Histopathological aberrations and oxidative stress responses in Nile tilapia Oreochromis niloticus as influenced by dietary florfenicol and its metabolites

The intensification of aquacultural practices demands the regulated use of antibiotics to contain diseases. This study investigated the accrual and depletion of florfenicol (FFC) and its metabolite florfenicol amine (FFA) in Oreochromis niloticus juveniles following dietary administration of 15 and 45 mg FFC/kg biomass/day for 10 days, the oxidative stress responses and histopathological alterations in the kidney and liver tissues. The therapeutic dose caused no mortalities but reduced the feed intake significantly. The induction of oxidative stress in the liver and kidney tissues upon FFC-dosing was revealed by the increase in malondialdehyde, ferric reducing antioxidant power, total nitric oxide, and decrease in glutathione-S-transferase on day 10. The dietary FFC caused degeneration of renal tubular epithelium, inflammation, mineralization, hydropic swelling and necrosis in the kidney and glycogen-type vacuolation, cytoplasmic degeneration, cellular hypertrophy, and nuclear abnormalities in the liver signifying its nephrotoxic and hepatotoxic potential. The elimination of FFC was rapid in the liver and kidney but it persevered in muscle for 3 weeks. The depletion of FFA was faster in the liver and muscle, while it persevered in the kidney, signifying the probable reaction between free radicals and FFC metabolites. The withdrawal period was computed to be 6 days. Within 3 weeks of termination of dosing, the changes in biomarkers and histoarchitecture were recuperated. Though the dietary FFC induced oxidative stress and alterations in the kidney and liver histoarchitecture, our findings suggested that FFC was well tolerated by O. niloticus and is practically safe at the therapeutic dose.