부산대학교 도서관

Vitamin B2 deficiency-associated with normal dietary intake has been reported in patients wire Parkinson's 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 (Colmbra & Junqueim, 2003), This study rested this hypothesis by verifying the effects of dietary riboflavin restriction associated with heroin administration on rat brain. After 8 months of riboflavin restriction, riboflavin deficiency with or without oral administration of hemin (assessed by etythrocyte glutathione reductase 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 & Junqueira, (2003). possibly due to an intact mechanism of nutritional privilege that preserves riboflavin content in the normal rat brain during deficiency states. Contrastingly, polynorphic enzymes or receptors involved in the human cellular uptake of riboflavin 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, thereby annulling the nutritional privilege of the nervous system. [ABSTRACT FROM AUTHOR]