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Dalian D, Haiyan J, Yong F, et al. Ototoxic Model of Oxaliplatin and Protection from Nicotinamide Adenine Dinucleotide. J Otol. 2013;8(1):63-71doi: 10.1016/s1672-2930(13)50009-2.
Dalian, D., Haiyan, J., Yong, F., Yongqi, L., Salvi, R., Someya, S., & Tanokura, M. (2013). Ototoxic Model of Oxaliplatin and Protection from Nicotinamide Adenine Dinucleotide. Journal of otology, 8(1), 63-71. https://doi.org/10.1016/s1672-2930(13)50009-2
Dalian, Ding, et al. "Ototoxic Model of Oxaliplatin and Protection from Nicotinamide Adenine Dinucleotide." Journal of otology vol. 8,1 (2013): 63-71. doi: https://doi.org/10.1016/s1672-2930(13)50009-2
Dalian D, Haiyan J, Yong F, Yongqi L, Salvi R, Someya S, Tanokura M. Ototoxic Model of Oxaliplatin and Protection from Nicotinamide Adenine Dinucleotide. J Otol. 2013;8(1):63-71. doi: 10.1016/s1672-2930(13)50009-2. PMID: 25419212; PMCID: PMC4240522.
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J Otol. 2013;8(1):63-71. doi: 10.1016/s1672-2930(13)50009-2.

Ototoxic Model of Oxaliplatin and Protection from Nicotinamide Adenine Dinucleotide.

Journal of otology

Ding Dalian, Jiang Haiyan, Fu Yong, Li Yongqi, Richard Salvi, Shinichi Someya, Masaru Tanokura

Affiliations

  1. Center for Hearing and Deafness, State University of New York at Buffalo, USA ; Sixth People's Hospital, Shanghai Oriental Otolaryngology Institute, Shanghai Jiao Tong University, China ; Xiangya Hospital, Central South University, China ; Department of Applied Biological Chemistry, University of Tokyo, Japan.
  2. Center for Hearing and Deafness, State University of New York at Buffalo, USA.
  3. The First Officiated Hospital, College of Medicine, Zhejiang University.
  4. The Third Affiliated Hospital of Sun Yat-Sen University.
  5. University of Florida, USA.
  6. Department of Applied Biological Chemistry, University of Tokyo, Japan.

PMID: 25419212 PMCID: PMC4240522 DOI: 10.1016/s1672-2930(13)50009-2

Abstract

Oxaliplatin, an anticancer drug commonly used to treat colorectal cancer and other tumors, has a number of serious side effects, most notably neuropathy and ototoxicity. To gain insights into its ototoxic profile, oxaliplatin was applied to rat cochlear organ cultures. Consistent with it neurotoxic propensity, oxaliplatin selectively damaged nerve fibers at a very low dose 1 μM. In contrast, the dose required to damage hair cells and spiral ganglion neurons was 50 fold higher (50 μM). Oxailiplatin-induced cochlear lesions initially increased with dose, but unexpectedly decreased at very high doses. This non-linear dose response could be related to depressed oxaliplatin uptake via active transport mechanisms. Previous studies have demonstrated that axonal degeneration involves biologically active processes which can be greatly attenuated by nicotinamide adenine dinucleotide (NAD+). To determine if NAD+ would protect spiral ganglion axons and the hair cells from oxaliplatin damage, cochlear cultures were treated with oxaliplatin alone at doses of 10 μM or 50 μM respectively as controls or combined with 20 mM NAD+. Treatment with 10 μM oxaliplatin for 48 hours resulted in minor damage to auditory nerve fibers, but spared cochlear hair cells. However, when cochlear cultures were treated with 10 μM oxaliplatin plus 20 mM NAD+, most auditory nerve fibers were intact. 50 μM oxaliplatin destroyed most of spiral ganglion neurons and cochlear hair cells with apoptotic characteristics of cell fragmentations. However, 50 μM oxaliplatin plus 20 mM NAD+ treatment greatly reduced neuronal degenerations and hair cell missing. The results suggested that NAD+ provides significant protection against oxaliplatin-induced neurotoxicity and ototoxicity, which may be due to its actions of antioxidant, antiapoptosis, and energy supply.

Keywords: apoptosis; copper transporter; nicotinamide adenine dinucleotide; oxaliplatin

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