Paracetamol causes endocrine disruption and hepatotoxicity in male fish Rhamdia quelen after subchronic exposure

- Males of Rhamdia quelen were exposed during 21 d to paracetamol.
- Paracetamol disrupted the hypothalamic-pituitary-gonadal axis in males fish.
- Paracetamol caused oxidative stress and hematologic changes.
- Paracetamol caused hepatotoxicity in Rhamdia quelen.
- Paracetamol release to the environment can be hazardous to the fish.

Paracetamol is one of the most widely sold non-prescription drugs. This study aimed to evaluate the effects of the paracetamol on reproductive, biochemical, genetic, histopathological and hematogical biomarkers by waterborne exposure. Male fish of Rhamdia quelen were exposed to environmental concentrations of paracetamol (0, 0.25, 2.5 μg/L) in a semi-static bioassay for 21 days. Hemoglobin and hematocrit were reduced upon exposure to 0.25 μg/L of paracetamol. Leukocytes and thrombocytes increased after paracetamol exposure. Paracetamol reduced testosterone levels in all exposed groups and increased estradiol levels at higher concentration. Serotonin and dopamine levels increased at exposure to 0.25 μg/L. Paracetamol also caused protein carbonyls and increased SOD activity in fish exposed to 2.5 μg/L and in addition led to an inhibition of EROD and GST activities in both concentrations. Hepatic genotoxicity occurred at the 0.25 μg/L concentration. Hepatic tissues of exposed fish showed mild blood congestion and leucocytes infiltration. The results showed that paracetamol disrupted the hypothalamic-pituitary-gonadal axis, changed hematological parameters and caused hepatotoxicity in Rhamdia quelen. The findings suggest that this drug merits attention relative to its potential endocrine disrupter effect and hepatotoxicity, even at concentrations found in the aquatic environment.