Hydrogen Protects Cell Powerhouses from Dangerous Free Radicals
- Authors
- Genki Ishihara, Kosuke Kawamoto, Nobuaki Komori, Toru Ishibashi
- Journal
- Biochemical and Biophysical Research Communications
- Year
- 2020
- DOI
- 10.1016/j.bbrc.2019.11.135
- Study Type
- Molecular Assay
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Neurodegenerative Diseases
- Body System
- Cellular
TL;DR
Hydrogen gas (H2) can help protect cells by adjusting the flow of electrons in the cell's powerhouses, mitochondria, and reducing harmful oxygen-related molecules.
Key Finding
Molecular hydrogen suppressed superoxide generation at mitochondrial complex I by approximately 51% and reduced mitochondrial membrane potential by 11.3% in laboratory tests.
Summary
This laboratory study examined how molecular hydrogen (H2) affects mitochondria, the energy-producing structures inside cells. Researchers tested H2's effects on electron flow and superoxide (a harmful molecule produced during energy generation) in isolated mitochondria and cultured cells. They found that H2 reduced superoxide production by about 51% and lowered the electrical charge across the mitochondrial membrane by 11.3%, suggesting H2 may work by regulating how electrons move through the energy-making machinery rather than just by neutralizing harmful free radicals.
Practical Takeaway
This is a laboratory study using isolated mitochondria and cultured cells, not human testing, so it cannot yet tell us whether these effects occur in the human body or translate to health benefits. The findings suggest a potential mechanism by which hydrogen water might protect cells from oxidative damage, but much more research—including human studies—would be needed before drawing any conclusions about therapeutic use.
Abstract
Molecular hydrogen (H2) is recognized as a medical gas applicable to numerous diseases including neurodegenerative diseases, metabolic disorders, and rheumatoid arthritis. Although the efficacy of H2 is reportedly attributed to its scavenging capability against the hydroxyl radical, the mechanisms underlying its therapeutic efficacy are not fully understood. Herein, we estimated the role of H2 in the energy converting system of the mitochondria, the source of reactive oxygen species. To investigate the effects of H2 on mitochondrial function, direction of electron flow, superoxide generation, and mitochondrial membrane potential were investigated. Forward electron transport (FET) or reverse electron transport (RET) was assessed by monitoring the decrease or increase of β-nicotinamide adenine dinucleotide hydrate (NADH, - or +, μM, respectively) in the presence of β-nicotinamide adenine dinucleotide (NAD+) and/or succinate in the isolated mitochondria. H2O2 converted from superoxide by superoxide dismutase (SOD) was measured to estimate electron leakage in the mitochondria. The effects of H2 on mitochondrial membrane potential were observed by staining cells with the fluorescence probe, teramethylrhodamine ethyl ester (TMRE). Despite the absence of succinate, a distinct RET was observed (from +0.0313 ± 0.0106 μM to +1.20 ± 0.302 μM) by adding 25 μM H2. In the presence of 5 μM NADH, RET by succinate inverted to FET from +1.62 ± 0.358 μM to -1.83 ± 0.191 μM, accompanied by a suppression of superoxide generated predominantly from complex I by 51.1%. H2 solely reduced mitochondrial membrane potential of the cultured cells by 11.3% as assessed by TMRE. The direction of electron flow was altered by H2 depending on the NAD+/NADH ratio, accompanied by suppression of superoxide generation H2 could suppress superoxide generation in complex I in vitro and reduce membrane potential in vivo. H2 may also neutralize semiquinone radicals to reduce superoxide produced in complex III. H2 may function as a rectifier of the electron flow affecting the mitochondrial membrane potential to suppress oxidative damage in mitochondria.