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• W2068510785 abstract "Ethacrynic acid (EA) significantly enhances the ototoxic effects of cisplatin. To gain insights into the mechanisms underlying Cis/EA ototoxicity, cochleas were labeled with several apoptotic markers. Cis/EA treatment caused extensive outer hair cell (OHC) and inner hair cell (IHC) damage; OHC lesions decreased from the base towards apex of the cochlea whereas the IHC lesion was relatively constant (25–60%) along the length of the cochlea. Propidium iodide labeled OHC nuclei appeared relatively normal at 6 h post-treatment, were condensed and fragmented at 12 h post-treatment and were frequently missing 48 h post-treatment. Initiator caspase 8, associated with membrane death receptors, and TRADD, a protein that recruits caspase 8, were present in OHC at 6 h post-treatment. Caspase 8 labeling increased from 6 to 24 h, but was largely absent at 48 h post-treatment. Executioner caspase 3 and caspase 6, which lie downstream of caspase 8, were expressed in OHC 12–24 h post-treatment. Initiator caspase 9, associated with mitochondrial damage, was only expressed at low levels at 48 h post-treatment. These results suggest that the rapid onset of Cis/EA induced programmed cell death is initiated by membrane death receptors associated with TRADD and caspase 8." @default.
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• W2068510785 date "2007-04-01" @default.
• W2068510785 modified "2023-10-11" @default.
• W2068510785 title "Cell death after co-administration of cisplatin and ethacrynic acid" @default.
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• W2068510785 doi "https://doi.org/10.1016/j.heares.2006.07.015" @default.
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