Objective: To compare how and to what extent ingestion of hydrogen water and milk increase breath hydrogen in adults. Methods: Five subjects without specific diseases, ingested distilled or hydrogen water and milk as a reference material that could increase breath hydrogen. Their end-alveolar breath hydrogen was measured. Results: Ingestion of hydrogen water rapidly increased breath hydrogen to the maximal level of approximately 40 ppm 10-15 min after ingestion and thereafter rapidly decreased to the baseline level, whereas ingestion of the same amount of distilled water did not change breath hydrogen (p < 0.001). Ingestion of hydrogen water increased both hydrogen peaks and the area under the curve (AUC) of breath hydrogen in a dose-dependent manner. Ingestion of milk showed a delayed and sustained increase of breath hydrogen in subjects with milk intolerance for up to 540 min. Ingestion of hydrogen water produced breath hydrogen at AUC levels of 2 to 9 ppm hour, whereas milk increased breath hydrogen to AUC levels of 164 ppm hour for 540 min after drinking. Conclusion: Hydrogen water caused a rapid increase in breath hydrogen in a dose-dependent manner; however, the rise in breath hydrogen was not sustained compared with milk.
Recent studies have revealed that inhaled or ingested hydrogen gas (H 2) inactivates reactive oxygen species such as hydroxyl radicals in various kinds of diseases and disorders in animal models and that H2 reduces oxidative stress-induced damage in brain, heart, and other peripheral tissues. These reports suggested that exogenous H2 is partially trapped by oxygen radicals. This study was conducted to evaluate H2 consumption after the ingestion of H2-rich water. Seven adult subjects ingested H2-rich water. The H2 content of their expired breath was measured by gas chromatography with a semiconductor. The ingestion of H2-rich water rapidly increased breath H2 content to its maximal level of approximately 36 ppm at 10 min after ingestion and thereafter decreased it to the baseline level within 60 min. Taken together with simultaneous measurements of expiratory minute volume, 59% of the ingested H2 was exhaled. The loss of H2 from the water during the experimental procedures accounted for 3% or less of the H2. H 2 release from the skin surface was estimated as approximately 0.1%. Based on the remaining H2 mass balance, approximately 40% of the ingested H2 was consumed in the body. As the H2 molecule is reported to be a weak scavenger of hydroxyl radicals and is not effective against superoxide or hydrogen peroxide, the rate of hydroxyl radical production was estimated to be at least 1.0 μmol/min/m2 (equivalent to 29 nmol/min/kg), assuming that the H2 molecules were all used to scavenge hydroxyl radicals and that bacterial consumption in the alimentary tract and on the skin surface could be excluded. In summary, 59% of ingested H2 was exhaled, and most of the remainder was consumed in the body.
Inhaling or ingesting hydrogen (H2) gas improves oxidative stress-induced damage in animal models and humans. We previously reported that H2 was consumed throughout the human body after the ingestion of H2-rich water and that the H2 consumption rate ([Formula: see text]) was 1.0 μmol/min/m(2) body surface area. To confirm this result, we evaluated [Formula: see text]during the inhalation of low levels of H2 gas. After measuring the baseline levels of exhaled H2 during room air breathing via a one-way valve and a mouthpiece, the subject breathed low levels (160 ppm) of H2 gas mixed with purified artificial air. The H2 levels of their inspired and expired breath were measured by gas chromatography using a semiconductor sensor. [Formula: see text] was calculated using a ventilation equation derived from the inspired and expired concentrations of O2/CO2/H2, and the expired minute ventilation volume, which was measured with a respiromonitor. As a result, [Formula: see text] was found to be approximately 0.7 μmol/min/m(2)BSA, which was compatible with the findings we obtained using H2-rich water. [Formula: see text] varied markedly when pretreatment fasting to reduce colonic fermentation was not employed, i.e., when the subject’s baseline breath hydrogen level was 10 ppm or greater. Our H2 inhalation method might be useful for the noninvasive monitoring of hydroxyl radical production in the human body.
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