Hydrogen Gas Protects Cells from Oxygen Damage in Lab Study
- Authors
- Mizuki Seya, Toshiyuki Aokage, Ying Meng, Takahiro Hirayama, Takafumi Obara, Tsuyoshi Nojima, Kosaki Yoshinori, Tetsuya Yumoto, Akihiro Watanabe, Taihei Yamada, Hiromichi Naito, Atsunori Nakao
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2025
- DOI
- 10.1016/j.bbrc.2025.152753
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Ischemia-Reperfusion Injury
- Body System
- Digestive System
TL;DR
Molecular hydrogen restores mitochondrial function and reduces oxidative damage in intestinal ischemia-reperfusion injury.
Key Finding
Hydrogen-rich gas significantly restored mitochondrial function and energy production in intestinal cells recovering from simulated ischemia-reperfusion injury, while reducing cell damage and death.
Summary
Researchers exposed intestinal cells to conditions mimicking lack of oxygen and blood flow (ischemia-reperfusion injury), then treated some cells with hydrogen-rich gas during recovery. Hydrogen treatment helped cells restore their mitochondria (the energy-producing structures in cells), produce more energy (ATP), and reduce harmful molecules called reactive oxygen species. The hydrogen also prevented cells from dying and appeared to work by affecting genes related to low-oxygen stress.
Practical Takeaway
This is a laboratory study using isolated cells, not human subjects, so findings cannot yet be applied to health recommendations. The results suggest hydrogen may help protect cells during oxygen deprivation and recovery, but much more research—including animal and human studies—would be needed to determine if hydrogen water or hydrogen gas has practical benefits for people.
Abstract
Background: Ischemia-reperfusion (I/R) injury induces oxidative stress, leading to damage in highly susceptible intestinal tissues. Molecular hydrogen (H2) has shown therapeutic potential in I/R injuries, with our prior research showing its efficacy in improving outcomes in rat intestinal transplantation models. However, its impact on mitochondrial function remain insufficiently understood. This study aims to elucidate how H2 modulates mitochondrial function impaired by I/R injury. Methods: To assess the effects of H2 on I/R injury, cells were divided into three groups: a control group, a hypoxic group (99 % N2, 1 % O2, without H2 for 3, 6, or 24 h), and a hypoxic-H2 group (99 % H2, 1 % O2, for the same durations). After treatment, cells were reoxygenated under normoxic conditions (21 % O2) for 1, 2, 4, or 6 h. Mitochondrial membrane potential, oxygen consumption, and ATP production were measured. Reactive oxygen species production and apoptotic and metabolic regulators were also assessed. Results: H2 markedly promoting mitochondrial recovery following I/R injury, by enhancing ATP production, restoring mitochondrial membrane potential, and improving oxygen consumption. It also reduced ROS levels and suppressed pro-apoptotic signaling. Notably, H2 suppressed the expression of HIF1α and PDK1, suggesting that H2 may act upstream of hypoxia-driven signaling pathways. These changes promoted oxidative phosphorylation and overall cellular function during reperfusion. Conclusions: Our findings reveal that H2 therapy supports mitochondrial function, suppresses ROS, and modulates hypoxia-driven pathways in I/R injury. These insights advance the understanding of H2's potential in addressing I/R injury and provide a foundation for its application in other hypoxia-related conditions.