Early-gestational binge ethanol exposure induces persistent motor dysfunction associated with cerebellar redox and cytokine dysregulation in rat offspring.

Ethanol (EtOH) exposure frequently occurs before pregnancy recognition, making early embryonic development particularly vulnerable to inadvertent alcohol exposure. This study evaluated the effects of binge-like EtOH exposure during early gestation on neurobehavioral, oxidative, and inflammatory outcomes in male and female rat offspring. Pregnant rats received EtOH (3 g/kg/day, intragastric gavage) on gestational days 6, 7, and 8, while control animals received distilled water. Offspring were evaluated at postnatal day 23 (PN23) and postnatal day 42 (PN42) using the pole, open field, and rotarod tests. The cerebellum was collected for analysis of oxidative stress markers and cytokines. Data were analyzed by two-way ANOVA followed by Tukey's post hoc test (p < 0.05). EtOH exposure induced locomotor alterations at both PN23 and PN42, mainly characterized by reduced total distance traveled, accompanied by impaired balance and forced locomotion. In the cerebellum, both ages exhibited reduced glutathione levels and total antioxidant capacity, together with increased lipid peroxidation. Cytokine alterations displayed a temporal pattern, with reduced IL-1β and TNF-α levels at PN23 and increased levels at PN42, whereas IL-6 and IL-10 remained elevated at both time points. Females exhibited more pronounced impairments in spontaneous locomotion, particularly at PN42. These findings demonstrate that brief binge-like EtOH exposure during early gestation is sufficient to induce persistent motor dysfunction accompanied by cerebellar redox imbalance and cytokine dysregulation, with evidence of sex-dependent behavioral susceptibility.