NADH stimulates endogenous dopamine biosynthesis

NADH stimulates endogenous dopamine biosynthesis

Abstract
Treatment of Parkinson patients with L-DOPA 3,4-dihydroxy-L-phenylalanine. leads to endproduct inhibition of tyrosine
hydroxylase, the key enzyme in dopamine biosynthesis and the enzyme needing tetrahydrobiopterin and iron as cofactors.
To overcome this problem an alternative treatment was investigated which attempted to stimulate endogenous dopamine
biosynthesis. Incubation of rat PC 12 cells with NADH  b-nicotinamide adeninedinucleotide. leads to increased dopamine
production. We investigated the possibility that this increase of dopamine biosynthesis was due to stimulation of quinonoid
dihydropteridine reductase, the enzyme which recycles the inactive dihydrobiopterin to the active tetrahydrobiopterin. The
experiments showed that whereas NADH is able to increase dopamine production in PC 12 cells rat phaeochromocytoma
cells, clone PC 12. up to three-fold, no influence is exerted by NADH on pteridine metabolism; neither are tetrahydrobiopterin
concentrations nor the de novo-biosynthesis of pteridines from guanosine triphosphate altered by NADH. Further
no influence of NADH on protein de novo synthesis of quinonoid dihydropteridine reductase was observed. However,
NADH was able to directly increase the catalytic activity of this enzyme. Our results suggest that the stimulation of
dopamine biosynthesis by NADH is due to more rapid regeneration of quinonoid dihydrobiopterin to tetrahydrobiopterin…

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