Main content area

Hexavalent chromium-induced toxic effects on the antioxidant levels, histopathological alterations and expression of Nrf2 and MT2 genes in the branchial tissue of Ctenopharyngodon idellus

Jindal, Rajinder, Handa, Kriti
Chemosphere 2019 v.230 pp. 144-156
Ctenopharyngodon idella, aneurysm, antioxidants, bioaccumulation, catalase, chromium, enzyme activity, epithelial cells, epithelium, fish, genes, gills, glutathione, histopathology, hyperplasia, lipid peroxidation, mitochondria, necrosis, oxidative stress, pavements, superoxide dismutase, toxicity
Ability of hexavalent chromium to accumulate and induce oxidative stress has been studied in the gills of Ctenopharyngodon idellus, with the resulting damage in the form of altered endogenous antioxidant enzyme activity and, histopathology in the tissue. The fish were exposed to 5.3 (C1) and 10.63 mg/L (C2) of hexavalent chromium and were scrutinised on 15th, 30th and 45th day of toxicant exposure. Oxidative stress studied in terms of lipid peroxidation and glutathione levels and the antioxidant enzymes activity also exhibited alterations. The histopathological modifications in gills announced lesions in the form of hyperplasia, aneurysm, lamellar fusion, focal proliferation, epithelial degeneration and necrosis with loss of lamellae, bringing irreversible damage on 45th day with mean degree of tissue change value of 100.35 ± 10.69. Bioaccumulation of chromium, and increased anomalies in branchial tissue exhibited damage in concentration and time-dependent manner. The ultrastructural anomalies in the cellular morphology in the epithelial cells of filaments and lamellae, exhibited pleomorphic nuclei, swollen mitochondria, extensive vacuolation and loss of microridges in pavement cells. The tissue also displayed altered regulation of Nrf2 and Mt2 following Cr(VI) exposure with maximum downregulation on 45th day by 61 and 53%, respectively. PCA generated two principal components, PC1 (GSH, GST, CAT and SOD) and PC2 (DTC, MDA and Cr(VI) concentration). Thus, it can be concluded that accumulation of Cr(VI) induces alteration in the gene expression of Nrf2 and Mt2 leading to the development of oxidative stress, ensuing various pathological changes creating hindrance in fish survival.