黄素腺嘌呤二核苷酸 (FAD) 是一种氧化还原辅助因子，更具体地说是蛋白质的辅基，参与代谢中的几个重要酶促反应。
Animal experiment: | Dogs[1]The dogs are divided into 3 groups and they are received the following treatments. Each group consists of 6 dogs. Dogs in group I as control, are given 2 mL/kg of physiological saline by intravenous injection. Ten min after the start of the first injection, another dose of saline, 1 mL/kg, is injected intravenously. Dogs in group II are given i.v. 2 mL saline/kg. Ten min afterwards, 1 mg chlorpromazine(CPZ)/kg is injected. Dogs in group III are given i.v. Flavin Adenin Dinucleotide, 2 mg/kg. Ten min later, they are given CPZ, 1 mg/kg. All solutions is administrated in 1 min or 2. Blood samples are taken before and 10, 20, 30, and 40 min after the intravenous injection of saline (groups I and II) or Flavin Adenin Dinucleotide (group III). Serum K+ and blood pH are also measured. Heart rate, blood pressure and ventricular fibrillation threshold (VFT) of each dog are recorded at the same intervals[1]. |
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| 产品描述 | Flavin Adenin Dinucleotide is a redox cofactor, more specifically a prosthetic group of a protein, involved in several important enzymatic reactions in metabolism.
Poly(Flavin Adenin Dinucleotide, FAD) characterized by an additional polymer-type redox reaction is a highly effective electrocatalyst for NADH oxidation: operating at the lowest potentials reported for NADH transducers (0.00 V, pH 7.4), poly(FAD) is characterized by the electrochemical rate constant of 1.8 ± 0.6×10-3 cm/s, which is at the level of the NADH mass-transfer constant. Poly(FAD)-modified electrodes are characterized by the dramatically improved stability and, is the most advantageous NADH transducers for analytical chemistry[2].
Flavin Adenin Dinucleotide (2 mg/kg, i.v.) significantly cancels chlorpromazine (CPZ)-induced decrease in ventricular fibrillation threshold (VFT). Flavin Adenin Dinucleotide cancels the effect of CPZ on canine heart mitochondria. After injection of Flavin Adenin Dinucleotide, the dogs show a transient hypotension within 10 min, then their blood pressures recover to the initial level. Flavin Adenin Dinucleotide also prevents mitochondrial dysfunction induced by chlorpromazine[1].
Reference：
[1]. Sugiyama S, et al. Protection of chlorpromazine-induced arrhythmia by flavin-adenine-dinucleotide in canine heart. Jpn Heart J. 1979 Sep;20(5):657-65.
[2]. Karyakin AA, et al. Electropolymerized flavin adenine dinucleotide as an advanced NADH transducer. Anal Chem. 2004 Apr 1;76(7):2004-9. |
