Triclosan at environmental concentration alters the hepatic antioxidant defence system in the fish, Anabas testudineus (Bloch, 1792)

Abstract

Triclosan has been detected in the aquatic environment ranging between nanogram and microgram levels. The present study focussed on the toxic effects of triclosan at environment relevant concentration, that is, 9 µg/L in the non-target fish, Anabas testudineus at the subcellular level. Fish were exposed to triclosan for 4, 7, 30 and 60 days, along with the control groups, and alterations in the antioxidant defence system were studied in various hepatic subcellular compartments. Triclosan declined the activities of superoxide dismutase and glutathione peroxidase along with a reduction in the glutathione level and glutathione-S-transferase activity suggesting the failure of antioxidant enzymes to eliminate the free radicals. Similarly, increased levels of hydrogen peroxide generation, lipid peroxidation and protein carbonyl contents confirmed the induction of oxidative stress. Further, the significant reduction in the total antioxidant capacity, and rise in the activities of alanine and aspartate aminotransferases suggests the liver tissue damage, mediated through oxidative stress. Histology of the liver showed severe lesions including melanomacrophage aggregation, cytoplasmic vacuolization, elongated nucleus, and degenerated hepatocytes. The study showed the hepatotoxicity of triclosan even at low concentrations at the subcellular level with more mitochondrial damage, thereby providing convincing evidence to demand its regulation and safe disposal in the environment.