Protective effects of dissolved molecular hydrogen against hydrogen peroxide‑, hydroperoxide‑, and glyoxal‑induced injuries to human skin keratinocytes

Abstract

Molecular hydrogen (H2) is recognized as a gaseous antioxidant, and it is expected to ameliorate various disorders related to oxidative stress and inflammation. However, there are still many unclear points regarding its effectiveness in the skin. Therefore, the purpose of this study was to examine the protective effect of H2 against ultraviolet (UV) irradiation-related stress injury in human epidermal HaCaT cells. We investigated the effects of H2 against three types of UV-derived oxidative stress using human skin keratinocytes: hydrogen peroxide (H2O2)-induced oxidative stress, tert-butyl hydroperoxide (t-BuOOH)-induced lipid peroxidation stress, and glyoxal-induced carbonyl stress. Our results showed that H2 exerted cytoprotective effects against stress induced by H2O2, t-BuOOH, and glyoxal. Furthermore, our results also revealed that H2 suppressed H2O2-induced increases in intracellular peroxide and H2O2 levels, and suppressed the progression of lipid peroxidation. Taken together, our results demonstrate that H2 can exert protective effects against oxidative stress-, lipid peroxidation-, and carbonyl stress-induced cellular injuries in human keratinocytes, partly mediated via suppression of intracellular oxidative stress and peroxide generation. Therefore, H2 is expected to be utilized as an effective and attractive component in cosmetic formulations in the future.

Study details

Article type

Original Research

Disease / injury model

Oxidative stress, lipid peroxidation, and carbonyl stress models in human keratinocytes (in vitro)

Dose-dependent effect

No

Outcome

Positive

Findings

Molecular hydrogen (H2) exerts cytoprotective effects against hydrogen peroxide-, tert-butyl hydroperoxide-, and glyoxal-induced injuries in human skin keratinocytes, suppressing oxidative stress, lipid peroxidation, and carbonyl stress. H2 was superior to ascorbic acid (Vit. C) and α-tocopherol (Vit. E) in protecting against H2O2-induced cell injury.