Experimental Study of Deltamethrin-Induced Nephrotoxicity in the Rat Model

The purpose of this study was to determine the nephrotoxic effect of deltamethrin in experimental animals at a dose of 43.5mg/kg (1/2 LD50). Materials and Methods: For the experiment, 48 male Wistar rats with a body weight of 240±10g were divided into 4 groups of 12 animals each. Groups 1 and 3 were control groups, which were administered a physiological solution intragastrically. The animals in Groups 2 and 4 received a single dose (43.5mg/kg) of the synthetic pyrethroid deltamethrin, which corresponds to 1/2 LD50. Rats were withdrawn from the experiment in two stages: 1) rats in Groups 1 and 2 – one day after the deltamethrin administration; 2) rats in Groups 3 and 4 – 3 days after the deltamethrin administration. Biochemical and pathomorphological changes in the kidneys were evaluated. The evaluation criteria were the content of pyruvate, inorganic phosphate, and glutathione and the activity of glutathione peroxidase activity (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) in the kidneys. Histological preparations of kidney tissue were studied. Results: The single administration of a toxic dose of deltamethrin caused a decrease in body weight of rats, an increase in kidney weight, and the accumulation of pyruvate and inorganic phosphate in the kidneys. A decrease in the GSH content in the kidney was accompanied by an increase in the activity of GPx, GR and GST. One day after the experiment, in the convoluted tubules, epithelial cells with blurred contours of the boundaries were enlarged; and the granularity of the cytoplasm containing vacuoles was expressed. The nuclei of epithelial cells had different sizes; some of them were in a state of pycnosis. In the organ parenchyma, large and small blood vessels full of blood were visible. Three days after the intoxication, these symptoms became more pronounced. In the intertubular connective tissue, hemorrhages and leukocyte infiltrates were detected. Conclusion: The study confirms the nephrotoxic effect of a single toxic dose (43.5mg/kg [1/2LD50]) of deltamethrin. Pathomorphological changes in the kidneys are accompanied by the disturbances in energy metabolism and activation of the glutathione antioxidant system with the development of glutathione deficiency

Impact of Acute Deltamethrin Poisoning on Rat Adrenal Glands: Biochemical and Pathomorphological Study

Background: Deltamethrin is known all over the world as an effective preparation for the control of insects. In connection with this, its role as a chemical stressor increases. The aim of the study was to determine the features of the functioning and structure of AG after a single administration of synthetic pyrethroid deltamethrin in experimental animals at a dose of 17.4 mg/kg (1/5 LD50). Material and Methods: For the experiment, 88 male Wistar rats with a body weight of 240±10 g were divided into 8 groups of 10–12 animals each. Groups 1, 3, 5, and 7 were control groups, which were administered physiological solution intragastrically. The animals in Groups 2, 4, 6, and 8 received a single dose (17.4mg/kg) of deltamethrin, which corresponds to 1/5 LD50. In the serum of rats, the content of ACTH, progesterone, DHEA-sulfate, corticosterone and aldosterone was determined by EIA. Histological preparations of adrenal glands were stained with H&E, picrofuxin according to Van Gieson, and with Bismarck brown according to Shubich. On frozen sections, lipids were detected by Sudan Black B. Results: One day after intoxication, we identified an increase in adrenal mass, edema of the parenchyma and blood capillary overflow, and a large number of lipids in corticocytes. In the blood serum, the concentration of ACTH and corticosteroids increased, but their level decreased in the adrenal cortex. After 3 days, the concentration of corticosterone in the blood serum of the experimental animals remained above the control value, but the content of other hormones decreased. At the border of the cortex and the medulla of the adrenal glands, there were mast cells in a state of degranulation; the amount of lipids decreased with time. In the subsequent terms of the study, a decrease in the weight of AG with a decrease in the concentration of hormones in the blood serum and adrenal tissue was detected. Conclusion: The intoxication of rats with deltamethrin causes morphofunctional changes in AG that characterize the development of the stress response. The hormonal background is not restored within a month, which indicates the possibility of developing post-toxic complications