Estimating the hepatotoxic impact of hexavalent chromium on Ctenopharyngodon idellus through a multi-biomarker study

Abstract

The toxic impact introduced by environmentally relevant sublethal concentrations of hexavalent chromium (5.3 and 10.63 mg/L) was measured in the hepatic tissue of Ctenopharyngodon idellus through altered oxidative stress levels, histopathological analysis (light and transmission electron microscopy) semi-quantified through DTC, accumulated Cr(VI) levels and molecular biomarkers. Hexavalent chromium altered oxidative stress resulting in increased malondialdehyde and decreased glutathione levels; with the antioxidant enzymes (SOD, Catalase and GST) diverging away from their normal activities. Histopathological alterations included dilation of sinusoidal space, enlarged nucleolus and dispersion of heterochromatin in the nucleus, intercellular vacuolation in cytoplasm displaying dilation of RER and depletion of the glycogen granules, myeloid bodies, swollen mitochondria enclosed by RER fragments, degeneration of mitochondrial cristae, autophagy, hepatic necrosis, lymphocyte infiltration, haemorrhage, dilated bile canaliculi with loss of microvilli, nuclear pleomorphism and degeneration of hepatopancreas. Chromium kept on accumulating in the tissue till the 30th day of metal exposure which thereafter decreased due to necrosis of the tissue. Nrf2, MT2 and Gadd45ab displayed abnormal gene expression with increasing duration of the experiment. From the present investigation, it can be presumed that the accumulated Cr(VI) and abnormal expression of Nrf2, Mt2 and Gadd45 persuaded in hampering the normal oxidative stress and establishment of hepatocytic anomalies leading to the destruction of normal histoarchitecture, thus, challenging its normal growth and survival.