The presence of pharmaceuticals in the aquatic environment and its impact on humans and the ecosystem are emerging issues in environmental health. This study evaluated the potential biochemical, genetic and reproductive effects of the diclofenac by waterborne exposure, in a semi-static bioassay for 21 days. The fish Rhamdia quelen were exposed to environmental concentrations of diclofenac (0, 0.2, 2 and 20µg/L). The results showed that in the liver, diclofenac reduced the catalase and ethoxyresorufin- O- deethylase activities in fish exposed to 2µg/L, and superoxide dismutase in all exposed groups. The levels of reduced glutathione and glutathione S-transferase (GST) activity increased at all tested concentrations. Lipid peroxidation (LPO) was reduced in the groups exposed to 0.2 and 20µg/L of diclofenac, but there was no protein oxidation. In the testis, the concentration of 0.2µg/L caused major changes as inhibition of SOD, glutathione peroxidase and GST activities and also LPO decrease. Diclofenac was not genotoxic and not altered plasma testosterone and estradiol levels and testicular morphology. In brain, there was a reduction of dopamine and its metabolite DOPAC (3, 4-dihydroxyphenylacetic acid) in exposure to diclofenac, but this not disrupted the hypothalamic-pituitary-gonadal axis.
Keywords: Genotoxicity; NSAIDs; Neurotransmitters; Oxidative stress; Steroids.
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