The toxicological effects of α-cypermethrin on placental oxidative balance in a rat model

α-Cypermethrin, a synthetic pyrethroid, is highly lipophilic, allowing it to accumulate in fatty tissues, the liver, and the brain, and potentially cross the placental barrier. Although α-cypermethrin primarily acts by disrupting neuronal sodium channel function, its potential to induce oxidative stress highlights an additional pathway of toxicity. Pyrethroids are nowadays recognized as potential endocrine disruptors, with oxidative stress suggested as a mechanism linking exposure to adverse health outcomes. This study aimed to investigate the effects of α-cypermethrin exposure on oxidative stress induction by analyzing relevant biomarkers (malondialdehyde, MDA; reactive oxygen species, ROS; reduced glutathione, GSH; and activities of catalase, CAT, superoxide dismutase, SOD, and glutathione peroxidase, GPx) in the placentas of pregnant rats exposed to 1, 10, or 19 mg/kg/day throughout gestation. A dose-dependent increase in ROS production and lipid peroxidation, as indicated by elevated MDA levels, was observed. These elevated MDA concentrations likely resulted from the lipophilic nature of α-cypermethrin, which facilitates its penetration into cell membranes, promoting lipid peroxidation. GSH levels remained unchanged across all exposure groups. Although CAT and GPx activities decreased, SOD activity was consistently elevated in all samples, indicating compensatory activation of the antioxidant defense system. The most pronounced disruption of oxidative--antioxidant balance occurred at the lowest tested dose (1 mg/kg). These findings suggest that α-cypermethrin induces oxidative stress in sensitive tissues such as the placenta, potentially contributing to disruption of the endocrine system.