Dietary ascorbic acid reduced micronucleus and nuclear abnormalities in Clarias gariepinus (Burchell 1822) exposed to hospital effluent.

Hospital effluents contain myriad of mutagens and genotoxins capable of increasing DNA damage in aquatic biota. African mudfish, Clarias gariepinus, are exposed to genotoxins when cultured in swamps and derelict water bodies often contaminated by effluents. Moreover, its DNA is susceptible to xenobiotic-induced lesions since it lacks L-gulonolactone oxidase and hence cannot synthesize L-ascorbic acid. This study investigated 96-h acute toxicity and protective effects of dietary ascorbic acid (AA) against micronucleus (MN) and abnormal nuclear (NAs) formation in C. gariepinus exposed to sub-lethal concentrations of hospital effluent. Six concentrations (0.5-3.0%) of the effluent were selected to determine the 96-h acute toxicity of the effluent in C. gariepinus, after range finding test. Fish were exposed to sub-lethal concentrations (0.08-1.30%) of the 96 h LC50. Two other groups were exposed to the 96 h LC50 (1.30%) of the effluent +50 and +100 mg/kg of dietary ascorbic for 7 days, and MN and NAs assessed in peripheral erythrocytes. The 96 h LC50 (1.30%) was 1.18 times more toxic than the 24 h LC50 (1.54%), indicating that the toxicity of the effluent increased with exposure duration. MN, nuclear bud, enucleated, fragmented nucleus (apoptosis), and necrotic erythrocytes significantly increase in effluent treated fish. Dietary AA reduced MN from 6.35-fold (1.30% treated group) to 3.72-fold (1.30% + 50 mg AA) and 3.54-fold (1.30% + 100 mg AA). Also, AA reduced total NAs from 2.26-fold (1.30%) to 1.40-fold (1.30% + 50 mg AA) and 1.06-fold (1.30% + 100 mg AA) compared to the control. Heavy metals and physicochemical parameters analyzed in the tested effluent possibly induced the mortality and cytogenotoxicity in C. gariepinus, and this was ameliorated by dietary AA.