Hydrogen Gas Protects Gut Cells from Toxic Damage in Lab Study
- Authors
- Xu Ji, Weijiang Zheng, Wen Yao
- Journal
- Toxins
- Year
- 2019
- DOI
- 10.3390/toxins12010005
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Mycotoxin Poisoning
- Body System
- Digestive
TL;DR
Hydrogen gas can protect pig intestine cells from damage and cell death caused by a toxic substance found in contaminated food.
Key Finding
Hydrogen gas reversed oxidative damage and cell death markers in intestinal cells exposed to deoxynivalenol, restoring antioxidant enzyme activity and suppressing apoptotic pathways.
Summary
This laboratory study tested whether hydrogen gas could protect intestinal cells from damage caused by deoxynivalenol, a toxic compound found in contaminated grains. Researchers exposed pig intestinal cells to this toxin alone, or to the toxin plus hydrogen-saturated liquid. Cells treated with hydrogen gas showed better survival, less oxidative stress (cellular damage from unstable molecules), and reduced signs of cell death compared to cells exposed to the toxin alone.
Practical Takeaway
This is a preliminary cell-culture study, not a human trial, so it cannot directly predict effects in people. While the results suggest hydrogen may have potential to protect intestinal cells from mycotoxin damage, much more research—including animal studies and eventually human trials—would be needed before any health claims could be supported.
Abstract
To explore the protective role of hydrogen gas (H2) on oxidative damage and apoptosis in intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol (DON), cells were assigned to four treatment groups, including control, 5 μM DON, H2-saturated medium, and 5 μM DON + H2-saturated medium treatments. After 12 h of different treatments, the cell viability, biomarkers of cell redox states, and gene expression of antioxidant enzymes and apoptosis were observed and detected. Furthermore, caspase-3 and Bax protein expressions were measured by Western blot analysis. Our results demonstrated that the 5 μM DON significantly caused cytotoxicity to IPEC-J2 cells by reducing cell viability and increasing lactate dehydrogenase release in culture supernatants. Moreover, DON treatments significantly increased levels of 8-hydroxy-2'-deoxyguanosine, 3-nitrotyrosine, and malonaldehyde; however, they decreased total superoxide dismutase and catalase activities and downregulated messenger RNA (mRNA) expression related to antioxidant enzymes in cells. The 5 μM DON treatment also downregulated Bcl-2 expression and upregulated caspase-3 and Bax expression. However, the H2-saturated medium significantly improved cell growth status and reversed the change of redox states and expression of genes and proteins related to apoptosis induced by DON in IPEC-J2 cells. In conclusion, H2 could protect IPEC-J2 cells from DON-induced oxidative damage and apoptosis in vitro.