Hydrogenology
Source-linked study record

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.

PreclinicalOther formsPublished 2017Source checked
Study record, not medical adviceThis record reports what the source states. It is not medical advice and does not establish that molecular hydrogen is effective, safe or appropriate for any person.
Quick summary

Study at a glance

Evidence type

Preclinical

Population or model

Primary keratinocytes isolated from foreskin samples collected during routine circumcision and cultured for up to five generations.

Intervention and dose

H₂-containing balanced salt solution applied before or with 500 μM hydrogen peroxide in cell assays completed within a few hours. · 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.

Duration

Short cell exposures and pretreatments completed within hours; hydrogen-peroxide pretreatment was commonly 30 minutes.

Reported result

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.

Main limitation

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.

Evidence and classification

What kind of evidence is this?

Evidence type

Preclinical

Reported design

Primary human-keratinocyte oxidative-stress and calcium-signaling laboratory study

Research topic

Skin, wound and aging research

Administration form

Other forms

Information not yet classified

Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.

Reported in the source

Methods

Population or model

Primary keratinocytes isolated from foreskin samples collected during routine circumcision and cultured for up to five generations.

Sample

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.

Duration

Short cell exposures and pretreatments completed within hours; hydrogen-peroxide pretreatment was commonly 30 minutes.

Intervention

H₂-containing balanced salt solution applied before or with 500 μM hydrogen peroxide in cell assays completed within a few hours.

Hydrogen form

H₂ dissolved in balanced salt solution — H₂ only, not Brown's gas and not inhalation.

Dose or H₂ specification

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.

Comparator

Vehicle buffer, hydrogen peroxide alone and the reducing agent β-mercaptoethanol, with ATP or photoreleased IP3 stimulation.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

ROS, ATP/IP3-evoked intracellular calcium signaling, IP3-receptor disulfide-bond formation/phosphorylation and mass-spectrometry peptide labeling.

Reported result

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.

Extraction completeness

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.

Interpretation limits

Limitations and applicability

Main methodological cautions

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.

Applies directly to

Cultured primary human keratinocytes; it does not establish anti-aging or dermatologic treatment in people.

No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.

Sources and status

Sources and record status

Identifiers

PMID: 28620198 · DOI: 10.1038/s41598-017-03513-2

Publisher access

Free full article in PubMed Central.

Extraction basis

Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.

Last reviewed

10 August 2026

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