Oxidative parameters of Rhamdia quelen in response to commercial herbicide containing clomazone and recovery pattern

[Display omitted] ► Clomazone exposure at environmental relevant concentrations causes oxidative stress. ► The study provided some toxicity biomarkers for fish poisoning with herbicide clomazone. ► Concentrations tested seem to be safe to Rhamdia quelen, however new evaluations are necessary. In this study, fish Rhamdia quelen, were exposed to different concentrations of herbicide clomazone: 0.0 (control), 0.45 and 0.91 mg L −1. After exposure for 8 days to herbicide, fish were transferred to clean water for a recovery period (8 days). Oxidative stress indicators such as thiobarbituric acid reactive substances (TBARS) levels and protein carbonyl content, as well as antioxidant defenses, such as catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), ascorbic acid and non-protein thiols levels were studied, using the liver, brain and muscle tissues. Herbicide exposure increased TBARS in muscle and in liver at higher concentration. In liver protein carbonylation increased and catalase activity did not change in fish exposed to herbicide. SOD enhanced in liver at concentration of 0.91 mg L −1. GST, ascorbic acid and non-protein thiols levels increase at both concentrations. At the end of the recovery period the most of the parameters recovered whereas GST and ascorbic acid remain elevated. The present study demonstrates the occurrence of disorders in antioxidant parameters and importance in the assessment of the potential risk of herbicides as clomazone on fish species.