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

- Acute toxicity of Sencor was studied on goldfish gills.
- Increase of the activities of glutathione-related antioxidant enzymes was observed.
- Sencor increased level of low and high molecular mass thiols.
- Sencor changed intensity of protein and lipid oxidation.

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 96 h to 7.14, 35.7 or 71.4 mg L−1 Sencor 70 WG (corresponding to 5, 25 and 50 mg L−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 (7.14 mg L−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 (71.4 mg L−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 71.4 mg L−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.

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