Combating oxidative stress and inflammation in gentamicin-induced nephrotoxicity using hydrogen-rich water.

Gentamicin-induced nephrotoxicity primarily results from renal inflammatory cascades and increased oxidative stress. This study aims to examine the effects of hydrogen-rich water (HRW) on gentamicin-induced renal damage in rats. Thirty-two rats were equally divided into four groups, including control (no treatment), hydrogen, gentamicin, and gentamicin+hydrogen. At the end of one week, all animals were euthanized following ethical rules, and blood and tissue samples were analyzed for examining Malondialdehyde (MDA), glutathione (GSH), Tumor Necrosis Factor-Alfa (TNF-α), Tumor Necrosis Factor-Beta (TNF-β), Interleukin 6 (IL-6), endoglin, endocan, urea, creatinine, Na, and K parameters. Levels of 8-Hydroxyguanosine (8-OHdG), MDA, and Bax were immunohistochemically analyzed. Data showed that while MDA (control P<0.0001, HP<0.0001, ‎Genta+HP<0.0007), TNF-α (control P<0.0002, HP<0.0040, ‎Genta+HP<0.0381), IL-6 (control P<0.0044, HP<0.0070, ‎Genta+HP<0.0109), endocan (control P<0.0460, HP<0.0286, ‎Genta+HP<0.0452), and endoglin (control P<0.0131, HP<0.0164, ‎Genta+HP<0.0397), urea (control P<0.0024, HP<0.0001, ‎Genta+HP<0.0180), and creatinine parameters (control P<0.0017, HP<0.0178, ‎Genta+HP<0.0011) increased in the gentamicin group compared to the other groups, a decrease in these parameters was observed in the gentamicin+hydrogen group compared to the gentamicin group. The Genta group had greater levels of TNF-β than the control (P<0.0042) and H2 groups (P<0.0268). GSH content was higher in the hydrogen group compared to the gentamicin group. Immunohistochemically, 8-OHdG, MDA, and Bax expressions increased in the gentamicin group compared to the control group, whereas they decreased in the gentamicin+hydrogen group compared to the gentamicin group. Hydrogen may be an alternative treatment for oxidative stress-induced nephrotoxicity.