Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress

Chi-Yu Lu, Chia-Jung Yen, Ching-Ying Wu, Chu-Huang Chen, Hsin-Su Yu, Jian-He Lu, Jui-Lin Liang, Mami Noda, Ming-Hsien Tsai, Shain-Jang Yan, Tohru Yoshioka, Wen-Li Hsu

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DOI: 10.1038/s41598-017-03513-2 DOI is the universal ID for this study.

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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.

Publish Year 2017
Country Taiwan
Rank Positive
Journal Nature Scientific Reports
Primary Topic Whole Body
Secondary TopicAging
Model Cell Culture
Tertiary TopicOxidative Stress
Vehicle Medium (Dissolved)
pH Neutral
Application Culture Media