Effects of trophic exposure to dexamethasone and diclofenac in freshwater fish.

Steroidal and non-steroidalanti-inflammatories are pharmaceutical prescribed in human medicine and have the potential to contaminate water and sediments via inputs from sewage treatment plants. Their impacts on humans and ecosystems are emerging issues in environmental health. The aim of the present work was to evaluate the effects of diclofenac and dexamethasone in male fish Hoplias malabaricus after trophic exposure. Fish were fed twice every week with Astyanax sp. submitted to intraperitoneal inoculation with diclofenac (0; 0.2; 2.0 or 20.0 µg/kg) or dexamethasone (0; 0.03; 0.3 or 3.0 µg/kg). After 12 doses, blood was collected for testosterone dosage. The gonad and liver were collected to calculate gonadosomatic (GSI) and hepatosomatic index (HSI). Antioxidants enzymes activity and biotransformation were also evaluated in liver and gonads. In liver, diclofenac caused oxidative stress with increased superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and lipoperoxidation (LPO). The GST activity was reduced by diclofenac in liver. Trophic exposure of H. malabaricus to dexamethasone caused an increase in antioxidant system (GPx, CAT, GST, and GSH) and LPO in liver. However, it reduced antioxidant system (GPX and GST activities and GSH) in gonads. Both diclofenac and dexamethasone reduced the levels of testosterone, causing impairment to reproduction. Diclofenac reduced HSI at the 0.2 µg/kg, but not GSI. Our results suggest that the anti-inflammatory drugs diclofenac and dexamethasone caused oxidative stress and reduced testosterone levels that can have a negative impact in aquatic organisms.

Modulatory effect of nano TiO2on Pb in Hoplias malabaricus trophically exposed.

This study investigated the hepatic and neural effects of TiO2 nanoparticle and Pb in Hoplias malabaricus trophically exposed. The alanine transaminase activity was altered at the high dose of exposed group to Pb and at the lowest doses of co-exposed groups. It may reflect the hepatic effects of TiO2 on Pb toxicity, but the aspatate transaminase activity was not altered. The decreased injury index observed at the highest dose of co-exposed group compared to TiO2 may be related to the increased energy demand and can explain the more pronounced toxic effects observed in this group. The liver authomethallography revealed the metals presence at high dose groups. Serotonin concentration increased at the Pb lowest dose and at the highest dose of co-exposed group compare to control. Most importantly, when associated the contaminants were able to interact and altered some biomarkers. However, further studies, about action mechanisms of this co-exposure are needed.