Antioxidant effects on the intracerebroventricular galactose damage in rats

We investigated the effects of the intracerebroventricular infusion of galactose and the influence of pretreatment with antioxidants on oxidative stress parameters and acethylcholinesterase (AChE) activity in the brain of 60-day-old Wistar rats (6 per group). The animals were divided into naïve group (did not undergo surgery); procedure group (only underwent surgery); sham group (underwent surgery and received 5 μL saline) and galactose group (received 5 μL of galactose solution (5.0 mM) by intracerebroventricular injection), and were killed by decapitation after 1 h. Other groups were pretreated daily for 1 week with saline (sham and galactose groups) or antioxidants, α-tocopherol (40 mg/kg) plus ascorbic acid (100 mg/kg, i.p.) (antioxidants and galactose + antioxidants groups). Twelve hours after the last antioxidants injection, animals received an intracerebroventricular infusion of 5 μL of galactose solution (galactose and galactose + antioxidants groups) or saline (sham and antioxidants groups) and were sacrificed 1 h later. Galactose elevated thiobarbituric acid reactive substances (TBA-RS), protein carbonyl content and glutathione peroxidase (GSH-Px) activity and decreased total sulfhydryl content and catalase (CAT) activity in the cerebral cortex. In the hippocampus, galactose enhanced TBA-RS, decreased total sulfhydryl content and increased AChE activity, while in the cerebellum it decreased total sulfhydryl content and increased CAT and superoxide dismutase (SOD) activities. Pretreatment with antioxidants prevented the majority of these alterations, indicating the participation of free radicals in these effects. Thus, intracerebroventricular galactose infusion impairs redox homeostasis in the brain; the administration of antioxidants should be considered as an adjuvant therapy to specific diets in galactosemia.