Hydrogen Water Protects Bone Marrow from Radiation Damage in Mice
- Authors
- Junling Zhang, Xiaolei Xue, Xiaodan Han, Yuan Li, Lu Lu, Deguan Li, Saijun Fan
- Journal
- Oxidative Medicine and Cellular Longevity
- Year
- 2017
- DOI
- 10.1155/2017/8241678
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Radiation Injury
- Body System
- Hematopoietic System
TL;DR
Drinking hydrogen-rich water helps protect the blood-forming stem cells in mice from damage caused by full-body radiation exposure.
Key Finding
Hydrogen-rich water reduced harmful free radicals and DNA damage in blood-forming stem cells of irradiated mice, improving their survival and ability to multiply.
Summary
Researchers gave mice exposed to whole-body radiation either regular water or hydrogen-rich water to see if it could protect blood-forming stem cells in the bone marrow. Mice that drank hydrogen-rich water showed less damage to these stem cells, including reduced harmful molecules called hydroxyl radicals, less DNA damage, and better cell survival and growth compared to mice that received regular water.
Practical Takeaway
This is an early-stage mouse study showing hydrogen-rich water may help protect bone marrow cells from radiation damage. However, this is animal research only—human studies would be needed to determine if these effects apply to people undergoing cancer treatment. The study does not yet support using hydrogen water as a medical treatment.
Abstract
We examined whether consumption of hydrogen-rich water (HW) could ameliorate hematopoietic stem cell (HSC) injury in mice with total body irradiation (TBI). The results indicated that HW alleviated TBI-induced HSC injury with respect to cell number alteration and to the self-renewal and differentiation of HSCs. HW specifically decreased hydroxyl radical (∙OH) levels in the c-kit+ cells of 4 Gy irradiated mice. Proliferative bone marrow cells (BMCs) increased and apoptotic c-kit+ cells decreased in irradiated mice uptaken with HW. In addition, the mean fluorescence intensity (MFI) of γ-H2AX and percentage of 8-oxoguanine positive cells significantly decreased in HW-treated c-kit+ cells, indicating that HW can alleviate TBI-induced DNA damage and oxidative DNA damage in c-kit+ cells. Finally, the cell cycle (P21), cell apoptosis (BCL-XL and BAK), and oxidative stress (NRF2, HO-1, NQO1, SOD, and GPX1) proteins were significantly altered by HW in irradiated mouse c-kit+ cells. Collectively, the present results suggest that HW protects against TBI-induced HSC injury.