Heterobranchus longifilis juveniles (n = 450, Mean length ± SD = 10.28 ± 1.34 cm) were exposed to varying concentrations (0 = control, 6.00, 8.00, 10.00, 12.00 mg/l) of zinc oxide nanoparticles (ZnO-NPs) for 60 days to determine its effects on the histopathology of the gill and liver. To evaluate recovery from ZnO-NPs exposure, fish were subjected to a 30-day depuration. Ascorbic acid (AA) ameliorative potential against ZnO-NPs toxicity was assessed by augmenting fish basal diet with different AA (50.00, 250.00, 500.00, 1000.00 mg.kg^-1) levels. After each experiment, fish gills and liver were removed for histopathological analysis. Gills of exposed fish revealed different alterations like epithelial hyperplasia, epithelial lifting, lamellar fusion, oedema, aneurysms, and necrosis; while alterations such as nuclear vacuolation, fatty degeneration, cytoplasmic degeneration, focal fibrosis and necrosis were recorded in the liver. The mean degree tissue change (DTC) in both organs of ZnO-NPs-exposed fish gradually increased with an increase in ZnO-NPs concentration and exposure period. After 30-day depuration, some of the lesions in both organs attained recovery, while others did not. AA administration to ZnO-exposed fish at 500 mg.kg^-1 completely reversed the lesions in both organs compared to the normal tissue architecture in the control. The results suggest that ZnO-NPs could trigger structural alterations in both the branchial and hepatic tissues of H. longifilis, and full recovery under depuration was slow. However, 500 mg.kg^-1 AA dietary supplementation have the propensity to ameliorate the ZnO-NPs-induced pathological lesions in H. longifilis.