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Malproduction of endogenous hydrogen gas in COVID-19.

COVID-19における内因性水素ガス産生異常の可能性

review not specified not assessed

Abstract

COVID-19 is associated with extensive alterations in gut microbiota composition, including a reduction in hydrogen-producing bacterial species, which may lead to decreased endogenous dihydrogen (H2) output. As a biologically active gaseous molecule, H2 exerts cytoprotective, antioxidant, anti-inflammatory, and antiapoptotic effects. This review proposes that diminished H2 production could contribute to disease progression and severity in COVID-19. Exogenous H2 supplementation is discussed as a potential approach to restore physiological H2 levels, with the possibility of combining H2 measurement and supplementation as a combined diagnostic and interventional strategy. The paper also situates H2 alongside other gasotransmitters such as nitric oxide and hydrogen sulfide in the context of COVID-19-related gaseous signaling disruption.

Mechanism

COVID-19-induced gut dysbiosis reduces the abundance of H2-producing bacteria, lowering endogenous dihydrogen levels. Because H2 normally exerts antioxidant, anti-inflammatory, and antiapoptotic effects, its deficiency may impair host defense mechanisms and contribute to disease worsening.

Bibliographic

Authors
Ostojic SM
Journal
Front Cell Infect Microbiol
Year
2022
PMID
35967841
DOI
10.3389/fcimb.2022.924832
PMC
PMC9366905

Tags

Disease:COVID-19 Mechanism:抗酸化酵素 アポトーシス抑制 免疫調節 炎症抑制 酸化ストレス 活性酸素種

Delivery context

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 35967841. https://h2-papers.org/en/papers/35967841
Source: PubMed PMID 35967841