Background Trichlorfon is a widely used organophosphorus pesticide, but the relationship between its neurotoxicity and reproductive toxicity and oxidative stress has not been fully elucidated.

Objective This experiment observes the pathological changes of brain tissues and gonads of pregnant rats and their offspring after prenatal trichlorfon exposure, and explores whether trichlorfon causes neurotoxicity and reproductive toxicity through oxidative stress.

Methods Forty-eight pregnant SD rats were randomly divided into a control group and 2, 10, and 50 mg·kg^-1 trichlorfon exposure groups, with 12 rats in each group, and continuously received designed oral administration from proestrus to parturition. After delivery, the brains and gonads (ovaries/testicles) of the dams and their offspring were isolated, and the whole blood samples of the dams were collected. The pathological changes of the brains and gonads were observed by HE staining; the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) were detected by ELISA; the concentration of trichlorfon metabolite dimethyl phosphate (DMP) in the blood of mother rats were measured by gas chromatography. The correlations between maternal DMP and offspring's oxidative stress indicators were evaluated.

Results In the brains of postpartum mother rats, the SOD activities of the 10 and the 50 mg·kg^-1 trichlorfon exposure groups were higher than that of the control grouprespectively (15.72±2.31), (15.50±2.29), and (13.00±1.72) U·mg^-1, calculated by protein, thereafter (P < 0.05), and mild cerebral edema accompanied. In the brains of neonatal rats, the MDA content of the 50 mg·kg^-1 trichlorfon exposure group was higher than that of the control grouprespectively (1.42±0.49) and (1.02±0.18) nmol·g^-1, calculated by protein, thereafter (P < 0.05), and cerebral edema also occurred. In the ovaries of postpartum mother rats, the 50 mg·kg^-1 trichlorfon exposure group formed more atresia follicles, and their average MDA content was higher than the control group's(1.37±0.30) and (1.03±0.18) nmol·g^-1 respectively (P < 0.05). In the gonads of neonatal rats, both sexes of the 50 mg·kg^-1 trichlorfon exposure group had increased MDA content and decreased SOD and GSH-Px activities compared with the control group (P < 0.05), and the histopathological changes were damaged ovarian structure and follicle formation in the female offspring rats, and testicular congestion and irregular and reduced spermatogenic cells in the male offspring rats. In addition, the blood DMP concentrations of postpartum mother rats of the 50 mg·kg^-1 trichlorfon exposure group was higher than that of the 10 mg·kg^-1 trichlorfon exposure group(984.52±207.94) and (271.83±80.97) mg·L^-1 respectively (P < 0.01); as the maternal blood DMP concentration increased, the offspring's testicular SOD activity decreased, and the two showed a linear negative correlation (r=-0.638, P < 0.05).

Conclusion After prenatal exposure to trichlorfon at designed doses, both pregnant rats and their progeny produce neurotoxicity and reproductive toxicity, and oxidative stress may be one of their mechanisms.