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

Abstract

A rat model of gentamicin-induced nephrotoxicity was used to evaluate the renal protective potential of hydrogen-rich water (HRW). Thirty-two rats were allocated equally to four groups: control, HRW alone, gentamicin alone, and gentamicin combined with HRW. After one week, blood and kidney tissue were collected for biochemical analysis of MDA, GSH, TNF-α, TNF-β, IL-6, endoglin, endocan, urea, creatinine, sodium, and potassium. Immunohistochemical staining assessed 8-OHdG, MDA, and Bax expression. Gentamicin administration elevated all oxidative, inflammatory, and renal function markers compared with controls. Co-administration of HRW significantly attenuated these elevations, while GSH levels were higher in the HRW-alone group relative to the gentamicin group. Immunohistochemical findings corroborated the biochemical data, showing reduced 8-OHdG, MDA, and Bax expression in the combined group versus the gentamicin-only group.

Mechanism

HRW lowered renal oxidative stress markers (MDA, 8-OHdG) and pro-inflammatory cytokines (TNF-α, TNF-β, IL-6), while increasing GSH levels and reducing Bax expression, collectively attenuating gentamicin-induced apoptotic and inflammatory cascades in kidney tissue.