Hydrogen Water Protects Kidneys from Antibiotic Damage in Rats
- Authors
- Mustafa Oguz Cumaoglu, Mustafa Makav, Serpil Dag, Ayfer Yildiz Uysal, Lale Baser, Tyler W. LeBaron, Duried Alwazeer
- Journal
- Tissue & Cell
- Year
- 2024
- DOI
- 10.1016/j.tice.2024.102604
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Turkey
- Health Condition
- Nephrotoxicity
- Body System
- Renal
TL;DR
Drinking hydrogen-rich water reduced kidney damage caused by the antibiotic gentamicin in rats.
Key Finding
In rats, hydrogen-rich water reduced oxidative stress markers, inflammatory molecules, and kidney damage caused by gentamicin, while improving kidney function parameters like creatinine and urea levels.
Summary
Gentamicin is an antibiotic that can damage the kidneys by triggering inflammation and oxidative stress (cellular damage from harmful molecules). Researchers gave rats gentamicin with or without hydrogen-rich water to see if hydrogen could protect kidney function. Rats that received hydrogen-rich water alongside gentamicin showed reduced markers of oxidative stress and inflammation, and better kidney function tests compared to rats that received gentamicin alone.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen-rich water may help protect against kidney damage from certain antibiotics. However, this was only tested in rats over one week, so it's unclear whether these results would apply to humans or in real-world conditions. More research, including human studies, would be needed before drawing any conclusions about hydrogen water's usefulness for this purpose.
Abstract
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, H2P<0.0001, Genta+H2P<0.0007), TNF-α (control P<0.0002, H2P<0.0040, Genta+H2P<0.0381), IL-6 (control P<0.0044, H2P<0.0070, Genta+H2P<0.0109), endocan (control P<0.0460, H2P<0.0286, Genta+H2P<0.0452), and endoglin (control P<0.0131, H2P<0.0164, Genta+H2P<0.0397), urea (control P<0.0024, H2P<0.0001, Genta+H2P<0.0180), and creatinine parameters (control P<0.0017, H2P<0.0178, Genta+H2P<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.