Role of Vitamin-A on the Cerebral Cortex of Adult Male Wistar Rats Exposed to Methamphetamine

Abstract

Methamphetamine (METH) can induce oxidative stress and structural injury in the cerebral cortex, whereas vitamin A participates in antioxidant defence and neural maintenance. This study evaluated the effect of low-dose vitamin A on methamphetamine-induced cortical changes in adult male Wistar rats. Twenty rats were allocated to four groups (n = 5): control, METH only, vitamin A only and combined METH plus vitamin A. METH was administered orally at 5 mg/kg at 3-hour intervals within 12 hours per day, while vitamin A was administered orally at 0.7 mg/kg once daily for 28 consecutive days. Body weight, elevated plus-maze performance, cerebral-cortex malondialdehyde, glutathione and superoxide dismutase levels, and cortical histoarchitecture were assessed. METH-only exposure was associated with reduced body weight, a higher malondialdehyde level, lower glutathione and superoxide dismutase activities, altered open-arm time and marked cortical degeneration. Co-administration of vitamin A was associated with improved body-weight change, oxidative-stress indices closer to control values and better preservation of cortical architecture than METH-only treatment. The vitamin A-only group showed weight gain, antioxidant-marker values near those of the control group and largely preserved cortical morphology. Under the experimental conditions, low-dose vitamin A was associated with partial attenuation of methamphetamine-induced oxidative and histological changes in the cerebral cortex. These findings are limited to the measured outcomes in a small animal model and require confirmation through larger studies with clearly defined dosing and additional molecular assessments.