Hydrogen Water Protects Kidneys and Prevents Cancer in Rats
- Authors
- Fang-Yin Li, Shao-Xing Zhu, Zong-Ping Wang, Hua Wang, Yang Zhao, Gui-Ping Chen
- Journal
- Food and Chemical Toxicology
- Year
- 2013
- DOI
- 10.1016/j.fct.2013.10.004
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Nephrotoxicity
- Body System
- Renal
TL;DR
Drinking hydrogen-rich water reduced kidney damage and lowered the risk of early signs of cancer in rats treated with a harmful substance.
Key Finding
In rats exposed to a kidney-damaging toxin, hydrogen-rich water reduced kidney injury markers, suppressed inflammatory responses, and decreased the incidence of kidney cancer.
Summary
Researchers gave rats a toxic chemical (ferric nitrilotriacetate) that damages the kidneys and causes cancer, then treated some rats with hydrogen-rich water. The rats drinking hydrogen-rich water showed less kidney damage, reduced markers of inflammation and oxidative stress (cellular damage from unstable molecules), and developed fewer kidney tumors compared to untreated rats.
Practical Takeaway
This rat study suggests hydrogen-rich water may have protective effects against oxidative stress and inflammation in the kidneys. However, this is animal research only—results in rats do not automatically translate to humans—and much more research, including human trials, would be needed before any health claims could be made.
Abstract
The aim of this work was to test whether consumption with hydrogen-rich water (HW) alleviated renal injury and inhibited early tumor promotional events in Ferric nitrilotriacetate (Fe-NTA)-treated rats. Rats were injected with Fe-NTA solution (7.5mg Fe/kg body weight) intraperitoneally to induce renal injury and simultaneously treated with HW (1.3 ± 0.2mg/l). We found that consumption with HW ameliorated Fe-NTA-induced renal injuries including suppressing elevation of serum creatinine and blood urea nitrogen and inhibited early tumor promotional events including decreasing ornithine decarboxylase activity and incorporation of [3H]thymidine into renal DNA. Consumption with HW suppressed Fe-NTA-induced oxidative stress through decreasing formation of lipid peroxidation and peroxynitrite and activities of NADPH oxidase and xanthine oxidase, increasing activity of catalase, and restoring mitochondrial function in kidneys. Consumption with HW suppressed Fe-NTA-induced inflammation marked by reduced NF-κB, IL-6, and MCP-1 expression and macrophage accumulating in kidneys. In addition, consumption with HW suppressed VEGF expression, STAT3 phosphorylation and PCNA expression in kidneys of Fe-NTA-treated rats. Consumption with HW decreased the incidence of renal cell carcinoma and suppressed tumor growth in Fe-NTA-treated in rats. In conclusion, drinking with HW attenuated Fe-NTA-induced renal injury and inhibited early tumor promotional events in rats.