Assessment of Industrial Effluent-Induced Multi-Organ Toxicity, Genotoxicity, DNA Damage, and Esterase Activities Changes in the Brain, Liver, and Muscle of Oreochromis niloticus.

Industrial effluents frequently contain a variety of toxic substances that can seriously threaten aquatic life. Pollutants discharged in industrial effluents can significantly induce genetic damage in aquatic organisms, leading to long-term ecological consequences and impairments in fish health and reproduction. The present study provides an integrated assessment of neurotoxic, genotoxic, biochemical, and histopathological response of Oreochromis niloticus against composite of industrial effluents. Fish were exposed to 1/5th of sublethal LC50 concentration of composite untreated industrial effluents from Sundar Industrial Estate for 14 days, alongside an untreated control group. Neurotoxicity and biochemical analyses were done by measuring acetylcholinesterase (AChE) and carboxylesterase (CbE) activities in liver, muscle, and brain tissues, while cytogenotoxicity was evaluated by micronucleus, erythrocyte nuclear alterations, cellular abnormalities, and comet assay. Results showed significant (p < 0.05) inhibition of AChE activity by 1.28-fold in muscle, 2.53-fold in liver, and 1.35-fold in brain tissues. CbE activity was significantly induced (2.17-fold) in liver, while inhibited by 1.2-fold in muscle and 1.62-fold in brain tissues. Micronuclei formation and erythrocyte nuclear abnormalities including notched, elongated, and blebbed nuclei along with cellular deformities such as spindle-shaped, swollen, and vacuolated cells were observed in exposed fish. The comet assay revealed minor to moderate DNA damage, with significant differences in comet parameters compared to control. Histopathological alterations in liver, muscle, and brain tissues were also evident. The present findings demonstrate that these industrial effluents have the potential to induce toxic effect at multiple biological levels in exposed fish. Overall, industrial effluents caused enzymatic disruption, genetic damage, and tissue injury, posing risks to fish and human consumers.