scholarly journals Adenine Nucleotide and Nicotinamide Adenine Dinucleotide Measurements in Plants

2020 ◽  
Vol 5 (3) ◽  
Author(s):  
Youjun Zhang ◽  
Ina Krahnert ◽  
Antje Bolze ◽  
Yves Gibon ◽  
Alisdair R. Fernie
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Adenine Nucleotide ◽  
Nicotinamide Adenine

scholarly journals Changes in Levels of Nicotinamide Adenine Nucleotides and Krebs Cycle Intermediates in Mung Bean Leaves after Illumination

1967 ◽  
Vol 20 (2) ◽  
pp. 319 ◽  
Author(s):  
D Graham ◽  
Judith E Cooper
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Time Course ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Krebs Cycle ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Rapid Decline ◽  
Second Phase ◽  
Krebs Cycle Intermediates

Changes in levels of nicotinamide adenine nucleotides were measured during a short (30 min) period of illumination following a dark period. Two phases in the time course were found. In the first phase, during the first minute of illumination, a rapid decline in oxidized nicotinamide adenine dinucleotide occurred which represented a net loss of nicotinamide adenine nucleotide. In the subsequent, second phase during illumination, a slower decline in oxidized nicotinamide adenine dinucleotide was found which was coincident with increases in nicotinamide adenine dinucleotide phosphate(s). The changes in the reduced nicotinamide adenine nucleo� tides were relatively small during illumination.

scholarly journals Adenine Nucleotide Metabolites in Uremic Erythrocytes as Metabolic Markers of Chronic Kidney Disease in Children

2021 ◽  
Vol 10 (21) ◽  
pp. 5208
Author(s):  
Joanna Piechowicz ◽  
Andrzej Gamian ◽  
Danuta Zwolińska ◽  
Dorota Polak-Jonkisz
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Nicotinic Acid ◽  
Nicotinamide Adenine Dinucleotide ◽  
Positive Impact ◽  
Adenine Nucleotide ◽  
Group Iv ◽  
Nicotinamide Adenine ◽  
Reduced Form ◽  
Group Ii

Chronic kidney disease (CKD) is associated with multifaceted pathophysiological lesions including metabolic pathways in red blood cells (RBC). The aim of the study was to determine the concentration of adenine nucleotide metabolites, i.e., nicotinamide adenine dinucleotide (NAD)-oxidized form, nicotinamide adenine dinucleotide hydrate (NADH)-reduced form, nicotinic acid mononucleotide (NAMN), β-nicotinamide mononucleotide (NMN), nicotinic acid adenine dinucleotide (NAAD), nicotinic acid (NA) and nicotinamide (NAM) in RBC and to determine a relationship between NAD metabolites and CKD progression. Forty-eight CKD children and 33 age-matched controls were examined. Patients were divided into groups depending on the CKD stages (Group II-stage II, Group III- stage III, Group IV- stage IV and Group RRT children on dialysis). To determine the above-mentioned metabolites concentrations in RBC liquid chromatography-mass spectrometry was used. Results: the only difference between the groups was shown concerning NAD in RBC, although the values did not differ significantly from controls. The lowest NAD values were found in Group II (188.6 ± 124.49 nmol/mL, the highest in group IV (324.94 ± 63.06 nmol/mL. Between Groups II and IV, as well as III and IV, the differences were statistically significant (p < 0.032, p < 0.046 respectively). Conclusions. CKD children do not have evident abnormalities of RBC metabolism with respect to adenine nucleotide metabolites. The significant differences in erythrocyte NAD concentrations between CKD stages may suggest the activation of adaptive defense mechanisms aimed at erythrocyte metabolic stabilization. It seems that the implementation of RRT has a positive impact on RBC NAD metabolism, but further research performed on a larger population is needed to confirm it.

CONTROL OF REDUCED NICOTINAMIDE-ADENINE DINUCLEO-TIDE OXIDATION BY PIGEON-HEART MITOCHONDRIA

1966 ◽  
Vol 44 (11) ◽  
pp. 1527-1537 ◽  
Author(s):  
M. C. Blanchaer ◽  
Thomas J. Griffith
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Adenine Nucleotide ◽  
Respiratory Control ◽  
Adenosine Diphosphate ◽  
Nadh Oxidation ◽  
Heart Mitochondria ◽  
Nicotinamide Adenine ◽  
Nucleotide Inhibition ◽  
Reduced Nicotinamide Adenine Dinucleotide ◽  
A Site

The rate of oxidation of 10–35 μM reduced nicotinamide–adenine dinucleotide (NADH) by pigeon-heart mitochondria was increased not only by osmotic swelling and sonic disruption of the organelles but also by milder procedures such as washing or dilution, which had no deleterious effect on the P: O and respiratory control ratios when glutamate was the substrate. In all cases, the enhanced oxidation of 10 μM NADH was suppressed by 5 mM adenosine triphosphate (ATP). From these and other findings it was concluded that the access of extra-mitochondrial NADH to the respiratory chain is controlled at a minimum of two sites. Control of NADH flux through the first site is lost after treatment of the mitochondria by procedures which increase their permeability. A second level of NADH control survives sonic disruption of the mitochondria and is a site at which the oxidation of 10 μM NADH is stimulated by Pi and inhibited by ATP, adenosine diphosphate (ADP), and oxidized nicotinamide–adenine dinucleotide (NAD+). The ATP and ADP effects at this level are not blocked by oligomycin. Magnesium releases the adenine nucleotide inhibition of NADH oxidation under certain conditions, but its site and mode of action is not clear as yet. In these experiments, NADH oxidation was determined polarographically and photometrically at 28° in a medium containing 0.23 M mannitol, 0.07 M sucrose, 0.02 M Tris–chloride, and 0.02 mM ethylenediamine tetra-acetic acid (EDTA) at pH 7.2.

Effect of Niacin on Mitochondria of Allium Cepa Root Cells

1967 ◽  
Vol 25 ◽  
pp. 78-79
Author(s):  
M. Arif Hayat
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Hydrogen Transfer ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Root Tips ◽  
Root Cells ◽  
Transfer Processes ◽  
Standard Procedures ◽  
A Cell ◽  
Critical Interest

Although it is recognized that niacin (pyridine-3-carboxylic acid), incorporated as the amide in nicotinamide adenine dinucleotide (NAD) or in nicotinamide adenine dinucleotide phosphate (NADP), is a cofactor in hydrogen transfer in numerous enzyme reactions in all organisms studied, virtually no information is available on the effect of this vitamin on a cell at the submicroscopic level. Since mitochondria act as sites for many hydrogen transfer processes, the possible response of mitochondria to niacin treatment is, therefore, of critical interest.Onion bulbs were placed on vials filled with double distilled water in the dark at 25°C. After two days the bulbs and newly developed root system were transferred to vials containing 0.1% niacin. Root tips were collected at ¼, ½, 1, 2, 4, and 8 hr. intervals after treatment. The tissues were fixed in glutaraldehyde-OsO4 as well as in 2% KMnO4 according to standard procedures. In both cases, the tissues were dehydrated in an acetone series and embedded in Reynolds' lead citrate for 3-10 minutes.

Nicotinamide Adenine Dinucleotide and the Metabolism of Ethanol and Acetaldehyde

1967 ◽  
Vol 28 (2) ◽  
pp. 213-224 ◽  
Author(s):  
E. Majchrowicz ◽  
B. L. Bercaw ◽  
W. M. Cole ◽  
D. H. Gregory
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine
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