Genotoxicity and behavioral alterations induced by retene in adult zebrafish

Retene (1-methyl-7-isopropylphenanthrene; RET), a non-priority polycyclic aromatic hydrocarbon (PAH), is one of the most widely produced PAHs following cellulose burning. Despite RET toxicity observed in various aquatic organisms, the underlying mechanisms remain unclear. In this study, the genotoxic and neurotoxic effects of RET were investigated using zebrafish as experimental model. Adult zebrafish were exposed to 250, 500, 750, and 1000 µg/L RET for 96 h. RET increased micronuclei frequency, demonstrating its genotoxic potential. After RET exposure, adult zebrafish exhibited alterations in locomotion and exploration endpoints. RET also increased the levels of the reactive oxygen species (ROS) in the zebrafish brains, indicating an imbalance in the redox status. Moreover, in its initial concentration, the mRNA levels of superoxide dismutase ( sod1 and sod2 ), glutathione-disulfide reductase ( gsr ), glutathione peroxidase 1 A ( gpx1a ) were up-regulated; however, in the two highest RET concentrations, the transcriptional level of nuclear factor erythroid 2 like 2 ( nfe2l2 ) was down-regulated, leading to the reduction of mRNA levels of all the antioxidant defense genes investigated. Furthermore, RET decreased the mRNA levels of genes encoding components of the cholinergic, serotoninergic, and gamma-amino butyric acid (GABA) neurotransmitter systems. Taken together, these results demonstrate that RET affects DNA generating micronuclei and provide new evidence suggesting that the behavioral alterations in zebrafish could be due to changes in oxidative stress and the mRNA expression of the neurotransmitter systems. These results reinforce the risk posed by environmental pollutants to aquatic ecosystems, especially those whose toxic potentials remain underestimated. • RET leads to genotoxic effects in erythrocytes of adult zebrafish. • RET changes locomotion and exploratory endpoints in adult zebrafish. • Aberrant redox status may explain the behavioral alterations after RET exposure. • RET exposure alters the mRNA expression of neurotransmitter pathways.