Bio-chemical markers in Nile tilapia (Oreochromis niloticus) exposed to sublethal concentrations of fenitrothion.

Abstract

Fenitrothion is a widely used organophosphate insecticide, which poses potential threats to aquatic ecosystems. This study investigated the effect of sub-lethal concentrations of fenitrothion on total soluble protein, glycogen, gulathione-S-transferase (GST), acetylcholinestrase activity (AchE) and Na+/K+, Ca2+ and Mg2+/-ATPase activities in brain and liver of Nile tilapia Oreochromis niloticus. The potential of the fish to recover from the toxic effects of fenitrothion was also evaluated. Results showed significant decrease in total soluble protein and glycogen levels in both brain and liver, indicating impaired protein synthesis and energy metabolism. The activities of GST and AChE decreased in brain and liver, suggesting impairment of detoxification ability and neurotoxicity. Na+/K+-ATPase and Mg2+-ATPase activities were also reduced, indicating disruption of osmoregulation and energy production. Ca2+-ATPase activity was inhibited, potentially affecting calcium homeostasis. After the recovery period, most biomarkers showed significant rebounding which indicated possible restoration of cellular function. This study highlighted the sub-lethal toxicity of fenitrothion on O. niloticus and demonstrated its ability to recover from these toxic effects. The observed recovery potential suggests resilience of O. niloticus. Importantly, during the post-exposure recovery period, significant rebounding of most biomarkers was observed, demonstrating the Nile tilapia's ability to partially repair cellular damage and restore physiological functions.