Prenatal methamphetamine exposure induces oxidative stress and apoptosis in the ovaries of rat offspring.

Methamphetamine abuse among women of reproductive age is a growing concern, necessitating investigation of its intrauterine effects on offspring. In this study, we examined the induction of oxidative stress and apoptosis in the ovaries of rat offspring following maternal methamphetamine exposure. Pregnant Wistar rats received methamphetamine (2 mg/kg or 5 mg/kg) from gestational day 10 until delivery. Control rats received 0.9% saline (1 mL/kg) on the same schedule. Female offspring were raised to puberty and their ovaries were examined, compared to controls. Protein expression levels of FASL and TRAIL were assessed by immunohistochemistry, and antioxidant enzyme levels (superoxide dismutase, SOD) and oxidative stress marker levels (malondialdehyde, MDA) were evaluated by ELISA1. Histological examination of the ovaries was performed using H&E staining. Maternal methamphetamine treatment significantly increased ovarian FASL and TRAIL protein expression in the pubertal offspring (p ≤ 0.001). In utero methamphetamine exposure led to a dose-dependent increase in ovarian MDA levels and a corresponding decrease in SOD activity (p ≤ 0.05). Histologically, exposed offspring showed a reduction in the number of primordial, primary, secondary, and Graafian follicles, as well as a reduction in corpora lutea, compared to controls (p < 0.05). Conversely, the number of atretic follicles increased significantly in a dose-dependent manner (p < 0.05). Prenatal methamphetamine exposure induces oxidative stress and promotes apoptosis in the ovaries of offspring, leading to reduced ovarian follicle reserves. These findings raise concerns that methamphetamine use during pregnancy may impair female reproductive health in offspring.