Hydrogen Gas Protects Cells from Harmful Radicals in Breakthrough Study
- Authors
- Ikuroh Ohsawa, Masahiro Ishikawa, Kumiko Takahashi, Megumi Watanabe, Kiyomi Nishimaki, Kumi Yamagata, Ken-Ichiro Katsura, Yasuo Katayama, Sadamitsu Asoh, Shigeo Ohta
- Journal
- Nature Medicine
- Year
- 2007
- DOI
- 10.1038/nm1577
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Hydrogen gas can significantly reduce brain damage caused by oxidative stress by targeting the most harmful toxins without affecting the beneficial ones.
Key Finding
Hydrogen gas selectively neutralized the most cytotoxic free radical (hydroxyl radical) while preserving free radicals that play normal roles in cells, and it reduced brain injury in a rat model of stroke.
Summary
Researchers tested whether hydrogen gas could act as an antioxidant—a substance that protects cells from damage caused by harmful molecules called free radicals. In lab experiments and in rats with brain injury, hydrogen selectively neutralized the most damaging type of free radical (hydroxyl radicals) while leaving beneficial free radicals alone. Hydrogen gas was able to quickly pass through cell membranes and reduce brain damage in the rat model.
Practical Takeaway
This early research in cells and animals suggests hydrogen may have potential as an antioxidant therapy for conditions involving acute oxidative stress, but human studies are needed to determine if these effects apply to people. The study used lab conditions and animal models, not human trials, so it's too early to make health recommendations based on this work alone.
Abstract
Acute oxidative stress induced by ischemia-reperfusion or inflammation causes serious damage to tissues, and persistent oxidative stress is accepted as one of the causes of many common diseases including cancer. We show here that hydrogen (H(2)) has potential as an antioxidant in preventive and therapeutic applications. We induced acute oxidative stress in cultured cells by three independent methods. H(2) selectively reduced the hydroxyl radical, the most cytotoxic of reactive oxygen species (ROS), and effectively protected cells; however, H(2) did not react with other ROS, which possess physiological roles. We used an acute rat model in which oxidative stress damage was induced in the brain by focal ischemia and reperfusion. The inhalation of H(2) gas markedly suppressed brain injury by buffering the effects of oxidative stress. Thus H(2) can be used as an effective antioxidant therapy; owing to its ability to rapidly diffuse across membranes, it can reach and react with cytotoxic ROS and thus protect against oxidative damage.