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

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 ?-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.

SUBMITTER: Wu CY 

PROVIDER: S-EPMC5472599 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature