Histopathological and biochemical changes in goldfish kidney due to exposure to the herbicide Sencor may be related to induction of oxidative stress

Molecular mechanisms of toxicity by the metribuzin-containing herbicide Sencor to living organisms, particularly fish, have not yet been extensively investigated. In the present work, we studied the effects of 96h exposure to 7.14, 35.7, or 71.4mgL-1 of Sencor (corresponding to 5, 25, or 50mgL-1 of its herbicidal component metribuzin) on goldfish (Carassius auratus L.), examining the histology, levels of oxidative stress markers, and activities of antioxidant and related enzymes in kidney as well as hematological parameters and leukocyte profiles in blood. The treatment induced various histopathological changes in goldfish kidney, such as hypertrophy of intertubular hematopoietic tissue, small and multiple hemorrhages, glomerular shrinkage, a decrease in space between glomerulus and Bowman's capsule, degeneration and necrosis of the tubular epithelium. Sencor exposure also decreased activities of selected enzymes in kidney; activities of catalase decreased by 31-34%, glutathione peroxidase by 14-33%, glutathione reductase by 17-25%, and acetylcholinesterase by 31%. However, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities increased by 25-30% and 22% in kidney after treatment with 7.14 or 35.7mgL-1 and 71.4mgL-1 Sencor, respectively. Kidney levels of protein carbonyls increased by 177% after exposure to 35.7mgL-1 of Sencor indicating extensive damage to proteins. Lipid peroxide concentrations also increased by 25% after exposure to 7.14mgL-1 of Sencor, but levels were reduced by 42% in the 71.4mgL-1 exposure group. The data indicate that induction of oxidative stress is one of the mechanisms responsible for Sencor toxicity to fish

Hepatotoxicity of herbicide Sencor in goldfish may result from induction of mild oxidative stress

The effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L-1 of Sencor were studied on liver and plasma parameters in goldfish, Carassius auratus L. Goldfish exposure to 71.4 mg L-1 of Sencor for 96 h resulted in a decrease in glucose concentrations in plasma and liver by 55%, but did not affect liver glycogen levels. An increase in the activity of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (by 24-27%, 32-72%, and 87-102%, respectively) occurred in plasma of Sencor exposed goldfish, whereas in liver activities of these enzymes decreased (by 15-17%, 19%, and 20%, respectively). Lactate concentration in plasma increased by 22-36% in all treated fish groups, whereas in liver it increased by 64% only after exposure to 35.7 mg L-1 of Sencor. Herbicide exposure enhanced lipid peroxide levels by 49-75% and decreased activities of catalase by 46%, glutathione reductase by 25-48% and glutathione peroxidase by 21-26% suggesting development of oxidative stress in liver. The treatment induced various histological changes in goldfish liver, such as dilated sinusoids, hypertrophy and dystrophy of hepatic cells and detachment of endothelial cytoplasm with diffuse hemorrhage. The data collectively let us propose that mild oxidative stress might be responsible for the hepatotoxicity of Sencor