Dihydronicotinamid-adenin-dinucleotid

140.0-142.0 °C

140.0 - 142.0 °C

Chemical: Adenosine 5′-(trihydrogen diphosphate), P′.fwdarw.5′-ester with 1,4-dihydro-1-.beta.-D-ribofuranosyl-3-pyridinecarboxamide

Adenosine 5'-(trihydrogen diphosphate), P'→5'-ester with 1,4-dihydro-1-.beta.-D-ribofuranosyl-3-pyridinecarboxamide, disodium salt: Does not have an individual approval but may be used under an appropriate group standard

Chemical: Adenosine 5′-(trihydrogen diphosphate), P′.fwdarw.5′-ester with 1,4-dihydro-1-.beta.-D-ribofuranosyl-3-pyridinecarboxamide

Adenosine 5'-(trihydrogen diphosphate), P'→5'-ester with 1,4-dihydro-1-.beta.-D-ribofuranosyl-3-pyridinecarboxamide, disodium salt: Does not have an individual approval but may be used under an appropriate group standard

A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). The action of supplemental NADH is unclear. Oral NADH supplementation has been used to combat simple fatigue as well as such mysterious and energy-sapping disorders as chronic fatigue syndrome and fibromyalgia. Researchers are also studying the value of NADH supplements for improving mental function in people with Alzheimer's disease, and minimizing physical disability and relieving depression in people with Parkinson's disease. Some healthy individuals also take NADH supplements orally to improve concentration and memory capacity, as well as to increase athletic endurance. However, to date there have been no published studies to indicate that using NADH is in any way effective or safe for these purposes.

NADH is synthesized by the body and thus is not an essential nutrient. It does require the essential nutrient nicotinamide for its synthesis, and its role in energy production is certainly an essential one. In addition to its role in the mitochondrial electron transport chain, NADH is produced in the cytosol. The mitochondrial membrane is impermeable to NADH, and this permeability barrier effectively separates the cytoplasmic from the mitochondrial NADH pools. However, cytoplasmic NADH can be used for biologic energy production. This occurs when the malate-aspartate shuttle introduces reducing equivalents from NADH in the cytosol to the electron transport chain of the mitochondria. This shuttle mainly occurs in the liver and heart.

11-beta-hydroxylase deficiency (CYP11B1)；17-alpha-hydroxylase deficiency (CYP17)；17-Beta Hydroxysteroid Dehydrogenase III Deficiency；2-aminoadipic 2-oxoadipic aciduria；2-Hydroxyglutric Aciduria (D And L Form)；2-ketoglutarate dehydrogenase complex deficiency；2-Methyl-3-Hydroxybutryl CoA Dehydrogenase Deficiency；21-hydroxylase deficiency (CYP21)；27-Hydroxylase Deficiency；3-Beta-Hydroxysteroid Dehydrogenase Deficiency；Total 46220 pathways, visit the HMDB page for details