関: FAD、flavin-adenine dinucleotide

WordNet

a silvery soft waxy metallic element of the alkali metal group; occurs abundantly in natural compounds (especially in salt water); burns with a yellow flame and reacts violently in water; occurs in sea water and in the mineral halite (rock salt) (同)Na, atomic number 11
(biochemistry) purine base found in DNA and RNA; pairs with thymine in DNA and with uracil in RNA (同)A
a ketone that forms the nucleus of certain natural yellow pigments like riboflavin

PrepTutorEJDIC

ソジウム,ナトリウム(金属元素;化学記号はNa)
アデニン(肝臓・茶の葉から採れる塩基の一種)

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1. 母体血中の無細胞胎児核酸を使った出生前診断 prenatal diagnosis using cell free fetal nucleic acids in maternal blood
2. 小児におけるエタノール中毒：疫学、毒性の推定、および毒性作用 ethanol intoxication in children epidemiology estimation of toxicity and toxic effects
3. 塩分摂取量および塩分摂取量制限と本態性高血圧 salt intake salt restriction and essential hypertension
4. 尿酸による腎疾患 uric acid renal diseases
5. 分子遺伝学の原理 principles of molecular genetics

English Journal

Diabetic Cardiomyopathy: Mechanisms and New Treatment Strategies Targeting Antioxidant Signaling Pathways.

Huynh K1, Bernardo BC2, McMullen JR3, Ritchie RH4.Author information 1Baker IDI Heart & Diabetes Institute Melbourne; Department of Medicine, Monash University, Clayton, Victoria, Australia.2Baker IDI Heart & Diabetes Institute Melbourne.3Baker IDI Heart & Diabetes Institute Melbourne; Department of Medicine, Monash University, Clayton, Victoria, Australia; Department of Physiology, Monash University, Clayton, Victoria, Australia. Electronic address: julie.mcmullen@bakeridi.edu.au.4Baker IDI Heart & Diabetes Institute Melbourne; Department of Medicine, Monash University, Clayton, Victoria, Australia. Electronic address: rebecca.ritchie@bakeridi.edu.au.AbstractCardiovascular disease is the primary cause of morbidity and mortality amongst the diabetic population. Both experimental and clinical evidence suggest that diabetic subjects are predisposed to a distinct cardiomyopathy, independent of concomitant macro- and microvascular disorders. 'Diabetic cardiomyopathy' is characterized by early impairments in diastolic function, accompanied by the development of cardiomyocyte hypertrophy, myocardial fibrosis and cardiomyocyte apoptosis. The pathophysiology underlying diabetes-induced cardiac damage is complex and multifactorial, with elevated oxidative stress a key contributor. We now review the current evidence of molecular disturbances present in the diabetic heart, and their role in the development of diabetes-induced impairments in myocardial function and structure. Our focus incorporates both the contribution of increased reactive oxygen species production and reduced antioxidant defenses to diabetic cardiomyopathy, together with modulation of protein signaling pathways and the emerging role of protein O-GlcNAcylation and miRNA dysregulation in the progression of diabetic heart disease. Lastly, we discuss both conventional and novel therapeutic approaches for the treatment of left ventricular dysfunction in diabetic patients, from inhibition of the renin-angiotensin-aldosterone-system, through recent evidence favoring supplementation of endogenous antioxidants for the treatment of diabetic cardiomyopathy. Novel therapeutic strategies, such as gene therapy targeting the phosphoinositide 3-kinase PI3K(p110α) signaling pathway, and miRNA dysregulation, are also reviewed. Targeting redox stress and protective protein signaling pathways may represent a future strategy for combating the ever-increasing incidence of heart failure in the diabetic population.
Pharmacology & therapeutics.Pharmacol Ther.2014 Jan 22. pii: S0163-7258(14)00026-6. doi: 10.1016/j.pharmthera.2014.01.003. [Epub ahead of print]
Cardiovascular disease is the primary cause of morbidity and mortality amongst the diabetic population. Both experimental and clinical evidence suggest that diabetic subjects are predisposed to a distinct cardiomyopathy, independent of concomitant macro- and microvascular disorders. 'Diabetic cardio
PMID 24462787

The role of cyclophilin D in interspecies differences in susceptibility to hepatotoxic drug-induced mitochondrial injury.

Sekine S, Kimura T, Motoyama M, Shitara Y, Wakazono H, Oida H, Horie T.Author information Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.AbstractTest compound A ((5Z)-6-[(2R,3S)-3-({[(4-Chloro-2-methylphenyl)sulfonyl]amino}methyl) bicyclo[2.2.2]oct-2-yl]hex-5-enoic acid) was withdrawn from premarketing clinical trials due to severe liver injury. Intracellular accumulation of lipids (steatosis) has been observed in human-derived cells and may account for the severe hepatotoxicity. Mitochondrial β-oxidation and ketogenesis play a fundamental role in energy homeostasis. Mitochondrial dysfunction can therefore cause severe deficiency in fatty acid oxidation and apoptosis which finally triggers the hepatocellular injury. Some of hepatotoxic drugs (e.g., salicylic acid, diclofenac and troglitazone) are known to induce mitochondrial dysfunction. This study therefore examined the effect of compound A on the mitochondrial permeability transition (MPT) and membrane potential in mitochondria isolated from mouse, rat and monkey livers. The incubation of rat and monkey mitochondria energized by succinate in the presence of Ca(2+) (20μM) and compound A (2.5-10μM) resulted in cyclosporin A (CsA)-sensitive MPT pore opening and a decline in mitochondrial membrane potential in a concentration-dependent manner. However, mouse mitochondria showed low susceptibility to compound A-induced dysfunction. Rat mitochondrial expression of cyclophilin D (CyPD) was about twice that of mouse mitochondria, but the expression levels of other MPT pore proteins (adenine nucleotide translocator and voltage-dependent anion channel) were comparable in both species. An assessment of the effect of compound A on CyPD knockdown cells demonstrated that mitochondrial susceptibility to compound A was attenuated in CyPD knockdown cells. These results suggest that an interspecies difference in the susceptibility to mitochondrial dysfunction induced by compound A exists as a result of species-specific discrepancies in CyPD expression.
Biochemical pharmacology.Biochem Pharmacol.2013 Nov 15;86(10):1507-14. doi: 10.1016/j.bcp.2013.08.027. Epub 2013 Sep 3.
Test compound A ((5Z)-6-[(2R,3S)-3-({[(4-Chloro-2-methylphenyl)sulfonyl]amino}methyl) bicyclo[2.2.2]oct-2-yl]hex-5-enoic acid) was withdrawn from premarketing clinical trials due to severe liver injury. Intracellular accumulation of lipids (steatosis) has been observed in human-derived cells and may
PMID 24012842

