Effect of the Neonicotinoid Insecticide Thiacloprid on Oxidative Stress, Genotoxic, and Immunotoxic Biomarkers in Greater Wax Moth, Galleria mellonella

Abstract

The aim of this study was to investigate the effect of the neonicotinoid insecticide Thiacloprid on oxidative stress, genotoxic, and immunotoxic biomarkers in Galleria mellonella. The effects of neonicotinoid insecticide thiacloprid on antioxidant enzyme activities, malondialdehyde (MDA) levels, hemocyte number, micronucleus frequency of greater wax moth (Galleria mellonella) larvae at different doses (5, 10, 15, 20, 25, and 30 µg) and periods (24, 48, 72, and 96 hrs) were explored. Superoxide dismutase (SOD) activity increased significantly at 5, 10, and 15 µg thiacloprid doses compared to the control and negative control in all periods tested, while significantly decreased at 20, 25, and 30 µg doses. Catalase (CAT) activity showed significant increases at 5, 10 and 15 µg thiacloprid doses at 24 and 96h compared to the control and negative control. MDA concentrations showed significant increases in all periods compared to the control and negative control. At 24th, 48th, 72nd and 96th, total hemocyte count (THC) decreased significantly at all doses except 5 µg thiacloprid concentration. During all the tested periods, there was a significant increase in the number of micronuclei, particularly at high doses of thiacloprid (20, 25, and 30 µg) compared to both the control and negative control. Additionally, a positive correlation was observed between MDA and the number of micronuclei, while other markers showed a negative correlation with micronucleus (MN). These results suggest that high doses of thiacloprid induce significant increases in micronuclei formation and are positively correlated with MDA levels, indicating oxidative damage and genotoxicity caused by thiacloprid exposure in the tested organism. Overall, our findings suggest that the measured parameters can be considered reliable biomarkers to demonstrate oxidative damage from thiacloprid exposure.