Hydrogenology
Hydrogenology editorial study record

Molecular hydrogen protects against oxidative stress-induced SH-SY5Y neuroblastoma cell death through the process of mitohormesis

Murakami Y, Ito M, Ohsawa I. · PLOS ONE. 2017;12(5):e0176992.

PreclinicalOther formsPublished 2017
Study record, not medical adviceThis page reports one source and Hydrogenology’s source-text extraction. It does not establish that molecular hydrogen is effective, safe or appropriate for any person. Human, animal and laboratory evidence must not be treated as equivalent.
Source and classification

What kind of evidence is this?

Evidence stream

Preclinical

Reported design

Controlled SH-SY5Y neuroblastoma-cell gas-exposure and oxidative-stress experiment

Research topic

Other neurological conditions

Administration classification

Other forms

Study result signal

Not reported in this record.

Outcome type

Not reported in this record.

Reported in the source

Methods at a glance

Population or model

Human SH-SY5Y neuroblastoma cells cultured in glucose- or galactose-containing media.

Sample

Experiments were repeated two or three times with n=4–5 per group; selected protein measurements used n=5–6.

Duration

30-minute box fill followed by sealed exposures from one to 18 hours; oxidative-stress outcome timing varied by assay.

Intervention

Pretreatment or post-treatment in sealed culture boxes with gas containing 1–50% H₂, principally 50% for up to 18 hours, around hydrogen-peroxide exposure.

Hydrogen form

50% H₂ with 10% O₂, 5% CO₂ and 35% N₂ — H₂ alone as the active gas component, not Brown's gas.

H₂ specification

Boxes were filled at 1 L/min for 30 minutes and then sealed. At 50% H₂, the fill stream contained 500 mL/min H₂ and 100 mL/min O₂; these are filling flows, not continuous 18-hour exposure flows. Medium H₂ was 390±40 μM.

H₂ flow

500 mL/min during the 30-minute box fill at 50% H₂; no continuous flow during sealed incubation.

O₂ delivered with H₂

100 mL/min during the box fill at 10% O₂; no continuous flow during sealed incubation.

Comparator

Matched 10% O₂/5% CO₂/85% N₂ gas without H₂, multiple H₂ concentrations/durations and pretreatment versus post-treatment.

Reported, not endorsed

Outcomes and reported result

Outcomes measured

Cell death, mitochondrial membrane potential, ATP, oxygen consumption, mitochondrial DNA, glutathione/superoxide/ROS and Nrf2-pathway gene/protein expression.

Reported result

H₂ pretreatment of at least three hours reduced later hydrogen-peroxide cell death and changed mitochondrial and Nrf2-linked measures. Post-treatment did not protect; mitochondrial DNA copy number did not change, DCFDA-indicated ROS did not increase, and the induced stress included lower glutathione and higher superoxide in one metabolic condition.

Results-extraction completeness

The complete free PMC article, figures and gas-system methods were checked for exact mixture and filling flow, concentration/duration comparisons, positive and null/adverse-direction 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.

Interpretation limits

Cautions and applicability

Design and reporting cautions

Cancer-derived cell line, high gas concentrations, sealed-box exposure, small laboratory replicate counts, pretreatment paradigm and many mechanistic endpoints. Japanese public grants funded the work; authors declared no competing interests.

Applies directly to

SH-SY5Y cells under induced oxidative stress; it does not establish neuroprotection or cancer treatment in animals or people.

Preliminary appraisal framework

Not reported in this record.

Preliminary risk-of-bias status

Not reported in this record.

Appraisal rationale

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.

Provenance

Sources and record status

Identifiers

PMID: 28467497 · DOI: 10.1371/journal.pone.0176992

Publisher access

Free full article in PubMed Central.

Extraction basis

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

Record revision

2026-08-10