Hydrogen gas protects IP3Rs by reducing disulfide bridges in human keratinocytes under oxidative stress
Wu CY, Hsu WL, Tsai MH, Liang JL, Lu JH, Yen CJ, Yu HS, Noda M, Lu CY, Chen CH, Yan SJ, Yoshioka T. · Scientific Reports. 2017;7:3606.
What kind of evidence is this?
Preclinical
Primary human-keratinocyte oxidative-stress and calcium-signaling laboratory study
Skin, wound and aging research
Other forms
Not reported in this record.
Not reported in this record.
Methods at a glance
Primary keratinocytes isolated from foreskin samples collected during routine circumcision and cultured for up to five generations.
32 foreskin samples were collected. Functional experiments typically report three or five independent replicates and imaging averages over defined cell fields rather than one participant-level treatment sample.
Short cell exposures and pretreatments completed within hours; hydrogen-peroxide pretreatment was commonly 30 minutes.
H₂-containing balanced salt solution applied before or with 500 μM hydrogen peroxide in cell assays completed within a few hours.
H₂ dissolved in balanced salt solution — H₂ only, not Brown's gas and not inhalation.
H₂ water was mixed with concentrated balanced salt solution to pH 7.4 and measured with an H₂ electrode. The article reports an estimated six-hour half-life and cites 0.08 ppm as a lower effective limit, but does not state one numeric starting H₂ concentration for the experimental solution.
Not applicable — H₂-containing cell buffer, not gas inhalation; preparation flow was not reported.
No O₂ was co-delivered as part of the H₂ intervention.
Vehicle buffer, hydrogen peroxide alone and the reducing agent β-mercaptoethanol, with ATP or photoreleased IP3 stimulation.
Outcomes and reported result
ROS, ATP/IP3-evoked intracellular calcium signaling, IP3-receptor disulfide-bond formation/phosphorylation and mass-spectrometry peptide labeling.
H₂-containing buffer preserved several calcium responses and reduced selected IP3R1 disulfide-bond signals. It did not reduce hydrogen-peroxide-induced ROS production, did not restore IP3R2/IP3R3 in the same way, and hydrogen peroxide did not change IP3R1 phosphorylation/density in a reported comparison.
The complete free PMC article, figures, methods and supplement-linked analyses were checked for tissue source, replicate counts, H₂ preparation and missing numeric concentration, positive and null receptor/ROS findings, funding and conflicts.
A reported association, difference or mechanism is not automatically a clinical benefit. Null findings, outcome type, study design and precision all matter.
Cautions and applicability
In-vitro oxidative-stress model, small experiment-level replicate counts, mixed tissue-donor and cell-level units, no numeric starting H₂ concentration stated, many mechanistic assays and no clinical aging or skin-disease outcome. Taiwanese academic/public and named donor support funded the work; authors declared no competing interests and identified the commercial H₂-water machine.
Cultured primary human keratinocytes; it does not establish anti-aging or dermatologic treatment in people.
Not reported in this record.
Not reported in this record.
Not reported in this record.
No single-study GRADE certainty rating is assigned. Certainty is assessed by important outcome across a complete eligible evidence set, not by attaching a final grade to one source.
Sources and record status
PMID: 28620198 · DOI: 10.1038/s41598-017-03513-2
Free full article in PubMed Central.
Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
2026-08-10