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.