Prenatal Ethion Exposure Disrupts Reproductive Health in First‐Generation Rats

Ethion is a commonly used OP (Organophosphate) pesticide. The present study evaluated the transgenerational reproductive effects of prenatal ethion exposure in rats. Different doses of ethion were orally administered to pregnant rats from gestational day (GD) 6-19, at doses of 0.86, 1.7, 3.43, and 6.9 mg/kg in groundnut oil. On post-natal day (PND) 1, body weight, crown-rump length (CRL), anogenital distance (AGD), tail length, and physical status of pups were evaluated. Post-natal survival was assessed by weekly monitoring of body weight, day of pinna detachment, teeth eruption, fur development, and eye and ear opening. Pubertal onset and oestrus cycle duration were recorded in female and male offspring and they were sacrificed on PND 60, and 75 respectively. Sperm parameters and levels of malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD), catalase, mRNA expression of 3β-Hydroxysteroid dehydrogenase (3βHSD), DNA fragmentation, and histology of reproductive organs were evaluated. Lower ethion doses increased body weights, CRL, AGD, and tail lengths in pups. However, the highest dose showed significant weight reduction. Ethion delayed all postnatal developmental milestones in Filial (F1) offspring. In females, ethion-exposed groups showed prolonged oestrus cycle duration. MDA levels were elevated in the uterus, ovary, and testis. The uterus of ethion groups showed marked papillary projections and severe myometrial degeneration. The ovary showed disrupted ovarian stroma architecture and fewer developing and matured follicles in the ethion groups. mRNA expression of the 3βHSD gene revealed decreased fold change except in the 1.7 mg/kg group where an increase in the fold change was recorded. Ethion advanced the testis descent and delayed pubertal onset in males. It also reduced sperm count, motility, intact acrosome percentage, and increased sperm abnormalities. Ethion caused severe testicular degeneration with necrosis of spermatogonial cells and the formation of giant cells. It caused a decrease in the fold change of mRNA expression of the 3βHSD gene in the ovary and testis. No DNA fragmentation was observed. The findings indicate that prenatal ethion exposure induced marked transgenerational reproductive toxicity in rats.