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The principle and the potential approach to ROS-dependent cytotoxicity by non-pharmaceutical therapies: optimal use of medical gases with antioxidant properties.

医療ガスの抗酸化特性とROS依存性細胞毒性への応用:CO・H₂S・H₂の分子機序に関するレビュー

review not specified not assessed

Abstract

Maintaining cellular redox equilibrium is fundamental to human health, and numerous conditions—including inflammation, diabetes, glaucoma, cancer, ischemia, and neurodegeneration—are linked to dysregulated reactive oxygen species (ROS) and oxidative stress. This review examines two principal strategies for counteracting oxidative damage: direct ROS scavenging by medical gases (carbon monoxide, hydrogen sulfide, and molecular hydrogen), and the induction of endogenous ROS-resistant proteins and antioxidant enzymes. The molecular mechanisms by which each gas exerts antioxidant activity are discussed, along with the physiological pathways governing antioxidant enzyme expression. The authors suggest that targeted approaches to ROS elimination may have future relevance for a range of oxidative stress-related conditions.

Mechanism

Medical gases including CO, H2S, and H2 are reviewed for their capacity to directly scavenge ROS and to upregulate endogenous ROS-resistant proteins and antioxidant enzymes, thereby restoring intracellular redox balance.

Bibliographic

Authors
Noda M, Fujita K, Lee CH, Yoshioka T
Journal
Curr Pharm Des
Year
2011
PMID
21736540
DOI
10.2174/138161211797052600

Tags

Disease:糖尿病・代謝症候群 虚血再灌流障害 Mechanism:抗酸化酵素 ヒドロキシルラジカル消去 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 21736540. https://h2-papers.org/en/papers/21736540
Source: PubMed PMID 21736540