Chlorantraniliprole (Coragen® 20% SC) exposure induced reproductive toxicity mediated by oxidative stress, apoptosis, and sperm quality deficient in male Wistar rats.

Abstract

Pesticides can adversely affect reproduction by causing congenital abnormalities, fetal demise, and infertility. The reproductive toxicity of coragen, a modified ryanodine receptor-targeting insecticide with chlorantraniliprole concentrations of 20%, was examined in male rats. Twenty-one healthy male rats were randomly assigned to one of three groups: the control group, two orally administered with low (500 mg/kg) and high (1000 mg/kg) doses of coragen for 8 weeks. Exposure to coragen resulted in significant, dose-dependent changes in male reproductive hormones, steroidogenic enzymes, and an imbalance in the oxidant-antioxidant system. The treated groups revealed significantly higher lipid peroxidation levels than the control group. The effects were accompanied by damage to testicular tissue, modified testicular lactate dehydrogenase, reduced sperm motility and viability, and heightened sperm abnormalities. Elevated levels of pro-apoptotic proteins (caspase-3 and Bax) and decreased levels of anti-apoptotic protein (Bcl-2) provided evidence of apoptosis in both treatment groups. Moreover, coragen induced substantial DNA damage in the testicular tissue. The results indicate that the reproductive impairment caused by coragen may be ascribed to oxidative stress, hormonal disturbance, apoptosis, and damage to testicular DNA and finally might result in infertility and compromised reproductive function.