Document Detail


Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway.
MedLine Citation:
PMID:  21519324     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Aminoglycoside ototoxicity is a common cause of drug-induced hearing loss. Toxicity is dose related, but some patients may still develop hearing loss even under safe dosage. Apart for genetic idiosyncrasy, indirect evidences imply that ischemia may increase the aminoglycoside ototoxic sensitivity because common clinical situations associated with cochlear ischemia such as noise, sepsis, and shock are known to augment the development of aminoglycoside ototoxicity. At present, a direct interaction of cochlear ischemia and aminoglycoside ototoxicity is still lacking. This study demonstrated a direct evidence of increased gentamicin (GM) ototoxic sensitivity in chronic guinea pig models of transient cochlear ischemia. No permanent auditory changes were observed after a single dose of GM (125 mg/kg) or after transient cochlear ischemia for 30 min. Persistent and significant auditory threshold shift was detected when GM was given after transient cochlear ischemia. Cochlear hair cells and spiral ganglion neurons are the major regions affected. Apoptosis contributes to hair cell death during acute interaction of ischemia and GM ototoxicity. Increased apoptotic cell death was also depicted when GM crossreacted with hypoxia in vitro, using cochlear cell lines. Generation of reactive oxygen species, loss of mitochondrial membrane potential, calcium release, and caspase-dependent apoptotic cell death were shown during the interaction of hypoxia and GM ototoxicity in vitro. This synergistic ototoxicity may be critical to aminoglycoside-induced hearing loss in clinical scenarios. The results should improve our understanding of the interacting mechanism and potential preventive strategy to aminoglycoside ototoxicity.Laboratory Investigation advance online publication, 25 April 2011; doi:10.1038/labinvest.2011.69.
Authors:
Chia-Der Lin; Ming-Ching Kao; Ming-Hsui Tsai; Chih-Ho Lai; I-Hua Wei; Mang-Hung Tsai; Chih-Hsin Tang; Cheng-Wen Lin; Chuan-Jen Hsu; Ching-Yuang Lin
Related Documents :
9264404 - C-myc plays a role in cellular susceptibility to death receptor-mediated and chemothera...
21507984 - Rhinovirus-induced barrier dysfunction in polarized airway epithelial cells is mediated...
21073944 - Progallin a isolated from the acetic ether part of the leaves of phyllanthus emblica l....
21344504 - Ah receptor antagonism inhibits constitutive and cytokine inducible il6 production in h...
19364504 - Tnf-related apoptosis-inducing ligand suppresses prdx4 expression.
23530934 - The role of flagella and chemotaxis genes in host pathogen interaction of the host adap...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-4-25
Journal Detail:
Title:  Laboratory investigation; a journal of technical methods and pathology     Volume:  -     ISSN:  1530-0307     ISO Abbreviation:  -     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-4-26     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376617     Medline TA:  Lab Invest     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
1] Department of Otolaryngology-Head and Neck Surgery, China Medical University Hospital, Taichung, Taiwan [2] Graduate Institute of Clinical Medical Science, School of Medicine, China Medical University, Taichung, Taiwan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Is there a role for immune and anti-in-flammatory therapy in type 2 diabetes?
Next Document:  Quantitative assessment shows loss of antigenic epitopes as a function of pre-analytic variables.