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Background: Modification of the nitrate (NO 3 )-nitrite (NO 2 )-nitric oxide (NO) pathway can be induced by oral intake of inorganic NO 3 (NIT) or NO 3 -rich products, such as beetroot juice (BRJ)., Objectives: The primary aim of this study was to evaluate the plasma changes in betaine, choline, trimethylamine (TMA), trimethylamine N-oxide (TMAO), and NO 3 /NO 2 (NO x ) concentrations over 4 h after single oral ingestion of NIT or BRJ. The flow-mediated skin fluorescence (FMSF) method was applied to measure the changes in nicotinamide adenine dinucleotide reduced form (NADH) in response to transient ischemia and reperfusion. We hypothesized that various sources of NO 3 may differently affect endothelial and mitochondrial functions in healthy human subjects., Methods: In a randomized crossover trial, 8 healthy young adults ingested 800 mg NO 3 from either NIT or BRJ on 2 separate days with ≥3 d apart. Venous blood samples were collected every hour, and FMSF determination was applied bihourly., Results: Plasma betaine and choline concentrations peaked at 1 h after BRJ ingestion, and remained significantly higher than baseline values at all time points (P < 0.001 and P < 0.001, compared to preingestion values). Over time, BRJ was more effective in increasing NOx compared with NIT (fixed-trial effect P < 0.001). Baseline fluorescence decreased after both NIT and BRJ consumption (fixed-time effect P = 0.005). Transient ischemia and reperfusion response increased because of NO 3 consumption (fixed-time effect P = 0.003), with no differences between trials (P = 0.451; P = 0.912; P = 0.819 at 0, 2, and 4 h, respectively)., Conclusions: Acute ingestion of BRJ elevated plasma betaine and choline, but not TMA and TMAO. Moreover, plasma NOx levels were higher in the BRJ trial than in the NIT trial. Various sources of NO 3 positively affected endothelial and mitochondrial functions. This trial was registered at clinicaltrials.gov as NCT05004935., (Copyright © 2023 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

In this work, we report that NADH can increase the autoxidation rate of hemoglobin (HbA) in a pH-dependent fashion. During this process, this cofactor is itself oxidized. The presence of superoxide dismutase (SOD) and/or catalase (CAT) can inhibit this result. At lower pH rates, the effect of NADH on the hemoglobin autoxidation rate is more enhanced; in addition, the rate of NADH oxidation is increased. Our data indicates that the reduced pyridine nucleotide may influence the redox state of human hemoglobin by a mechanism, which probably involves free radical species., (Copyright 2002 Elsevier Science B.V.)