Hydrogen Water Activates Heat Response and Repairs Liver Tissue

Authors
Journal
Free Radical Research
Year
DOI
10.1080/10715762.2018.1439166
Study Type
clinical
Peer Reviewed
Yes
Country
Japan
Health Condition
Liver Disease
Body System
Hepatic

TL;DR

Scientists studied how hydrogen water affects genes in the liver and found that it basically turns on the body's repair system (heat shock response) to fix and rebuild damaged tissue, while slowing down cell division—which is actually a good thing because it gives cells time to heal instead of just keep multiplying.

Key Finding

Molecular hydrogen upregulates heat shock response and collagen biosynthesis pathways while downregulating cell cycle genes in liver tissue, with heat shock response activation appearing to be the primary mechanism.

Summary

Researchers analyzed how molecular hydrogen affects gene activity in liver tissue by studying mice and rats that drank hydrogen water. They found that hydrogen water activated genes related to heat shock response (a protective cellular mechanism) and collagen production (important for tissue structure), while reducing genes involved in cell division. The researchers concluded that triggering the heat shock response is likely the main way hydrogen produces its effects in the liver.

Practical Takeaway

This laboratory study in rodents provides early molecular evidence for how hydrogen water might work in the body, but it is not a human study and does not demonstrate that these effects translate to health benefits in people. The findings suggest hydrogen may activate protective cellular mechanisms, but much more research is needed before drawing conclusions about practical health applications.

Abstract

Molecular hydrogen exerts its effect on multiple pathologies, including oxidative stress, inflammation, and apoptosis. However, its molecular mechanisms have not been fully elucidated. In order to explore the effects of molecular hydrogen, we meta-analysed gene expression profiles modulated by molecular hydrogen. We performed microarray analysis of the mouse liver with or without drinking hydrogen water. We also integrated two previously reported microarray datasets of the rat liver into meta-analyses. We used two categories of meta-analysis methods: the cross-platform method and the conventional meta-analysis method (Fisher's method). For each method, hydrogen-modulated pathways were analysed by (i) the hypergeometric test (HGT) in the class of over-representation analysis (ORA), (ii) the gene set enrichment analysis (GSEA) in the class of functional class scoring (FCS), and (iii) the signalling pathway impact analysis (SPIA), pathway regulation score (PRS), and others in the class of pathway topology-based approach (PTA). Pathways in the collagen biosynthesis and the heat-shock response were up-regulated according to (a) HGT with the cross-platform method, (b) GSEA with the cross-platform method, and (c) PRS with the cross-platform method. Pathways in cell cycles were down-regulated according to (a) HGT with the cross-platform method, (b) GSEA with the cross-platform method, and (d) GSEA with the conventional meta-analysis method. Because the heat-shock response leads to up-regulation of collagen biosynthesis and a transient arrest of cell cycles, induction of the heat-shock response is likely to be a primary event induced by molecular hydrogen in the liver of wild-type rodents.