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Molecular Hydrogen as a Novel Antitumor Agent: Possible Mechanisms Underlying Gene Expression.

抗腫瘍剤としての分子状水素:遺伝子発現調節を介した作用機序の考察

review not specified not assessed

Abstract

This review examines the antitumor potential and safety profile of molecular hydrogen (H₂). Cancer development is closely linked to mutations in both nuclear DNA and mitochondrial DNA (mtDNA), with hydroxyl radicals (·OH)—among the most potent oxidizing reactive oxygen species—identified as a key causative factor. H₂ selectively neutralizes ·OH and, unlike conventional antitumor agents, appears to lack significant side effects. Beyond direct radical scavenging, evidence suggests that H₂ may engage indirect biological defense pathways through modulation of gene expression. The review also addresses findings on H₂ efficacy in reducing adverse effects associated with cancer-related interventions, consolidating current knowledge on its mechanistic basis as a candidate antitumor agent.

Mechanism

H₂ selectively scavenges hydroxyl radicals (·OH), thereby reducing oxidative DNA mutations in both nuclear and mitochondrial DNA. Additionally, indirect biological defense mechanisms involving gene expression regulation are proposed as contributing pathways.

Bibliographic

Authors
Hirano S, Yamamoto H, Ichikawa Y, Sato B, Takefuji Y, Satoh F
Journal
Int J Mol Sci
Year
2021 (2021-08-13)
PMID
34445428
DOI
10.3390/ijms22168724
PMC
PMC8395776

Tags

Disease:がん化学療法 (副作用軽減) がん放射線療法 (副作用軽減) Mechanism:ヒドロキシルラジカル消去 炎症抑制 ミトコンドリア 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 34445428. https://h2-papers.org/en/papers/34445428
Source: PubMed PMID 34445428