Hydrogen Gas Protects Skin Cells from Aging Damage
- Authors
- Ching-Ying Wu, Wen-Li Hsu, Ming-Hsien Tsai, Jui-Lin Liang, Jian-He Lu, Chia-Jung Yen, Hsin-Su Yu, Mami Noda, Chi-Yu Lu, Chu-Huang Chen, Shian-Jang Yan, Tohru Yoshioka
- Journal
- Scientific Reports
- Year
- 2017
- DOI
- 10.1038/s41598-017-03513-2
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Taiwan
- Health Condition
- Skin Aging
- Body System
- Integumentary
TL;DR
Hydrogen gas can help protect skin cells from aging by preventing damage caused by harmful oxygen compounds.
Key Finding
Molecular hydrogen protected skin cells from oxidative damage by reducing disulfide bond formation in calcium-signaling proteins, rather than by directly neutralizing reactive oxygen species.
Summary
Researchers studied how hydrogen gas might protect skin cells from damage caused by hydrogen peroxide, which creates harmful molecules called reactive oxygen species. When skin cells were exposed to hydrogen peroxide, it damaged proteins involved in calcium signaling (a key process in cells), but adding hydrogen gas to the treatment reduced this damage by preventing the formation of disulfide bonds (chemical links between damaged proteins). The study suggests hydrogen gas works by repairing damaged proteins rather than simply neutralizing the harmful molecules.
Practical Takeaway
This laboratory study in skin cells suggests hydrogen gas may help protect against oxidative damage related to aging, but it is a very early-stage finding. The research was conducted only in cultured cells, not in living humans, so it's unclear whether these results would apply to actual skin aging. More research, including human studies, would be needed before any health claims could be made.
Abstract
Based on the oxidative stress theory, aging derives from the accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm. Hydrogen peroxide (H2O2) elicits ROS that induces skin aging through oxidation of proteins, forming disulfide bridges with cysteine or methionine sulfhydryl groups. Decreased Ca2+ signaling is observed in aged cells, probably secondary to the formation of disulfide bonds among Ca2+ signaling-related proteins. Skin aging processes are modeled by treating keratinocytes with H2O2. In the present study, H2O2 dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca2+ response, which was partially protected via co-treatment with β-mercaptoethanol, resulting in reduced disulfide bond formation in inositol 1, 4, 5-trisphosphate receptors (IP3Rs). Molecular hydrogen (H2) was found to be more effectively protected H2O2-induced IP3R1 dysfunction by reducing disulfide bonds, rather than quenching ROS. In conclusion, skin aging processes may involve ROS-induced protein dysfunction due to disulfide bond formation, and H2 can protect oxidation of this process.