DIETARY RIBOFLAVIN RESTRICTION AND CHRONIC HEMIN ADMINISTRATION DOES NOT ALTER BRAIN FUNCTION IN RATS: THE IMPORTANCE OF VITAMIN HOMEOSTASIS IN THE BRAIN

Vitamin B2 deficiency associated with normal dietary intake has been reported inpatients with Parkinson disease (PD), suggesting impaired absorption of this micronutrient. Elevated red meat consumption was thought to contribute as a triggering factor, as the catabolism of hemin (a neurotoxic substance) requires vitamin B2 (Coimbra &Junqueira, 2003). This study tested this hypothesis by verifying the effects of dietary riboflavin restriction associated with hemin administration on rat brain. After 8 months of riboflavin restriction, riboflavin deficiency with or without oral administration of hemin (assessed by erythrocyte glutathion ereductase activity) did not impair motor function or spatial learning; neither altered the volume of substantia nigra or brain concentrations of total glutathione. Partial dietary restriction of riboflavin may failed to induce oxidative stress in the rat brain and dopaminergic degeneration in the rat substantia nigra as suggested to occur in humans by Coimbra & Junqueita, (2003), possibly due to an intact mechanism of nutritional privilege that preserves riboflavin content in the normal rat brain during deficiency states. Contrastingly, polymorphic enzymes or receptors involved in the human cellular uptake of ribofiavin may conceivably impair the transport of this micronutrient not only through the intestinal wall and renal tubules, but also in the brain of PD patients, there by annulling the nutritional privilege of the nervous system.