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

Abstract

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.