BIFENTHRIN INDUCED BIOCHEMICAL AND HISTOPATHOLOGICAL ALTERATIONS IN RATS
Journal: International Journal of Advanced Research (Vol.7, No. 5)Publication Date: 2019-05-01
Authors : Enas A. Tahoun Shimaa M. Abou-Zeid; Huda O. AbuBakr.;
Page : 70-85
Keywords : Bifenthrin oxidative stress apoptosis inflammation histopathology.;
Abstract
Bifenthrinis a third-generation synthetic pyrethroid with a broad spectrum insecticidal and acaricidal activity used to control a wide range of insect pests in many applications. The current study was designed to investigate the toxic effects of bifenthrin in male rats exposed orally by stomach intubation at 7 mg/kg for 28 days. Liver and kidney functions were monitored in addition to oxidant/antioxidant parameters inserum, liver, kidney and brain. The immunohistochemical reactivity to iNOS, COX-2 and caspase-3 were studied and the histopathological findings were recorded. Our results revealed significant elevations in serum ALT, AST, LDH and ALP activities and blood BUN and creatinine levels while serum total protein was reduced. The level of MDA increased in liver, kidney and brain with reduction in GSH level and SOD, CAT and GPx activities. The activity of iNOS increased in hepatocytes, glomeruli and renal tubular cells. Strong immunoreactivity to COX-2 was observed in the brain. The expression of caspase-3 increased in both liver and brain. The liver revealed degeneration with loss of cellular outlines and areas of coagulative necrosis infiltrated with inflammatory cells. The kidney showed congestion of blood vessels and glomeruli, necrotic renal tubules and hyperplasia of fibrocytes with leucocyte infiltration in-between renal tubules. The brain revealed loss of some Purkinje cells, demyelination, neuronophagia, widespread neuronal necrosis with marked edema and proliferation of perineural satellite oligodendroglia cells around the cell body of motor neurons ?satellitosis?. In conlusion, bifenthrin produced toxic effects in rats which seem to be mediated by oxidative stress and release of inflammatory mediators.
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