Oxidative stress responses in gills of goldfish, Carassius auratus, exposed to the metribuzin-containing herbicide Sencor.

Metribuzin belongs to the family of asymmetrical triazine compounds and is an active ingredient in many commercial herbicides including Sencor. Effects on goldfish (Carassius auratus L.) of exposure for 96h to 7.14, 35.7 or 71.4mgL(-1) Sencor 70 WG (corresponding to 5, 25 and 50mgL(-1) of metribuzin) were examined by evaluating oxidative stress markers and activities of antioxidant and associated enzymes in gills. Fish exposed to the lowest Sencor concentration (7.14mgL(-1)) showed a 94% increase in levels of protein carbonyls in gills as well as 45% and 144% increases in the activities of glutathione peroxidase and glutathione-S-transferase. Exposure to the highest Sencor concentration (71.4mgL(-1)) resulted in reduced levels of protein carbonyls by 56% and lipid peroxides by 40%, as compared with controls, but enhanced levels of low and high molecular mass thiols by 71% and 36%, respectively. The activities of superoxide dismutase, glutathione peroxidase and glutathione-S-transferase were increased in gills of goldfish exposed to 71.4mgL(-1) Sencor. At any concentration tested, Sencor did not affect the activities of glutathione reductase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase or acetylcholine esterase in gills. The results of this study indicate that acute exposure of goldfish to Sencor had effect on free radical processes in gills and glutathione-dependent antioxidants effectively protect proteins and lipids from oxidation.

Toxicity of environmental Gesagard to goldfish may be connected with induction of low intensity oxidative stress in concentration- and tissue-related manners.

Prometryn is a selective herbicide commonly used in agriculture as the commercial preparation, Gesagard. Goldfish (Carassius auratus) exposure for 96h to 0.2, 1, or 5mgL(-1) Gesagard 500FW (corresponding to 0.1, 0.5, and 2.5mgL(-1) of prometryn) on indices of oxidative stress (lipid peroxides, protein carbonyls, and thiol content) and activities of antioxidant and related enzymes in gills, liver, and kidney was studied. Gills appeared to be the most resistant to Gesagard treatment, reacting to only the highest concentration of herbicide with enhanced levels of low molecular mass thiols and activities of glutathione S-transferase (GST) and glutathione reductase. Goldfish exposure to 0.2-5mgL(-1) Gesagard resulted in enhancement of carbonyl protein level and activity of superoxide dismutase (SOD), but reduced the lipid peroxide (LOOH) content and activity of glutathione peroxidase in liver. Kidney appeared to be the main target organ of Gesagard toxicity, showing the greatest number of parameters affected even under low concentrations of herbicide. An increase in the content of L-SH and activity of SOD was accompanied with decreased activities of catalase, GST, and glucose-6-phosphate dehydrogenase and reduced levels of LOOH in kidney of Gesagard treated fish. The treatment also induced various histological changes in goldfish liver and kidney which could be related to their dysfunction. The present study indicates that Gesagard induced oxidative stress of differing intensities in the three goldfish tissues and demonstrated that kidney would be the best target organ to analyze, reveal, and monitor Gesagard effects on 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.

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 96 h exposure to 7.14, 35.7, or 71.4 mg L(-1) of Sencor (corresponding to 5, 25, or 50 mg L(-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 35.7 mg L(-1) and 71.4 mg L(-1) Sencor, respectively. Kidney levels of protein carbonyls increased by 177% after exposure to 35.7 mg L(-1) of Sencor indicating extensive damage to proteins. Lipid peroxide concentrations also increased by 25% after exposure to 7.14 mg L(-1) of Sencor, but levels were reduced by 42% in the 71.4 mg L(-1) exposure group. The data indicate that induction of oxidative stress is one of the mechanisms responsible for Sencor toxicity to fish.

S-nitrosoglutathione-induced toxicity in Drosophila melanogaster: Delayed pupation and induced mild oxidative/nitrosative stress in eclosed flies.

The toxicity of the nitric oxide donor S-nitrosoglutathione (GSNO) was tested on the Drosophila melanogaster model system. Fly larvae were raised on food supplemented with GSNO at concentrations of 1.0, 1.5 or 4.0mM. Food supplementation with GSNO caused a developmental delay in the flies. Biochemical analyses of oxidative stress markers and activities of antioxidant and associated enzymes were carried out on 2-day-old flies that emerged from control larvae and larvae fed on food supplemented with GSNO. Larval exposure to GSNO resulted in lower activities of aconitase in both sexes and also lower activities of catalase and isocitrate dehydrogenase in adult males relative to the control cohort. Larval treatment with GSNO resulted in higher carbonyl protein content and higher activities of glucose-6-phosphate dehydrogenase in males and higher activities of superoxide dismutase and glutathione-S-transferase in both sexes. Among the parameters tested, aconitase activity and developmental end points may be useful early indicators of toxicity caused by GSNO.