scholarly journals Pyridine nucleotide cycle of Salmonella typhimurium: in vitro demonstration of nicotinamide adenine dinucleotide glycohydrolase, nicotinamide mononucleotide glycohydrolase, and nicotinamide adenine dinucleotide pyrophosphatase activities.

1981 ◽  
Vol 145 (2) ◽  
pp. 1002-1009 ◽  
Author(s):  
J W Foster
1986 ◽  
Vol 41 (1-2) ◽  
pp. 148-157 ◽  
Author(s):  
Ludger Schwenen ◽  
Dieter Komoßa ◽  
Wolfgang Barz

Abstract Application of [6-14C]-or [7-14C]nicotinic acid to parsley cell suspension cultures led to the accumulation of labelled nicotinamide mononucleotide, nicotinamide adenine dinucleotide, nicotinamide N-riboside, nicotinamide and nicotinic acid, indicating the operation of the pyridine nucleotide cycle in these cells. As main conjugates, nicotinic acid N-glucoside and nicotinic acid glucose ester were found. For nicotinic acid degradation the following sequence is suggested: nicotinic acid → 6-hydroxynicotinic acid → 2,5-dihydroxypyridine → a C4/C3 unit of unknown structure → CO2. In aseptically grown parsley seedlings nicotinic acid is also degraded to CO2


1974 ◽  
Vol 20 (2) ◽  
pp. 205-209 ◽  
Author(s):  
Gerald J. Tritz

The biosynthesis of nicotinamide adenine dinucleotide (NAD) is under the genetic control of the nadR+ locus. The nadR+ allele is dominant to the nadR allele in transheterogenotes, indicating that the regulation is of the positive type. Mutants of the nadR type are unable to synthesize quinolinic acid; however, they do retain the ability to convert quinolinic acid into NAD and to recycle this NAD through the pyridine nucleotide cycle. Thus, the nadR+ locus regulates only genes involved in the biosynthesis of quinolinic acid.


2021 ◽  
Author(s):  
Masaki Igarashi ◽  
Masaomi Miura ◽  
Yoshiko Nakagawa-Nagahama ◽  
Keisuke Yaku ◽  
Kosuke Kashiwabara ◽  
...  

Abstract Preclinical studies have revealed that the elevation of nicotinamide adenine dinucleotide (NAD+) levels on administration of an NAD+ precursor, nicotinamide mononucleotide (NMN), can mitigate aging-related disorders; however, human data are sparse. Therefore, we aimed to investigate whether the chronic oral supplementation of NMN can elevate blood NAD+ levels and alter physiological dysfunctions, including muscle weakness, in healthy elderly participants. We administered 250 mg NMN per day to aged men for 6 or 12 weeks (n=21 for 6 weeks, n=10 for 12 weeks) in a placebo-controlled, randomized, double blind, parallel-group trial. Chronic supplementation with NMN was well tolerated and did not cause any significant deleterious effect. Metabolomic analysis of whole blood demonstrated that the oral supplementation of NMN significantly increased the concentrations of NAD+ and NAD+ metabolites. Moreover, NMN significantly improved muscle strength and performance, which were evaluated using the 30-second chair stand test, walking speed, and grip strength, and it showed no significant effect on body composition. Thus, our evidence indicates that chronic oral NMN supplementation can be an efficient NAD+ booster for preventing aging-related muscle dysfunctions in humans.


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