NADH disodium salt is the sodium salt form of nicotinamide adenine dinucleotide phosphate (NADH), a coenzyme that serves as a regenerative electron donor in cellular energy metabolism, including glycolysis, beta oxidation, and citric acid Loop[1]. NADH can be used for the synthesis and regeneration of tetrahydrobiopterin (BH4), which is an essential cofactor for the rate-limiting enzyme in dopamine (DA) synthesis [2].
In vitro, NADH disodium salt (1mM) treated C2C12, Neuro2a and AML12 cells for 24h, significantly increased the NAD+ production of the three cells and protected the cells from genotoxicity [3]. NADH disodium salt (100µM) treated HUVEC and PIEC cells for 30 minutes had no significant effect on intracellular O2- production [4]. When treatment with NADH disodium salt (100µM) induces rodent β-cells, it cannot enhance depolarization-induced exocytosis [5].
In vivo, subcutaneous injection of NADH disodium salt (10 or 100 mg/kg) in SD rats did not affect the tissue contents of DA, 5-HT and their metabolites in the midbrain or striatum [2]. When treated with intraperitoneal injection of NADH disodium salt (1000mg/kg) in C57BL/6J mice, the NAD+ content in the blood, brain, fat and kidney increased several times, and the NAD+ content in the liver increased by more than 7 times within 4 hours [3]. Intraperitoneal injection of NADH disodium salt (5µM) into ICR mice significantly increased the urinary excretion of nicotinamide and its metabolites [6].
References:
[1] Ying W. NAD+ and NADH in cellular functions and cell death[J]. Front Biosci, 2006, 11(1): 3129-3148.
[2]Pearl S M, Antion M D, Stanwood G D, et al. Effects of NADH on dopamine release in rat striatum[J]. Synapse, 2000, 36(2): 95-101.
[3] Wu K, Li J, Zhou X, et al. NADH and NRH as potential dietary supplements or pharmacological agents for early liver injury caused by acute alcohol exposure[J]. Journal of Functional Foods, 2021, 87: 104852.
[4] Li,J. Differential NADPH-versus NADH-dependent superoxide production by phagocyte-type endothelial cell NADPH oxidase[J].Cardiovascular Research, 2001, 52(3):477.
[5] Ivarsson R, Quintens R, Dejonghe S, et al. Redox control of exocytosis: regulatory role of NADPH, thioredoxin, and glutaredoxin[J]. Diabetes, 2005, 54(7): 2132-2142.
[6]Kimura N, Fukuwatari T, Sasaki R, et al. Comparison of metabolic fates of nicotinamide, NAD+ and NADH administered orally and intraperitoneally; characterization of oral NADH[J]. Journal of nutritional science and vitaminology, 2006, 52(2): 142-148.
NADH disodium salt是烟酰胺腺嘌呤二核苷酸磷酸(NADH)的一种钠盐形式,NADH是一种辅酶,在细胞能量代谢中作为再生电子供体,包括糖酵解、β氧化和柠檬酸循环[1]。NADH可用于四氢生物蝶呤(BH4)的合成和再生,BH4又是多巴胺(DA)合成限速酶的必需辅因子[2]。
在体外,NADH disodium salt(1mM)处理C2C12, Neuro2a和AML12细胞24h,显著增加了三种细胞的NAD+的产量并保护细胞免受遗传毒性[3]。NADH disodium salt(100µM)处理HUVEC和PIEC细胞30分钟,对细胞内的O2-产量没有显著影响[4]。NADH disodium salt(100µM)处理诱导啮齿动物β细胞时,不能增强去极化诱发的胞吐作用[5]。
在体内,NADH disodium salt(10或100 mg/kg)皮下注射处理SD大鼠,不影响中脑或纹状体中DA、5-HT及其代谢产物的组织含量[2]。NADH disodium salt(1000mg/kg)腹膜内注射处理C57BL/6J小鼠,血液、脑、脂肪和肾脏中NAD+含量增加数倍,肝脏中4h内超过7倍[3]。NADH disodium salt(5µM)腹腔注射处理ICR小鼠,显著增加了体内烟酰胺及其代谢物的尿排泄[6]。