Cypermethrin-induced histopathological and biochemical changes in Nile tilapia (Oreochromis niloticus), and the protective and recuperative effect of ascorbic acid.

The objective of this study was to investigate the effects of ascorbic acid on the toxicity of cypermethrin's on histopathological lesions in tissues and protein, glycogen levels in Oreochromis niloticus. Nile tilapia was exposed to 0.22 and 0.44 µg/l cypermethrin+control diet, 0.22 and 0.44 µg/l cypermethrin+ascorbic acid supplemented diet for 20 days. The fish were allowed recuperation period of 15 days in pesticide-free water and fed with ascorbic acid suplementation diet. In light microscopic investigation, histopathological lesions were observed in the gill, liver and kidney. The severity of lesions accreted depending on increased pesticide concentration and control diet. Some of the lesions were reversible or at least were less pronounced after recuperation period. Protein levels decreased in some groups after treatment period according to control groups (p<0.05). The highest depletions in liver, muscle and gill protein levels were found in 0.44 µg/l cypermethrin+ascorbic acid supplemented diet group (62.23%), in 0.22 µg/l cypermethrin+control diet group (53.12%) and in 0.44 µg/l cypermethrin+control diet group (61.87%) after 10 days, respectively. These levels increased at the end of the recuperation period. The highest depletion in liver glycogen levels was found in 0.22 µg/l cypermethrin+control diet group (50.50%) after 10 days (p<0.05). At the end of recuperation period, there was no difference between the groups (except 0.22 µg/l cypermethrin+ascorbic acid supplemented diet group) and controls. The decrease of muscle glycogen, except 0.22 µg/l cypermethrin+ascorbic acid supplemented diet group, was recorded at the end of 10 and 20 days. In the recuperation period, an increase was observed at all groups. These results revealed that the histopathology, protein and glycogen can work as good indicators of stress of a toxicant on fish. Ascorbic acid serves fish as an antitoxic agent against pesticide toxicity.

The effects of monocrotophos to different tissues of freshwater fish Cirrhinus mrigala.

The histopathological effects of monocrotophos on the gill, kidney and intestine tissues of the Cirrhinus mrigala were determined by light microscopy. The changes in the gills were characterized by epithelial hyperplasia, aneurysm, epithelial necrosis, desquamation, epithelial lifting, oedema, lamellar fusion and curling of secondary lamellae. Pycnotic nuclei in tubular epithelium, hypertrophied epithelial cells of renal tubules, contraction of the glomerulus and expansion of space inside the Bowman's capsule were observed in the kidney tissues of fish after exposure to monocrotophos. In the intestine tissues of fish exposed to monocrotophos, oedema, necrosis and atrophy of epithelial cells were observed.

Histopathology of gills in mosquitofish, Gambusia affinis after long-term exposure to sublethal concentrations of malathion.

The histopathological effects of malathion, an organophosphate pesticide, on the gill tissues in mosquitofish, Gambusia affinis, were determined by light microscope. The fish were exposed to sublethal concentrations (0.01 and 0.02 mg/L) of malathion for 10, 20 and 30 days. Histological examination of the gills treated with malathion showed a variety of histopathological effects. The gill lesions included necrosis and desquamation of secondary lamellar epithelium, lifting up of epithelium, intraepithelial oedema, fusion of adjacent secondary lamellae, haemorrhage at primary lamellae, disorganization and rupture in seconder lamellae, hypertrophy and hyperplasia of epithelial cells. These alterations were time- and dose-dependent.

The histopathological effects of thiodan on the liver and gut of mosquitofish, Gambusia affinis.

Thiodan (33.7% endosulfan), a polychlorinated cyclodiene insecticide, was evaluated for its histopathological effects on mosquitofish, Gambusia affinis, by light microscopy. Fish were exposed to doses of 0.00 (control), 1.00, 2.50, and 5.00 microg/L on days 7, 14, 21, and 30. No histopathological effects were apparent at control group. The histopathological alterations were characterized as oedema, degeneration, accumulation of lymphocytes in the lamina propria, disintegration of villuses, pycnotic state of nuclei, and necrosis in gut; degeneration, hypertrophy, sinusoids enlargement, hemorrhage, pycnosis position of nuclei, vacuolization of cell cytoplasm, infiltration of mononuclear lymphocyte, and congestion in liver. These alterations were time- and dose-dependent.