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.
Highlights
The oxidative stress theory of aging suggests that aging results from the accumulation of aberrant proteins in the cytosol, chemical damage to macromolecules, and mitochondrial DNA changes[1]
H2O2 may be transported across the membrane by aquaporin channels[5] and act as superoxide anions, major reactive oxygen species (ROS) released from the mitochondria that are converted to H2O2 by superoxide dismutase[6], and the increased release of H2O2 mimics the aging process[7]
To examine the types of signaling molecules affected by aging in skin cells, different concentrations of H2O2 were used to mimic the aging process induced by ROS accumulation
Summary
The oxidative stress theory of aging suggests that aging results from the accumulation of aberrant proteins in the cytosol, chemical damage to macromolecules, and mitochondrial DNA changes[1]. The aging-related reduction of Ca2+ signaling may be mimicked by H2O2-induced disulfide bond formation. The protective effect of H2 treatment against ROS-induced dysfunctional disulfide bond formation and recovery Ca2+ signaling was examined. The data demonstrated that aging processes in KC was found to be selectively oxidized IP3Rs, especially IP3R1-mediated Ca2+ signaling by inducing the formation of H2O2-mediated disulfide bonds in the skin. A major protective effect of H2 was to reduce disulfide bond formation in the protein caused by oxidative stress, and not by eliminating the generation of ROS in the skin
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