Manganese-mediated acceleration of age-related hearing loss in mice | Zendy

Nobutaka Ohgami | Zendy; Ichiro Yajima | Zendy; Machiko Iida | Zendy; Xiang Li | Zendy; Reina Oshino | Zendy; Mayuko Y. Kumasaka | Zendy; Masashi Kato | Zendy

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Manganese-mediated acceleration of age-related hearing loss in mice

Author(s) -

Nobutaka Ohgami,

Ichiro Yajima,

Machiko Iida,

Xiang Li,

Reina Oshino,

Mayuko Y. Kumasaka,

Masashi Kato

Publication year - 2016

Publication title -

scientific reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.24

H-Index - 213

ISSN - 2045-2322

DOI - 10.1038/srep36306

Subject(s) - neurodegeneration , spiral ganglion , hearing loss , genetically modified mouse , endocrinology , transgene , medicine , lipofuscin , chemistry , biology , biochemistry , audiology , gene , disease

Despite the fact that manganese (Mn) is known to be a neurotoxic element relevant to age-related disorders, the risk of oral exposure to Mn for age-related hearing loss remains unclear. In this study, we orally exposed wild-type young adult mice to Mn (Mn-exposed WT-mice) at 1.65 and 16.50 mg/L for 4 weeks. Mn-exposed WT-mice showed acceleration of age-related hearing loss. Mn-exposed WT-mice had neurodegeneration of spiral ganglion neurons (SGNs) with increased number of lipofuscin granules. Mn-exposed WT-mice also had increased hypoxia-inducible factor-1 alpha (Hif-1α) protein with less hydroxylation at proline 564 and decreased c-Ret protein in SGNs. Mn-mediated acceleration of age-related hearing loss involving neurodegeneration of SGNs was rescued in RET -transgenic mice carrying constitutively activated RET . Thus, oral exposure to Mn accelerates age-related hearing loss in mice with Ret-mediated neurodegeneration of SGNs.

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