Pronounced chromosomal aberrations in kidney tissues and severe histopathological lesions in the liver and gills were evident following endosulfan exposure. These physiological and structural impairments were further corroborated by marked behavioral deviations from normal activity patterns in exposed fish.

CONCLUSIONS

Collectively, the findings demonstrate that endosulfan exposure induces substantial biochemical, cytogenetic, and histopathological disruptions in C. chanos, ultimately leading to metabolic dysregulation and organ damage.