Hydrogen Water Blocks Tumor Blood Vessel Growth in Cancer Cells

Authors
Journal
Biological & Pharmaceutical Bulletin
Year
DOI
10.1248/bpb.31.19
Study Type
Cell Culture
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Lung Adenocarcinoma
Body System
Cardiovascular

TL;DR

A special type of water called electrolyzed reduced water (ERW) can decrease the signals that lead to the growth of blood vessels in lung cancer cells, potentially slowing tumor growth.

Key Finding

Electrolyzed reduced water suppressed the production of VEGF—a protein that enables tumors to form new blood vessels—by reducing intracellular hydrogen peroxide and blocking the ERK1/2 signaling pathway in lung cancer cells.

Summary

Researchers tested electrolyzed reduced water (water treated with electrical current to add hydrogen) on lung cancer cells in laboratory dishes. They found that this water reduced harmful molecules called hydrogen peroxide inside cancer cells and decreased production of a protein (VEGF) that helps tumors grow new blood vessels. The water appeared to work by blocking a specific cellular signaling pathway (ERK1/2) that normally promotes VEGF production.

Practical Takeaway

This is an early-stage laboratory study using cancer cells in dishes, not animals or humans, so it cannot yet tell us whether hydrogen water would have any effect on cancer in people. The findings suggest a potential mechanism worth investigating further, but many compounds show promise in cell cultures and fail in living organisms. Much more research would be needed before any health claims could be considered.

Abstract

Vascular endothelial growth factor (VEGF) is a key mediator of tumor angiogenesis. Tumor cells are exposed to higher oxidative stress compared to normal cells. Numerous reports have demonstrated that the intracellular redox (oxidation/reduction) state is closely associated with the pattern of VEGF expression. Electrolyzed reduced water (ERW) produced near the cathode during the electrolysis of water scavenged intracellular H(2)O(2) and decreased the release of H(2)O(2) from a human lung adenocarcinoma cell line, A549, and down-regulated both VEGF transcription and protein secretion in a time-dependent manner. To investigate the signal transduction pathway involved in regulating VEGF expression, mitogen-activated kinase (MAPK) specific inhibitors, SB203580 (p38 MAPK inhibitor), PD98059 (ERK1/2 inhibitor) and JNKi (c-Jun N-terminal protein kinase inhibitor) were applied. The results showed that only PD98059 blocks VEGF expression, suggesting an important role for ERK1/2 in regulating VEGF expression in A549 cells. As well, ERW inhibited the activation of extracellular signal-regulated kinase (ERK) in a time-dependent manner. Co-culture experiments to analyze in vitro tubule formation assay revealed that A549 cell-derived conditioned medium significantly stimulated the formation of vascular tubules in all analyzed parameters; tubule total area, tubule junction, number of tubules, and total tubule length. ERW counteracted the effect of A549 cell-conditioned medium and decreased total tube length (p<0.01). The present study demonstrated that ERW down-regulated VEGF gene transcription and protein secretion through inactivation of ERK.