Abstract

<p>The present study addresses the deleterious impact of sub lethal exposure of butachlor 2-chloro-N-(2-6-diphenyl) acetamide on hepatic cells of air breathing fish <em>Clarias batrachus</em> (Linn.) based on light and transmission electron microscopy and estimation of oxidative stress biomarker enzymes <em>viz.</em> reduced glutathione and lipidperoxidase. Fishes were exposed to 1.0µl/L butachlor for 5, 10 and 15 days respectively. After schedule exposure, blood sample were collected and extracted serum were analyzed for quantitative estimation of serum reduced glutathione and lipid peroxidase activity by spectrophotometer. The liver tissues were processed for light and electron microscope. Light photomicrographs of hepatic cells reveal dose related abnormalities which increases with the duration of exposure. Major changes attributed to the hepatic cell were parenchyma degeneration, necrosis along with fibrosis, widening of sinusoids, vacuolation, and infiltration of eosinophilic inclusion, karyolysis, pyknosis and perivenular congestion. Transmission electron microscopy of hepatic cells also revealed degenerated hepatic parenchyma, accumulation of lipid and electron dense material, degenerated mitochondria, nuclear shrinkage and enlarged lysosomes engulfing cytoplasmic particles in contrast to control fish. On prolonged exposure, the most frequent pathological modifications were mitochondrial swelling with regression of cristae and giant lysosome with myelinated phospholipid membrane pointing towards phospholipidosis. The activities of all the marker enzymes showed high fluctuation indicating significant imbalance in comparison to control. The study highlights the oxidative stress caused by butachlor correlated with histopathological anomalies of hepatic cells. It can be used as sensitive index for assessing the magnitude of oxidative damage and physiological dysfunction of experimental fish under laboratory condition.</p>

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