scholarly journals On the Relative Efficacy of Nicotinamide and Nicotinic Acid as Precursors of Nicotinamide Adenine Dinucleotide

1966 ◽  
Vol 241 (10) ◽  
pp. 2367-2372
Author(s):  
Barbara Petrack ◽  
Paul Greengard ◽  
Helen Kalinsky
Blood ◽  
1990 ◽  
Vol 75 (8) ◽  
pp. 1705-1710 ◽  
Author(s):  
CR Zerez ◽  
EF Jr Roth ◽  
S Schulman ◽  
KR Tanaka

Abstract Plasmodium falciparum-infected red blood cells (RBCs) are characterized by increases in the activity of glycolytic enzymes. Because nicotinamide adenine dinucleotide (NAD) and NAD phosphate (NADP) are cofactors in the reactions of glycolysis and pentose phosphate shunt, we have examined NAD and NADP content in P. falciparum-infected RBCs. Although NADP content was not significantly altered, NAD content was increased approximately 10-fold in infected RBCs (66% parasitemia) compared with uninfected control RBCs. To determine the mechanism for the increase in NAD content, we examined the activity of several NAD biosynthetic enzymes. It is known that normal human RBCs make NAD exclusively from nicotinic acid and lack the capacity to make NAD from nicotinamide. We demonstrate that infected RBCs have readily detectable nicotinamide phosphoribosyltransferase (NPRT), the first enzyme in the NAD biosynthetic pathway that uses nicotinamide, and abundant nicotinamide deamidase, the enzyme that converts nicotinamide to nicotinic acid, thereby indicating that infected RBCs can make NAD from nicotinamide. In addition, infected RBCs have a threefold increase in nicotinic acid phosphoribosyltransferase (NAPRT), the first enzyme in the NAD biosynthetic pathway that uses nicotinic acid. Thus, the increase in NAD content in P falciparum-infected RBCs appears to be mediated by increases in NAD synthesis from both nicotinic acid and nicotinamide.


1969 ◽  
Vol 115 (4) ◽  
pp. 679-685 ◽  
Author(s):  
I. J. Ryrie ◽  
K. J. Scott

1. The relative efficiencies of nicotinate, quinolinate and nicotinamide as precursors of NAD+ were measured in the first leaf of barley seedlings. 2. In small amounts, both [14C]nicotinate and [14C]quinolinate were quickly and efficiently incorporated into NAD+ and some evidence is presented suggesting that NAD+ is formed from each via nicotinic acid mononucleotide and deamido-NAD. 3. [14C]Nicotinamide served equally well as a precursor of NAD+ and although significant amounts of [14C]NMN were detected, most of the [14C]NAD+ was derived from nicotinate intermediates formed by deamination of [14C]nicotinamide. 4. Radioactive NMN was also a product of the metabolism of [14C]nicotinate and [14C]quinolinate but most probably it arose from the breakdown of [14C]NAD+. 5. In barley leaves where the concentration of NAD+ is markedly increased by infection with Erysiphe graminis, the pathways of NAD+ biosynthesis did not appear to be altered after infection. A comparison of the rates of [14C]NAD+ formation in infected and non-infected leaves indicated that the increase in NAD+ content was not due to an increased rate of synthesis.


2020 ◽  
Author(s):  
Tae-Sik Nam ◽  
Dae-Ryoung Park ◽  
So-Young Rah ◽  
Tae-Gyu Woo ◽  
Hun Taeg Chung ◽  
...  

AbstractNicotinic acid adenine dinucleotide phosphate (NAADP) is an obligate driver of calcium signaling whose formation from other metabolites of nicotinamide adenine dinucleotide (NAD+) has remained elusive. In vitro, CD38-mediated NAADP synthesis requires an acidic pH and a nonphysiological concentration of nicotinic acid (NA). We discovered that the type II membrane form of CD38 catalyzes synthesis of NAADP by exchanging the nicotinamide moiety of nicotinamide adenine dinucleotide phosphate (NADP+) for the NA group of nicotinic acid adenine dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-activated killer cells. Upon IL8 stimulation, cytosolic NADP+ is transported to acidified endolysosomes via connexin 43 via cAMP-EPAC-RAP1-PP2A signaling. Luminal CD38 then performs a base exchange reaction with the donor NA group deriving from NAAD, produced by newly described endolysosomal activities of NA phosphoribosyltransferase and NMN adenyltransferase 3. Thus, the membrane organization of endolysosomal CD38, a signal-mediated transport system for NADP+ and luminal NAD+ biosynthetic enzymes integrate signals from a chemokine and cAMP to specify the spatiotemporal mobilization of calcium to drive cell migration.


