Disease relevance of nicotinamide adenine dinucleotide

• Nicotinamide-adenine dinucleotide phosphate oxidase assembly and activation in EBV-transformed B lymphoblastoid cell lines of normal and chronic granulomatous disease patients [1].
• Muscle fibers strongly reactive for both adenosinetriphosphatase and nicotinamide-adenine dinucleotide diaphorase, observed in central core disease and mitochondrial myopathy, were not associated with increased terminal innervation ratio [2].
• An enzyme degrading reduced nicotinamide-adenine dinucleotide in Proteus vulgaris [3].
• Mice deficient in nicotinamide-adenine dinucleotide phosphate oxidase activity (gp91(phox-/-)), nitric oxide synthase activity (NOS2(-/-)), or both (gp91(phox-/-)/NOS2(-/-)) were infected with Helicobacter organisms and evaluated for inflammation and bacteria load [4].
• Characterization of a nicotinamide-adenine dinucleotide-dependent cation channel in the CRI-G1 rat insulinoma cell line [5].

Psychiatry related information on nicotinamide adenine dinucleotide

• Elevated mitochondrial reduced nicotinamide-adenine dinucleotide-linked substrates suggest that reduced nicotinamide-adenine dinucleotide-ubiquinone oxidoreductase may be deficient in the brain in Rett syndrome patients [6].

High impact information on nicotinamide adenine dinucleotide

• The SIR2 protein family comprises a novel class of nicotinamide-adenine dinucleotide (NAD)-dependent protein deacetylases that function in transcriptional silencing, DNA repair, and life-span extension in Saccharomyces cerevisiae [7].
• Tumor necrosis factor and immune interferon synergistically induce cytochrome b-245 heavy-chain gene expression and nicotinamide-adenine dinucleotide phosphate hydrogenase oxidase in human leukemic myeloid cells [8].
• Distorted distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase neurons in temporal lobe of schizophrenics implies anomalous cortical development [9].
• Altered distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase cells in frontal lobe of schizophrenics implies disturbances of cortical development [10].
• In the present investigation in matched schizophrenic and control brains, we examined a particular population of neurons found in the prefrontal cortex and underlying white matter and characterized by histochemical staining for the enzyme nicotinamide-adenine dinucleotide phosphate-diaphorase [10].

Chemical compound and disease context of nicotinamide adenine dinucleotide

• Activation of nitrite reductase from Escherichia coli K12 by oxidized nicotinamide-adenine dinucleotide [11].
• Myocardial biopsy specimens were obtained before, during, and after ischemia, and levels of adenine nucleotides, nucleosides, oxypurines, and the oxidized form of nicotinamide-adenine dinucleotide were determined [12].
• This project consisted of a detailed histologic and histochemical analysis of the distribution of muscle spindles in paraspinal musculature of patients suffering from idiopathic scoliosis, using the reduced form of nicotinamide-adenine dinucleotide (NADH), adenosine triphosphatase (ATPase), and Tri-chrome stain techniques [13].
• Treatment with eplerenone, a selective aldosterone receptor blocker, almost completely prevented podocyte damage and proteinuria, with normalization of elevated reduced nicotinamide-adenine dinucleotide phosphate oxidase activity [14].
• The results confirmed that superoxide radicals play an important role in the pathogenesis of DDC-induced gastric ulcer in rats and suggested that NADPH (reduced nicotinamide-adenine dinucleotide phosphate) oxidase in PAF-activated polymorphonuclear leukocytes may be involved in the generation of these radicals [15].

Biological context of nicotinamide adenine dinucleotide

• Cocaine and its derivatives blunt neutrophil functions without influencing phosphorylation of a 47-kilodalton component of the reduced nicotinamide-adenine dinucleotide phosphate oxidase [16].
• Hydroxylation of aromatic compounds by reduced nicotinamide-adenine dinucleotide and phenazine methosulphate requires hydrogen peroxide and hydroxyl radicals, but not superoxide [17].
• Hydrolysis of nicotinamide-adenine dinucleotide by purified renal brush-border membranes. Mechanism of NAD+ inhibition of brush-border membrane phosphate-transport activity [18].
• The respiratory chain enzyme activity ratios, which are normally constant irrespective of the tissue tested, were markedly abnormal in all three patients (cytochrome c oxidase/reduced nicotinamide-adenine dinucleotide cytochrome c reductase, 4.6 to 10.4; normal mean +/- 1 SD, 2.9 +/- 0.5) [19].
• Calf-spleen nicotinamide-adenine dinucleotide glycohydrolase. Properties of the active site [20].

