Genotoxicity of quinclorac herbicide and protective effect of rosmarinic acid on gill tissue of adult zebrafish (Danio rerio, Hamilton 1822)

It is known that herbicides are used the most among pesticides in the world. In our country, the use of herbicides is increasing day by day and with this increase, the negative effects of herbicides on the environment and living organisms increase accordingly. Quinclorac (3,7-dichloro-8-quinolinecarboxylic acid), a quinolone carboxylic acid derivative, is a new, selective auxin group herbicide used in rice, turf, wheat and chemical fallow. In this study, DNA damage by Random Amplified Polymorphic DNA (RAPD) method and antioxidant, oxidative stress, gene repair, heat shock, cell cycle control by Quantitative Real Time PCR (qRT-PCR) in gill tissues of Zebrafish treated with quinclorac herbicide. It was aimed to reveal the mechanism of action of certain cell defense systems such as apoptosis pathway, to evaluate the protective effect of Rosmarinic acid (RA) obtained from rosemary plant against the toxic effect of quinclorac herbicide, and to reveal the relationship between genotoxic effect of quinclorac herbicide on tissue and RA. Zebrafish were treated with 177.00 mg/L, 88.50 mg/L, 44.25 mg/L and 100 μM RA separately and 100 μM RA+ 177.00 mg/L together with the highest quinclorac concentration for 48 hours with decreasing concentrations of quinclorac herbicide in multiples of the LC50 96 h value determined after the preliminary study. When the results were evaluated, the indicators detected in RAPD profiles after quinclorac exposure showed a change in percent genomic pattern stability (% GST). The expression levels of antioxidant (Cu-Zn SOD, Mn-SOD, GPX, GST, MT2), insulin-like growth factor (IGF2), heat shock protein (HSP70), cell cycle checkpoint (P21Kip1 and P27Kip1), DNA repair (XPA, XPC and XRCC3) and apoptosis pathway (P53, BAX, Caspase 3, Cytochrome C) genes increased after quinclorac exposure at the highest test concentration. After treatment with the highest test concentration of RA, results similar to the control group were obtained. As a result, it was determined that quinclorac exposure caused an increase in antioxidant defense system gene expressions, induced DNA damage, interrupted cell cycle progression, increased DNA repair system gene expressions, and triggered apoptotic pathway since it may have increased ROS formation. In the test groups in which RA was used, it was found to induce survival by protecting cells from toxic effects due to its antioxidant mechanism of action.