Hydrogen Therapy Protects Lungs from Radiation Damage in Mice Study
- Authors
- Yasuhiro Terasaki, Ikuroh Ohsawa, Mika Terasaki, Mikiko Takahashi, Shinobu Kunugi, Kang Dedong, Hirokazu Urushiyama, Shunsuke Amenomori, Mayuko Kaneko-Togashi, Naomi Kuwahara, Arimi Ishikawa, Naomi Kamimura, Shigeo Ohta, Yuh Fukuda
- Journal
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Year
- 2011
- DOI
- 10.1152/ajplung.00008.2011
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Radiation-Induced Lung Injury
- Body System
- Respiratory
TL;DR
Molecular hydrogen (H2) can protect lung cells from damage caused by radiation exposure.
Key Finding
Hydrogen treatment reduced both immediate and long-term radiation damage to mouse lungs by lowering oxidative stress and preventing the development of lung fibrosis, with no observed toxicity.
Summary
Researchers tested whether molecular hydrogen (H₂)—a gas that acts as an antioxidant—could protect lung tissue from damage caused by radiation. They exposed human lung cells and mice to high-dose radiation, with some receiving hydrogen treatment through inhaled gas and drinking hydrogen-enriched water. Hydrogen reduced harmful molecules called free radicals in the cells and lungs, decreased cell death markers, and prevented the development of lung scarring (fibrosis) in mice up to 5 months after radiation exposure.
Practical Takeaway
While this animal study suggests hydrogen may help protect lungs from radiation damage, it is not yet clear whether these results would apply to humans. The research was conducted in mice and cell cultures, not in people undergoing actual radiation therapy. More human studies would be needed before hydrogen water could be recommended as a protective measure for radiation patients.
Abstract
Molecular hydrogen (H(2)) is an efficient antioxidant that diffuses rapidly across cell membranes, reduces reactive oxygen species (ROS), such as hydroxyl radicals and peroxynitrite, and suppresses oxidative stress-induced injury in several organs. ROS have been implicated in radiation-induced damage to lungs. Because prompt elimination of irradiation-induced ROS should protect lung tissue from damaging effects of irradiation, we investigated the possibility that H(2) could serve as a radioprotector in the lung. Cells of the human lung epithelial cell line A549 received 10 Gy irradiation with or without H(2) treatment via H(2)-rich PBS or medium. We studied the possible radioprotective effects of H(2) by analyzing ROS and cell damage. Also, C57BL/6J female mice received 15 Gy irradiation to the thorax. Treatment groups inhaled 3% H(2) gas and drank H(2)-enriched water. We evaluated acute and late-irradiation lung damage after H(2) treatment. H(2) reduced the amount of irradiation-induced ROS in A549 cells, as shown by electron spin resonance and fluorescent indicator signals. H(2) also reduced cell damage, measured as levels of oxidative stress and apoptotic markers, and improved cell viability. Within 1 wk after whole thorax irradiation, immunohistochemistry and immunoblotting showed that H(2) treatment reduced oxidative stress and apoptosis, measures of acute damage, in the lungs of mice. At 5 mo after irradiation, chest computed tomography, Ashcroft scores, and type III collagen deposition demonstrated that H(2) treatment reduced lung fibrosis (late damage). This study thus demonstrated that H(2) treatment is valuable for protection against irradiation lung damage with no known toxicity.