5-methyltetrahydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: effects on vascular tetrahydrobiopterin availability and endothelial nitric oxide synthase coupling.

5-methyltetrahydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: effects on vascular tetrahydrobiopterin availability and endothelial nitric oxide synthase coupling.

BACKGROUND: The circulating form of folic acid, 5-methyltetrahydrofolate (5-MTHF), may have beneficial effects on endothelial function; however, its mechanisms of action remain uncertain. Decreased nitric oxide (NO) bioavailability and increased vascular superoxide production in vascular disease sta...

Disgrifiad llawn

Manylion Llyfryddiaeth
Prif Awduron:	Antoniades, C, Shirodaria, C, Warrick, N, Cai, S, de Bono, J, Lee, J, Leeson, P, Neubauer, S, Ratnatunga, C, Pillai, R, Refsum, H, Channon, K
Fformat:	Journal article
Iaith:	English
Cyhoeddwyd:	2006

Eitemau Tebyg

5-Methyl-tetrahydrofolate acid improves endothelial function and decreases superoxide production by improving eNOS coupling and increasing tetrahydrobiopterin bioavailability in human vessels in vivo
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Low- and high- dose treatment with folic acid, equally improve endothelial function and decrease superoxide production in human vessels via tetrahydrobiopterin-mediated eNOS coupling
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Effects of 5-methyl-tetrahydrofolic acid on endothelial function and vascular superoxide production in human coronary artery disease
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MTHFR 677 C>T Polymorphism reveals functional importance for 5-methyltetrahydrofolate, not homocysteine, in regulation of vascular redox state and endothelial function in human atherosclerosis.
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Altered plasma versus vascular biopterins in human atherosclerosis reveal relationships between endothelial nitric oxide synthase coupling, endothelial function, and inflammation.
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Mechanisms of increased vascular superoxide production in human diabetes mellitus: role of NAD(P)H oxidase and endothelial nitric oxide synthase.
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5-methyl-tetrahydrofolate increases eNOS activity by preventing peroxynitrite-induced oxidation of tetrahydrobiopterin in human vessels
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Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency.
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Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency
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Intravenous infusion of 5-methyl-tetrahydrofolate rapidly improves eNOS Coupling. In human vessels by increasing tetrahydrobiopterin bioavailability
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Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation.
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Endothelial cell tetrahydrobiopterin: going with the flow.
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Plasma asymmetrical-dimethyl-arginine (ADMA) regulates nitric oxide bioavailability and vascular superoxide production in human vessels
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Genetic Polymorphism On Methyl-Tetrahydrofolate-Reductase Affects Vascular Superoxide Generation and Nitric Oxide Bioavailability By Regulating eNOS Coupling in Human Arteries and Veins
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Plasma asymmetrical-dimethyl-arginine affects eNOS vascular superoxide radical production and nitric oxide bioavailability in human arteries and veins
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