Effects of neonicotinoid insecticide sulfoxaflor on oxidative stress and caspase-3 gene expression in the brain of Swiss albino mice (Mus musculus) and the protective role of fucoidan

The aim of this study is to investigate the effects of the neonicotinoid insecticide sulfoxaflor on GSH-dependent antioxidant system, lipid peroxidation and caspase-3 gene expression in the brain of male Swiss albino mice (Mus musculus) and the protective role of the sulfated polysaccharide fucoidan which has antioxidant properties, in these processes. For this purpose, sulfoxaflor were administered to mice at a dose of 15 mg/kg and fuciodan at a dose of 50 mg/kg by intragastric gavage for 24 hours and 7 days. The amounts of tGSH, TBARS, protein and the enzyme activities of GPx, GR, GST were determined by spectrophotometric methods and caspase-3 mRNA expression level was determined by RT-PCR in the brain of mice. It was determined that sulfoxaflor caused an increases in the amount of TBARS and enzyme activities of GPx, GR, GST and caspase-3 mRNA expression and decreased the amount of tGSH in the brain. It was also shown that coadministration of fucoidan and sulfoxaflor reduced the amount of TBARS, increased the amount of tGSH by raising the control levels, and increased the GPx, GR, GST enzyme activities in the brain. The increases in caspase-3 mRNA expression levels caused by sulfoxaflor were decreased to control levels with the effect of fucoidan. Results of the present study indicated that sulfoxaflor triggered apoptotic cell death by causing oxidative stress. Fucoidan supported the GSH-dependent antioxidant system with its antioxidant effect and played a protective role in the brain cells from oxidative conditions and apoptotic cell death caused by sulfoxaflor.