Abstract
ALUMINIUM OXIDE NANOPARTICLES INDUCED IRREVERSIBLE ALTERATIONS IN THE ANTIOXIDANT DEFENSE SYSTEM OF THE FISH, OREOCHROMIS MOSSAMBICUS (PETERS, 1852)

Puthan Variyam Vidya and Kumari Chidambaran Chitr

ABSTRACT

Aluminium oxide nanoparticles (Al2O3NPs) are the most abundantly produced nanoparticles having widespread applications in the field of physics, chemistry, engineering and biology. Therefore, exposure of Al2O3NPs to organisms and environment is definite with great concern on the fate, ecotoxicity and persistence in the environment. The present study was designed to evaluate the sublethal (4 mg/L) effects of Al2O3NPs in gill, liver and brain of the fish, Oreochromis mossambicus exposed for short-term (24, 72 and 96 h) and long-term (15, 30 and 60 days) durations. Gill tissue showed significant (P<0.05) decrease in the activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase with concomitant increase in the levels of hydrogen peroxide generation and lipid peroxidation. Liver tissue showed decreased activities of antioxidant enzymes in long-term exposure, with simultaneous increase in levels of hydrogen peroxide and lipid peroxidation. Brain tissue also showed significant reduction in the activities of all antioxidant enzymes along with rise in the levels of hydrogen peroxide generation and lipid peroxidation in short-term and long-term exposure groups. The activity of marker enzyme, alkaline phosphatase reduced in gill and increased in liver after 60 days. Brain marker acetylcholinesterase enzyme showed decreased activity in brain tissue after exposure to Al2O3NPs. Treatment withdrawal for 60 days also showed similar results like the treatment groups. In conclusion, aluminium oxide nanoparticles induced alterations in the antioxidant defense system, which is responsible for the persistent toxic effects in gill, liver and brain tissues of the freshwater fish, Oreochromis mossambicus.

Keywords: Al2O3NPs, Oreochromis mossambicus, antioxidant enzymes, lipid peroxidation, oxidative stress, treatment withdrawal.


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