Hydrogen gas mitigates acute hypoxia-induced oxidative and inflammatory brain injuries in medaka (Oryzias latipes)
Sato E, Shimamura N, Saiki C, Sunada K, Miwa N, Xiao L. · Antioxidants. 2025;14(9):1130.
Study at a glance
Preclinical
Mixed-sex adult Japanese medaka exposed to approximately nine minutes of severe low-oxygen water conditions.
After hypoxia, fish recovered for one hour in water bubbled with 4% H₂ in air. · The inlet mixture was 4% H₂ in air. Total gas flow and the resulting dissolved-H₂ concentration were not reported.
Nine-minute hypoxia exposure followed by one hour of recovery treatment.
H₂ recovery reduced several histologic/hypoxia/oxidative markers and restored antioxidant, respiratory and locomotor measures relative to air recovery. AChE did not differ among groups; IL-6/TNF-α tended lower with H₂ but did not differ significantly across H₂, air and ozone comparisons. Ozone worsened several measures.
Aquatic fish model, acute one-hour recovery, uncertain unique total n, unmeasured H₂ uptake/dissolved dose, multiple endpoints and no mammalian validation. Japanese public grants supported the work; authors declared no conflicts.
What kind of evidence is this?
Preclinical
Randomized medaka acute-hypoxia experiment with one-hour gas-bubbled-water recovery
Other neurological conditions
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.
Methods
Mixed-sex adult Japanese medaka exposed to approximately nine minutes of severe low-oxygen water conditions.
Figures commonly report n=20 fish/group with experiments repeated three or five times; the total number of unique fish across assays/repeats is not consolidated.
Nine-minute hypoxia exposure followed by one hour of recovery treatment.
After hypoxia, fish recovered for one hour in water bubbled with 4% H₂ in air.
4% H₂ premixed in air and bubbled into recovery water — H₂/air, not Brown's gas and not direct inhalation.
The inlet mixture was 4% H₂ in air. Total gas flow and the resulting dissolved-H₂ concentration were not reported.
No-hypoxia control, hypoxia followed by air-bubbled water, and selected assays with ozone-bubbled water (0.02–0.03 ppm).
Outcomes and reported result
Tissue hypoxia/vascular congestion, HIF-1α, apoptosis, 8-OHdG, COX-2, IL-6/TNF-α, antioxidant capacity, acetylcholinesterase, breathing and locomotion.
H₂ recovery reduced several histologic/hypoxia/oxidative markers and restored antioxidant, respiratory and locomotor measures relative to air recovery. AChE did not differ among groups; IL-6/TNF-α tended lower with H₂ but did not differ significantly across H₂, air and ozone comparisons. Ozone worsened several measures.
The complete free PMC article, methods, all result sections and disclosures were checked for randomization, concentration and missing flow/dissolved dose, sample reporting, positive and null endpoints, model limitations, funding and conflicts.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Aquatic fish model, acute one-hour recovery, uncertain unique total n, unmeasured H₂ uptake/dissolved dose, multiple endpoints and no mammalian validation. Japanese public grants supported the work; authors declared no conflicts.
Acute hypoxic brain injury in medaka; it does not establish neurologic treatment or dosing in mammals or people.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 41009034 · DOI: 10.3390/antiox14091130
Free full article in PubMed Central.
Complete PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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