1970 ◽  
Vol 48 (12) ◽  
pp. 2267-2278 ◽  
Author(s):  
H. R. Godavari ◽  
E. R. Waygood

Leaves of wheat (Triticum aestivum L. var. Selkirk) were incubated with nicotinic acid-7-14C and nicotinamide-7-14C for varying time periods from 5 min to 12 h. Aliquots of alcoholic extracts of leaves were subjected to paper chromatography and radioautography to isolate the intermediates of the synthesis and breakdown of nicotinamide adenine dinucleotide. Nine compounds were isolated quantitatively and identified as intermediates in the pathway of NAD metabolism. All the intermediates were labeled rapidly and the rapidity of labeling became a problem in rigorously proving the sequential operation of the pathway. The results indicate that the Preiss-Handler pathway: nicotinic acid→nicotinic acid mononucleotide→nicotinic acid adenine dinucleotide→NAD operates in wheat leaves. The degradation of NAD proceeded from NAD→nicotinamide mononucleotide→nicotinamide riboside→nicotinamide. Deamidation of the nicotinamide to nicotinic acid initiated a fresh cycle of biosynthesis. The total radioactivity recovered in the intermediates indicates that no measurable amount was lost to other metabolic pathways. Nicotinamide is recovered without significant loss and recycled. The rapid appearance of labeled nicotinamide indicates a possible interconversion of nicotinic acid and nicotinamide. About 80% of the radioactivity accumulated was present in trigonelline which is considered, on the basis of other evidence, to be a non-toxic form of nicotinic acid. Benzimidazole treatment of the leaves increased the incorporation of 14C into NADP.


1976 ◽  
Vol 83 (2) ◽  
pp. 357-364 ◽  
Author(s):  
Hans Tjälve ◽  
Erik Wilander

ABSTRACT The uptake of the nicotinamide adenine dinucleotide (NAD)-precursors nicotinamide, nicotinic acid and tryptophan in the pancreatic islets of mice was studied by use of autoradiographical methods. The ability of these substances to prevent streptozotocin diabetes was studied in the same species. It was found that only nicotinamide was strongly accumulated in the pancreatic islets and nicotinamide was also the only NAD-precursor which protected against the streptozotocin diabetes. Apparently there is a relationship between the ability of the NAD-precursors to be taken up in the pancreatic islets and their ability to prevent streptozotocin diabetes.


1974 ◽  
Vol 52 (4) ◽  
pp. 707-713 ◽  
Author(s):  
S. C. Chen ◽  
H. R. Godavari ◽  
E. R. Waygood

Incorporation of nicotinic acid-7-14C into nicotinamide adenine dinucleotide by the trifoliate leaves of the bean plant (Phaseolus vulgaris L. var. Brittle Wax) was studied for varying time periods from 5 min to 48 h. Nine radioactive compounds were isolated and identified as all the possible intermediates of NAD metabolism operating in a cyclic pattern. All the intermediates were labelled rapidly and N-methyl nicotinic acid (trigonelline) was detected within 5 min. About 80% of the nicotinic acid fed was accumulated in trigonelline. Senescence induced by floating detached leaves on water enhanced incorporation of the label into nucleotides, NAD > NADP. Treatment with growth regulators altered the NAD/NADP ratios. Benzimidazole and kinetin enhanced NADP synthesis while benzyladenine and ethionine reduced NADP synthesis. The regulator-mediated NADP synthesis is enhanced by light and appears to be inversely related to the synthesis of trigonelline.


2021 ◽  
Vol 10 (21) ◽  
pp. 5208
Author(s):  
Joanna Piechowicz ◽  
Andrzej Gamian ◽  
Danuta Zwolińska ◽  
Dorota Polak-Jonkisz

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.


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