Electrochemical behavior of flavin adenine dinucleotide adsorbed onto carbon nanotube and nitrogen-doped carbon nanotube electrodes.

Goran JM, Stevenson KJ.Author information Department of Chemistry, Center for Electrochemistry, Center for Nano- and Molecular Science and Technology, The University of Texas at Austin , 1 University Station, A5300, Austin, Texas 78712, United States.AbstractFlavin adenine dinucleotide (FAD) is a cofactor for many enzymes, but also an informative redox active surface probe for electrode materials such as carbon nanotubes (CNTs) and nitrogen-doped CNTs (N-CNTs). FAD spontaneously adsorbs onto the surface of CNTs and N-CNTs, displaying Langmuir adsorption characteristics. The Langmuir adsorption model provides a means of calculating the electroactive surface area (ESA), the equilibrium constant for the adsorption and desorption processes (K), and the Gibbs free energy of adsorption (ΔG°). Traditional ESA measurements based on the diffusional flux of a redox active molecule to the electrode surface underestimate the ESA of porous materials because pores are not penetrated. Techniques such as gas adsortion (BET) overestimate the ESA because it includes both electroactive and inactive areas. The ESA determined by extrapolation of the Langmuir adsorption model with the electroactive surface probe FAD will penetrate pores and only include electroactive areas. The redox activity of adsorbed FAD also displays a strong dependency on pH, which provides a means of determining the pKa of the surface confined species. The pKa of FAD decreases as the nitrogen content in the CNTs increases, suggesting a decreased hydrophobicity of the N-CNT surface. FAD desorption at N-CNTs slowly transforms the main FAD surface redox reaction with E1/2 at -0.84 V into two new, reversible, surface confined redox reactions with E1/2 at -0.65 and -0.76 V (vs Hg/Hg2SO4), respectively (1.0 M sodium phosphate buffer pH = 6.75). This is the first time these redox reactions have been observed. The new surface confined redox reactions were not observed during FAD desorption from nondoped CNTs.
Langmuir : the ACS journal of surfaces and colloids.Langmuir.2013 Nov 5;29(44):13605-13. doi: 10.1021/la403020y. Epub 2013 Oct 24.
Flavin adenine dinucleotide (FAD) is a cofactor for many enzymes, but also an informative redox active surface probe for electrode materials such as carbon nanotubes (CNTs) and nitrogen-doped CNTs (N-CNTs). FAD spontaneously adsorbs onto the surface of CNTs and N-CNTs, displaying Langmuir adsorption
PMID 24156654

Japanese Journal

2-haloacrylate hydratase, a new class of flavoenzyme that catalyzes the addition of water to the substrate for dehalogenation.

Mowafy Amr M,Kurihara Tatsuo,Kurata Atsushi,Uemura Tadashi,Esaki Nobuyoshi
Applied and environmental microbiology 76(18), 6032-6037, 2010-09
… Here we report the occurrence of a new reduced flavin adenine dinucleotide (FAD) (FADH(2))-dependent enzyme that catalyzes the removal of a halogen atom from an unsaturated aliphatic organohalogen compound by the addition of a water molecule to the substrate. … We found that 2-CAA is converted into pyruvate when the reaction was carried out with purified Caa67(YL) in the presence of FAD and a reducing agent [NAD(P)H or sodium dithionite] under anaerobic conditions. …
NAID 80021312186

ミクロゾームでのエタノールの代謝による脂質過酸化反応に対するフラビンアデニンジヌクレオチドの抑制効果

渡辺聡,河内佐十
ビタミン 68(2), 79-85, 1994-02-25
… The increase of TBARS was inhibited by the addition of flavin adenine dinucleotide (FAD), superoxide dismutase or catalase, and was also inhibited by uric acid or mannitol but not inhibited by sodium azide. …
NAID 110002847805

Purification and Properties of Reduced Nicotinamide Adenine Dinucleotide Dehydrogenase from Photobacterium phosphoreum

足立博一,古西清司,足立伊佐雄,堀越勇
Chemical & pharmaceutical bulletin 40(2), 427-431, 1992-02-25
… Reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase (EC 1.6.99.3) of Photobacterium phosphoreum was solubilized from membrane vesicles with 2% sucrose monolaurate, and was purified almost to homogeneity by use of diethylaminoethyl (DEAE)-Sephacel, hydroxylapatite, and Butyl-Toyopearl column chromatography in the presence of 0.5% sucrose monolaurate. …
NAID 110003629779