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- Title
3-Aminotriazole protects from CoCl-induced ototoxicity by inhibiting the generation of reactive oxygen species and proinflammatory cytokines in mice.
- Authors
Lee, Joon; Kim, Seul-Gi; Lim, Jae-Young; Dutta, Raghbendra; Kim, Se-Jin; Choe, Seong-Kyu; So, Hong-Seob; Park, Raekil
- Abstract
Cobalt is an essential heavy metal that is necessary for the formation of vitamin B12 (hydroxocobalamin). However, exposure to excess cobalt for a prolonged period can harm the human body, causing pulmonary fibrosis, blindness, deafness, and peripheral neuropathy. 3-Aminotriazole (3-AT) is a catalase inhibitor that is often used to investigate the physiological effects of catalase. The present study found that injection of 3-AT in mice significantly reduced CoCl-induced hearing impairment. In cultured organ of Corti explants from rats, 3-AT treatment protected hair cells from CoCl-induced cytotoxicity. To determine the mechanism by which 3-AT protected from CoCl-induced ototoxicity, we used the HEI-OC1 auditory cell line. Pretreatment with 10 mM 3-AT attenuated CoCl-induced accumulation of ROS and induction of proinflammatory cytokine expression. Interestingly, these protective effects of 3-AT did not require catalase activity, as demonstrated by a series of experiments using RNA interference-mediated catalase knockdown in HEI-OC1 cells and using catalase-deficient mouse embryonic fibroblasts. Our results demonstrated the mechanisms of CoCl-induced ototoxicity that may provide better ways to prevent the ototoxic effect of cobalt exposure.
- Subjects
OTOTOXICITY; COBALT chloride; REACTIVE oxygen species; CYTOKINES; LABORATORY mice; CATALASE; PULMONARY fibrosis
- Publication
Archives of Toxicology, 2016, Vol 90, Issue 4, p781
- ISSN
0340-5761
- Publication type
Article
- DOI
10.1007/s00204-015-1506-9