Hydrogen Therapy Delays Skin Cancer from UV Exposure in Mice
- Authors
- Fumiko Hori, Sayaka Sobue, Chisato Inoue, Yoshiki Murakumo, Masatoshi Ichihara
- Journal
- International Journal of Molecular Sciences
- Year
- 2026
- DOI
- 10.3390/ijms27020635
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Skin Cancer
- Body System
- Integumentary
TL;DR
Hydrogen slowed skin tumor development caused by UV exposure by reducing inflammation and suppressing cancer-related signaling pathways.
Key Finding
Continuous molecular hydrogen administration delayed the onset of UV-induced skin tumors and reduced tumor counts in mice by reducing skin inflammation through specific cellular pathways.
Summary
Researchers exposed hairless mice to repeated ultraviolet B (UVB) radiation—the type of UV light that causes skin cancer—while giving some mice molecular hydrogen through breathing it in and drinking hydrogen-rich water. Mice receiving hydrogen developed skin tumors more slowly and had fewer tumors overall compared to control mice. The hydrogen appeared to work by reducing inflammation in the skin rather than by protecting DNA from UV damage directly.
Practical Takeaway
This mouse study suggests hydrogen may help protect against UV-induced skin damage by reducing inflammation, but it is early-stage research in animals only. Whether these results would apply to humans, or whether hydrogen water or inhalation would be practical or effective for skin cancer prevention in people, remains unknown and requires human studies to determine.
Abstract
Molecular hydrogen (H2) exhibits anti-inflammatory and antioxidant properties. However, its role in ultraviolet B (UVB)-induced skin carcinogenesis remains unclear. Male HR-1 hairless mice received continuous H2 (2% hydrogen gas inhalation plus hydrogen-rich water (HRW)) or control treatment (normal air plus dehydrogenated water) during chronic dorsal UVB exposure (270 mJ/cm2, three times per week, 20 weeks), followed by a 10-week observation period. This protocol was replicated independently. H2 exposure consistently delayed the onset of papilloma and reduced cumulative tumor counts in both series, whereas prolonged survival and delayed squamous cell carcinoma (SCC) development each reached statistical significance in only one of the two experimental series. The cyclobutane pyrimidine dimer (CPD) levels remained unchanged, indicating no reduction in DNA photolesions. H2 exposure decreased epidermal T-cell infiltration, dermal IL-6 levels, and nuclear phosphorylated STAT3 levels. ERK and JNK phosphorylation levels were decreased. H2 preserved the GSH/GSSG ratio following acute UVB exposure and reduced nuclear Nrf2 accumulation during chronic exposure. Epidermal thickness and proliferation markers (Ki-67 and PCNA) were decreased. These findings suggest that continuous H2 administration attenuates inflammation-associated early UVB carcinogenesis through modulation of the IL-6/STAT3 and ERK/JNK pathways, supporting its use as a chemopreventive approach.