Anatomical context of nicotinamide adenine dinucleotide

• Four nicotinamide-adenine dinucleotide phosphate-requiring enzymes were measured in disrupted cultured skin fibroblasts from a 19-year-old patient with juvenile onset of a spinocerebellar and extrapyramidal syndrome [21].
• Extracellular synthesis of cADP-ribose from nicotinamide-adenine dinucleotide by rat cortical astrocytes in culture [22].
• The only compound found to be increased in the CLL B-lymphocytes when compared to their normal counterparts was nicotinamide-adenine dinucleotide [23].
• Cytolytic bursts were generally observed at 20-s intervals, which match the previously described reduced nicotinamide-adenine dinucleotide phosphate and superoxide release oscillation periods for neutrophils; we speculate that metabolic oscillations of the effector cell drive the membrane damage of the target [24].
• Since the KYN pathway leads to formation of nicotinamide-adenine dinucleotide (NADH), the present results may be a further indication of a defect in NADH:ubiquinone oxidoreductase (complex I) in mitochondria in PD [25].

Associations of nicotinamide adenine dinucleotide with other chemical compounds

• Purified PGH synthase when acting on arachidonic acid in the presence of reduced nicotinamide-adenine dinucleotide or reduced nicotinamide-adenine dinucleotide 3'-phosphate generated superoxide in burst-like fashion [26].
• Oxidized form of nicotinamide-adenine dinucleotide and cytochrome a,a3 quickly became reduced in the ischemic core, but a tardyspontaneous postischemic tissue perfusion resulted in their hyperoxidation [27].
• Adenosine diphosphate (ADP)/oxygen ratios with nicotinamide-adenine dinucleotide (NAD)-linked substrates, but not with succinate, were increased in brain mitochondria from experimental animals at each age [28].
• To induce in vitro superoxide anion (O2-) production, we used either particulate (e.g., opsonized bacteria or zymosan) or soluble (e.g., phorbol esters) stimuli, which allowed us to test two distinct pathways for reduced nicotinamide-adenine dinucleotide phosphate activation [29].
• Evaluation of equilibrium constants for the interaction of lactate dehydrogenase isoenzymes with reduced nicotinamide-adenine dinucleotide by affinity chromatography [30].

Gene context of nicotinamide adenine dinucleotide

• The final step in the biosynthesis of nicotinamide-adenine dinucleotide, a major coenzyme in cellular redox reactions and involved in intracellular signaling, is catalyzed by the enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT) [31].
• To this end, first we examined the abundance of several components of reduced nicotinamide-adenine dinucleotide phosphate oxidase (identified as the major source of reactive oxygen species), including gp91phox/Nox2, p22phox, p47phox, and Nox3 using real-time PCR [32].
• The maternally transmitted Ag is a cell surface product of three gene products: 1) H-2M3a (formerly Hmta), a class I MHC heavy chain; 2) beta 2-microglobulin; and 3) maternally transmitted factor (Mtf), the N-terminus of the mitochondrially encoded ND1 subunit of the reduced form of nicotinamide-adenine dinucleotide dehydrogenase [33].
• The involvement of nicotinamide-adenine dinucleotide diphosphate oxidase in the enhanced 02*- production was demonstrated by the finding that the cytosolic components of the enzyme, p47phox and p67phox, were both translocated to the plasma membrane of enriched but otherwise unmanipulated monocytes of SSc patients [34].
• The nadB gene encodes L-aspartate oxidase and has been shown in several bacteria to be essential for de novo nicotinamide-adenine dinucleotide (NAD) biosynthesis [35].

Analytical, diagnostic and therapeutic context of nicotinamide adenine dinucleotide

• The technique is sufficiently sensitive to detect increased (nicotinamide-adenine dinucleotide (NADH) during dissection of hepatic vessels before ligation 0.52 +/- 0.04 (n = 14, P < .03) compared with the in situ exposed liver, 0.43 +/- 0.02 n = 14) [36].
• Determination of nicotinamide-adenine dinucleotide and thiazole-4-carboxamide-adenine dinucleotide in human leukocytes by reversed-phase high-performance liquid chromatography [37].
• This study is the first to investigate the alteration in hepatic function during and after cardiopulmonary bypass in 30 patients by measuring the arterial ketone body ratio, an index of mitochondrial redox potential (oxidized nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide) [38].
• METHODS: We measured Ca(2+)-ATPase activity using a reduced nicotinamide-adenine dinucleotide-coupled reaction, determined sarcoplasmic reticulum Ca(2+)-dependent ATPase protein using Western blotting, and determined 4-hydroxyproline using amino-acid analysis [39].
• Real-time RT-PCR was performed to measure expression of transcripts of endogenous GTP cyclohydrolase-1 and components of reduced nicotinamide-adenine dinucleotide phosphate oxidase [40].

References