Hydrogen Gas Protects Hearing from Chemotherapy Drug Side Effects
- Authors
- Anette E. Fransson, Marta Kisiel, Kristian Pirttilä, Curt Pettersson, Pernilla Videhult Pierre, Göran F. E. Laurell
- Journal
- Frontiers in Cellular Neuroscience
- Year
- 2017
- DOI
- 10.3389/fncel.2017.00280
- Study Type
- Guinea Pig
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Sweden
- Health Condition
- Cisplatin Ototoxicity
- Body System
- Auditory
TL;DR
Inhaling hydrogen gas can lessen the hearing damage and tinnitus caused by the cancer drug cisplatin in guinea pigs.
Key Finding
Hydrogen gas inhalation reduced cisplatin-induced hearing damage in guinea pigs across multiple measures, including hearing thresholds, inner ear cell loss, and nerve cell connections.
Summary
This study tested whether breathing hydrogen gas could protect guinea pigs' hearing from damage caused by cisplatin, a chemotherapy drug known to cause hearing loss and ringing in the ears. Researchers gave some guinea pigs cisplatin alone, while others received cisplatin followed by 60 minutes of breathing hydrogen gas (2% hydrogen mixed with air). The guinea pigs that received hydrogen gas showed significantly less hearing damage, fewer lost inner ear cells, and better preservation of connections between nerve cells compared to those receiving cisplatin alone.
Practical Takeaway
While this preclinical study in guinea pigs suggests hydrogen gas may help protect hearing during cisplatin chemotherapy, it is too early to draw conclusions for humans. The researchers note that further studies are needed to confirm these findings in people and to ensure hydrogen doesn't interfere with cisplatin's cancer-fighting effectiveness. Anyone undergoing cisplatin treatment should discuss hearing protection options only with their oncology team.
Abstract
Introduction: Permanent hearing loss and tinnitus as side-effects from treatment with the anticancer drug cisplatin is a clinical problem. Ototoxicity may be reduced by co-administration of an otoprotective agent, but the results in humans have so far been modest. Aim: The present preclinical in vivo study aimed to explore the protective efficacy of hydrogen (H2) inhalation on ototoxicity induced by intravenous cisplatin. Materials and Methods: Albino guinea pigs were divided into four groups. The Cispt (n = 11) and Cispt+H2 (n = 11) groups were given intravenous cisplatin (8 mg/kg b.w., injection rate 0.2 ml/min). Immediately after, the Cispt+H2 group also received gaseous H2 (2% in air, 60 min). The H2 group (n = 5) received only H2 and the Control group (n = 7) received neither cisplatin nor H2. Ototoxicity was assessed by measuring frequency specific ABR thresholds before and 96 h after treatment, loss of inner (IHCs) and outer (OHCs) hair cells, and by performing densitometry-based immunohistochemistry analysis of cochlear synaptophysin, organic transporter 2 (OCT2), and copper transporter 1 (CTR1) at 12 and 7 mm from the round window. By utilizing metabolomics analysis of perilymph the change of metabolites in the perilymph was assessed. Results: Cisplatin induced electrophysiological threshold shifts, hair cell loss, and reduced synaptophysin immunoreactivity in the synapse area around the IHCs and OHCs. H2 inhalation mitigated all these effects. Cisplatin also reduced the OCT2 intensity in the inner and outer pillar cells and in the stria vascularis as well as the CTR1 intensity in the synapse area around the IHCs, the Deiters' cells, and the stria vascularis. H2 prevented the majority of these effects. Conclusion: H2 inhalation can reduce cisplatin-induced ototoxicity on functional, cellular, and subcellular levels. It is proposed that synaptopathy may serve as a marker for cisplatin ototoxicity. The effect of H2 on the antineoplastic activity of cisplatin needs to be further explored.