Abstract
Endocrine-disrupting chemicals (EDCs) are compounds that affect the way the endocrine system works in both humans and animals. The emphasis of the research was on the negative effects of mercaptophos exposure on Cyprinus carpio. Fish were subjected to sub-lethal amounts of mercaptophos at low (0.83 ppm) and high (2.1 ppm) concentrations for 12, 24, 48, and 96 h. The levels of lipid peroxidation (LPO), protein carbonyl (PC), and glutathione (GSH) were tested in the fish liver. Plasma cortisol and testosterone levels, as well as a histological examination of liver tissue, were also assessed. C. carpio treated with mercaptophos had lower testosterone levels and higher cortisol levels at all time intervals. Mercaptophos exhibited oxidative stress in C. carpio, which causes a time-and concentration-dependent augmentation of liver LPO and PC levels, which is linked to hepatic GSH depletion. A low concentration of mercaptophos caused atrophy of pancreatic acinar cells as well as the detection of karyolysis nuclei, according to histological alterations in hepatic tissue. Treatment with a high dosage of mercaptophos resulted in hypertrophy of Kupffer cells as well as coagulative necrosis of pancreatic tissue. Furthermore, short-term mercaptophos exposure reduced testosterone and cortisol levels in C. carpio, which are associated with the development of oxidative stress. Changes in hormone levels and oxidative stress markers in C. carpio may therefore aid in the prediction of disease.
•The C. carpio mortality caused by mercaptophos was directly proportional to its concentration.•Lipid peroxidation levels increase by increasing the time of exposure to mercaptophos.•GSH was depleted with a high concentration of mercaptophos.•The high-concentration of mercaptophos had coagulative necrosis of pancreatic tissue and hydropic hepatocyte degeneration.