Movatterモバイル変換


[0]ホーム

URL:


Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
Thehttps:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

NIH NLM Logo
Log inShow account info
Access keysNCBI HomepageMyNCBI HomepageMain ContentMain Navigation
pubmed logo
Advanced Clipboard
User Guide

Full text links

Elsevier Science full text link Elsevier Science
Full text links

Actions

Share

Review
.1986 Mar-Apr;7(2):73-99.
doi: 10.1016/s0196-0709(86)80037-0.

Effects of noise and ototoxic drugs at the cellular level in the cochlea: a review

Review

Effects of noise and ototoxic drugs at the cellular level in the cochlea: a review

D J Lim. Am J Otolaryngol.1986 Mar-Apr.

Abstract

Currently available information concerning the cellular mechanisms involved in acoustic trauma and aminoglycoside ototoxicity is reviewed to shed some new light on the cellular events that may be related to functional impairment of the auditory organ. Based on the available data, the following postulations can be made concerning the cellular mechanisms involved. 1) The macromolecular disruption of the stereocilia and cuticular plates is the initial cellular event in acoustic trauma. This disruption would affect the micromechanics of the transduction process, leading to temporary threshold shift. Further cellular impairment would involve basic cellular functions such as the protein, lipid, and glucose synthesis needed for cell repair and survival, and such impairment would result in permanent cell injury or cell death, leading to permanent threshold shift. 2) It can be postulated that the cellular mechanisms involved in aminoglycoside ototoxicity include two events. The early event is the reversible blockage of the transduction channels from the endolymph side of the hair cells. The later event is the interference in such cellular functions as protein and/or phospholipid synthesis because of binding of aminoglycoside to the phospholipids and/or protein, leading to cell death. The latter event may be facilitated by penetration or membrane-mediated internalization of the aminoglycoside from the perilymph side of the hair cell.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

MeSH terms

Substances

Related information

LinkOut - more resources

Full text links
Elsevier Science full text link Elsevier Science
Cite
Send To

NCBI Literature Resources

MeSHPMCBookshelfDisclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.


[8]ページ先頭

©2009-2025 Movatter.jp