The reported investigations were carried out in 6 young (20 years old) healthy males who performed a 10-minute exercise on a Monark cycle ergometer at workloads increasing the heart rate to 170/minute. Before the exercise, after its termination, and after 30 minutes of restitution the concentrations of adenosine-5' triphosphate, adenosine-5' diphosphate, adenosine-5' monophosphate, 2,3-diphosphoglycerate, nicotinamide-adenine dinucleotide and nicotinamide-adenine dinucleotide phosphate were assayed in erythrocytes. After the end of exercise a non-significant increase in ATP concentration and a non-significant decrease of 2,3-DPG were found in the erythrocytes. The concentrations of ADP and AMP were lower than at rest, both, after the end of exercise and after 30 minutes of restitution (p less than 0.05). The concentrations of nicotinamide-adenine dinucleotide and nicotinamide-adenine dinucleotide phosphate decreased after exercise (p less than 0.05) fell even more after 30 minutes of restitution (p less than 0.05).
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
SLC29A1 and SLC29A2 are human nicotinamide cell membrane transporters.
Nat Commun
January 2025
College of Pharmaceutical Sciences, National Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou, China.
Nicotinamide (NAM), a main precursor of NAD+, is essential for cellular fuel respiration, energy production, and other cellular processes. Transporters for other precursors of NAD+ such as nicotinic acid and nicotinamide mononucleotide (NMN) have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrate that equilibrative nucleoside transporter 1 and 2 (ENT1 and 2, encoded by SLC29A1 and 2) drive cellular nicotinamide uptake and establish nicotinamide metabolism homeostasis.
View Article and Find Full Text PDFCharacterization of human alcohol dehydrogenase 4 and aldehyde dehydrogenase 2 as enzymes involved in the formation of 5-carboxylpirfenidone, a major metabolite of pirfenidone.
Drug Metab Dispos
January 2025
Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kakuma-machi, Kanazawa, Japan; WPI Nano Life Science Institute (WPI-NanoLSI), Kanazawa University, Kakuma-machi, Kanazawa, Japan.
Pirfenidone (PIR) is used in the treatment of idiopathic pulmonary fibrosis. After oral administration, it is metabolized by cytochrome P450 1A2 to 5-hydroxylpirfenidone (5-OH PIR) and further oxidized to 5-carboxylpirfenidone (5-COOH PIR), a major metabolite excreted in the urine (90% of the dose). This study aimed to identify enzymes that catalyze the formation of 5-COOH PIR from 5-OH PIR in the human liver.
View Article and Find Full Text PDFThe protection of nicotinamide riboside against diabetes mellitus-induced bone loss via OXPHOS.
Bone
January 2025
School of Public Health, Qingdao University, Qingdao 266071, China. Electronic address:
Diabetes mellitus is a global disease that results in various complications, including diabetic osteoporosis. Prior studies have indicated a correlation between low levels of nicotinamide adenine dinucleotide (NAD) and diabetes-related complications. Nicotinamide riboside (NR), a widely utilized precursor vitamin of NAD, has been demonstrated to enhance age-related osteoporosis through the Sirt1/FOXO/β-catenin pathway in osteoblast progenitors.
View Article and Find Full Text PDFKinetic and Thermodynamic Characterization of Human 4-Oxo-l-proline Reductase Catalysis.
Biochemistry
January 2025
School of Biology, Biomedical Sciences Research Complex, University of St Andrews, St Andrews KY16 9ST, United Kingdom.
The enzyme 4-oxo-l-proline reductase (BDH2) has recently been identified in humans. BDH2, previously thought to be a cytosolic ()-3-hydroxybutyrate dehydrogenase, actually catalyzes the NADH-dependent reduction of 4-oxo-l-proline to -4-hydroxy-l-proline, a compound with known anticancer activity. Here we provide an initial mechanistic characterization of the BDH2-catalyzed reaction.
View Article and Find Full Text PDFRole of sirtuin 1 in depression‑induced coronary heart disease: Molecular pathways and therapeutic potential (Review).
Biomed Rep
March 2025
Department of Cardiology, Affiliated Renhe Hospital of China Three Gorges University, Yichang, Hubei 443001, P.R. China.
Depression and coronary heart disease (CHD) are two interconnected diseases that profoundly impact global health. Depression is both a complex psychiatric disorder and an established risk factor for CHD. Sirtuin 1 (SIRT1) is an enzyme that requires the cofactor nicotinamide adenine dinucleotide (NAD) to perform its deacetylation function, and its involvement is crucial in reducing cardiovascular risks that are associated with depression.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!