The toxicity of Acetamiprid in various tissues of rats and the protective role of sodium selenite

Acetamiprid is one of the most commonly used commercial neonicotinoids. Neonicotinoids have recently gained significant attention as a group of pesticides used in insect control. Selenium, on the other hand, is a naturally occurring antioxidant in food that is essential for human health. In this thesis, Acetamiprid, Sodium selenite, and a combination of Acetamiprid + Sodium selenite were administered via gavage to adult male Wistar rats for 28 days. After the administration period, kidney weights, serum levels of urea, uric acid, and creatinine (which are indicators of kidney function), as well as histopathological changes in kidney tissues under light microscopy, were examined comparatively with the control group. At the end of the 4th week of the experiment, no statistically significant differences were observed in absolute or relative kidney weights between the control group, the Sodium selenite group, the Acetamiprid group, and the Sodium selenite + Acetamiprid group. When comparing the control group and the Sodium selenite group, no significant differences were found in the serum levels of urea, uric acid, and creatinine. However, when the control group and Sodium selenite treated groups were compared with Acetamiprid and Sodium selenite+Acetamiprid treated groups, a statistically significant increase in serum urea levels and no change in uric acid and creatinine levels were observed. When Acetamiprid treated group was compared with Sodium selenite+Acetamiprid treated group, a statistically significant decrease was observed in serum urea, uric acid and creatinine levels in Sodium selenite+Acetamiprid treated group. When the kidney tissue was examined, severe tubular degeneration and vascular congestion, moderate glomerular atrophy, hemorrhage, infiltration and glomerular lobulation were observed in Acetamiprid treated group. Mild histopathologic changes were observed in the sodium selenite+acetamipride treated group. In conclusion, acetamiprid caused nephrotoxicity in rats and sodium selenite alleviated this nephrotoxicity, although not completely.