Hydrogen Gas Protects Hearing from Cancer Drug Side Effects

Authors
Journal
International Journal of Pediatric Otorhinolaryngology
Year
DOI
10.1016/j.ijporl.2011.10.014
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Cisplatin-induced Ototoxicity
Body System
Auditory

TL;DR

Inhaling hydrogen gas can reduce hearing loss and ear damage caused by the cancer drug cisplatin.

Key Finding

Inhaling hydrogen gas significantly reduced hearing loss and inner ear cell damage caused by cisplatin in rats, while also lowering oxidative stress markers in blood and ear tissue.

Summary

This rat study tested whether inhaling hydrogen gas could protect hearing from damage caused by cisplatin, a chemotherapy drug known to harm the inner ear. Rats given cisplatin plus hydrogen gas inhalation experienced less hearing loss and less damage to sound-sensing cells in the ear compared to rats given cisplatin alone. The researchers also found that hydrogen gas reduced markers of oxidative stress (cellular damage from harmful molecules) in both the blood and ear tissue.

Practical Takeaway

This is early-stage animal research suggesting hydrogen gas inhalation may help protect hearing during cisplatin chemotherapy. However, this was a rat study only, and the sample size and treatment duration were not reported. Much more research, including human trials, would be needed before this could be considered a viable protective strategy for cancer patients.

Abstract

Cisplatin, an anticancer drug used extensively to treat a broad range of tumors, has strong ototoxic side effects induced by reactive oxygen species (ROS). Recently, it has been reported that hydrogen gas (H(2)) is a new antioxidant by selectively reducing hydroxyl radical, the most cytotoxic ROS. The present study was designed to investigate whether H(2) treatment is beneficial to cisplatin-induced ototoxicity via reducing oxidative stress. The animals were intraperitoneally given a 30 min infusion of 16 mg/kg cisplatin or the same volume of saline. H(2) treatment was given twice with 2% H(2) inhalation for 60 min starting at 1h and 6h after cisplatin or saline injection, respectively. The hearing status of all animals was evaluated by auditory brainstem responses (ABR). The hair cell damage was observed by phalloidin staining. In addition, the levels of oxidative products in serum and cochlear tissue were measured. We found that H(2) treatment significantly attenuated cisplatin-induced hearing loss evaluated by click-evoked and tone burst ABR threshold. Furthermore, histological analysis revealed that 2% H(2) treatment significantly alleviated cisplatin-induced hair cell damage in the organ of corti. In addition, cisplatin significantly increased the levels of malondialdehyde (MDA) and 8-iso-prostaglandin F2α (8-iso-PGF2α) in serum and cochlear tissue, which was attenuated by H(2) treatment. These results demonstrate that H(2) is beneficial to cisplatin-induced ototoxicity via reducing oxidative stress. Therefore, H(2) has potential for improving the quality of life of patients during chemotherapy by efficiently mitigating the cisplatin ototoxicity.