Functional Water Triggers Immune Response in Oral Cancer Cells
- Authors
- Tomoko Takemoto, Ryo Kaetsu, Machiko Hanayama, Yuuichi Ishiyama, Masayuki Sadamura, Kensuke Nishio, Mariko Tsunoda, Masatake Asano, Mitsuru Motoyoshi
- Journal
- International Journal of Medical Sciences
- Year
- 2021
- DOI
- 10.7150/ijms.53999
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Oral Squamous Cell Carcinoma
- Body System
- Immune System
TL;DR
A special water created by electrolyzing salt water can trigger the release of an immune signaling protein from cancer cells in the mouth.
Key Finding
Acid-electrolyzed functional water triggered the release of interleukin-1α from existing intracellular storage in oral cancer cells, independent of new protein synthesis.
Summary
This laboratory study examined how acid-electrolyzed functional water (water treated with electrical current) affects cancer cells from oral tumors. Researchers found that this water caused cancer cells to release a protein called interleukin-1α (IL-1α), which is involved in immune responses. The release came from proteins already stored inside the cells rather than from newly made proteins.
Practical Takeaway
This is a preliminary laboratory study in cancer cells only—not in humans or animals—so it cannot yet inform health decisions about hydrogen water. While the finding is interesting for cancer biology research, much more work would be needed to determine if this effect occurs in living organisms or has any practical application for human health.
Abstract
The aim of this study was to examine the acid-electrolyzed functional water (FW)-mediated cytokine release in an oral squamous cell carcinoma-derived cell line (OSCC) following treatment with FW. FW is generated by the electrolysis of a sodium chloride solution and accelerate the burn wound healing. To elucidate the underlying mechanisms, the cytokine/chemokine secretion profile of HSC3 cells was examined using a cytokine array. FW treatment significantly induced interleukin (IL)-1α secretion, which was confirmed by enzyme-linked immunosorbent assay. Subsequently, the HSC3 cells were pre-treated with cycloheximide (CHX) for 1 h prior to FW stimulation to determine whether the augmented IL-1α secretion was due to enhanced protein synthesis. CHX pre-treatment did not affect IL-1α secretion suggesting that the secreted IL-1α might have been derived from intracellular storage sites. The amount of IL-1α in the cell lysate of the FW-treated HSC3 cells was significantly lower than that of the non-treated cells. Immunofluorescence staining using a polyclonal antibody against full-length IL-1α revealed a drastic reduction in IL-1α inside the FW- treated cells. IL-1α is synthesized in its precursor form (pIL-1α) and cleaved to produce pro-piece and mature IL-1α (ppIL-1α and mIL-1α) inside the cells. In the present study, only pIL-1α was detected within the HSC3 cells in its resting state. However, FW stimulation resulted in the release of the 33 kDa and two other smaller forms (about 19 kDa) of the protein. These results indicates that FW treatment induces IL-1α secretion, a typical alarmin, from the intracellular storage in OSCC cells.