Hydrogen Indirectly Suppresses Increases in Hydrogen Peroxide in Cytoplasmic Hydroxyl Radical-Induced Cells and Suppresses Cellular Senescence.
Takahiro Sakai, Ryosuke Kurokawa, Shin-Ichi Hirano, Jun Imai · International journal of molecular sciences · 2019
Research-use notice
Independent study record
Each H2HUBB study page organizes source-linked research details for educational use. Interpretation should remain proportional to the study design, population, controls, and limitations.
H2HUBB TAKEAWAY
In H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells, further, H₂ suppressed increased H₂O₂ by suppressing cyto •OH-mediated lipid peroxide formation and cellular senescence induction via two pathways. The authors concluded that the study suggests a model whereby the lipid peroxide produced by cyto •OH causes a decrease in GSH and heme storage, increases H₂O₂, and induces cellular senescence through the oxidative DNA damage/p-ATM ser1981 /p-p53 ser15 /p21 pathway and heme depletion/p-HRI/p-eIF2α ser51 /ATF4/p16 pathway. These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied. Molecular hydrogen was the intervention in this cellular study; hydrogen peroxide was evaluated as part of the oxidative-stress response and was not the therapeutic agent.
What Effects Did Molecular Hydrogen Have?
In H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells, further, H₂ suppressed increased H₂O₂ by suppressing cyto •OH-mediated lipid peroxide formation and cellular senescence induction via two pathways. MEFs were treated with vehicle or ROS inducer (30 μM pyocyanin) in normal medium or H₂ super-rich DMEM. The authors concluded that the study suggests a model whereby the lipid peroxide produced by cyto •OH causes a decrease in GSH and heme storage, increases H₂O₂, and induces cellular senescence through the oxidative DNA damage/p-ATM ser1981 /p-p53 ser15 /p21 pathway and heme depletion/p-HRI/p-eIF2α ser51 /ATF4/p16 pathway. Cyto •OH-generated lipid peroxide caused glutathione (GSH) and heme shortage, increased hydrogen peroxide (H₂O₂), and induced cellular senescence via the phosphorylation of ataxia telangiectasia mutated kinase serine 1981 (p-ATMser1981)/p53 serine 15 (p-p53ser15)/p21 and phosphorylation of heme-regulated inhibitor (p-HRI)/phospho-eukaryotic translation initiation factor 2 subunit alpha serine 51 (p-eIF2α)/activating transcription factor 4 (ATF4)/p16 pathways. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Findings Mean
H2HUBB reviewed how molecular hydrogen affected the outcomes measured in H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells. Further, H₂ suppressed increased H₂O₂ by suppressing cyto •OH-mediated lipid peroxide formation and cellular senescence induction via two pathways.
What the Researchers Studied
The researchers studied H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells. The study used a in vitro cell-culture laboratory experiment.
Why These Findings Matter
These findings from a laboratory model add evidence supporting molecular hydrogen's biological and therapeutic potential in the model studied.
How Strong Is This Evidence?
This is laboratory evidence from a in vitro cell-culture laboratory experiment. It is most informative for the biological mechanisms, cellular responses, or biochemical outcomes directly measured.
Technical Study Details
H2HUBB classifies this publication as laboratory study with laboratory or cellular evidence. The research population or model was H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells. The study used a in vitro cell-culture laboratory experiment.
Limitations and Safety
Reported limitations: One limitation of this study was that the researchers did not confirm whether the H₂ produced by intestinal bacteria suppresses cellular senescence and individual aging in vivo. Molecular hydrogen was the intervention in this cellular study; hydrogen peroxide was evaluated as part of the oxidative-stress response and was not the therapeutic agent.
Original Study and H2HUBB Research Context
H2HUBB presents this source-grounded research record as one contribution to the broader molecular-hydrogen evidence base.