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Titolo:
Oxidative stress in aging in the c57B16/J mouse cochlea.
Autore:
Staecker, H; Zheng, QY; Van de Water, TR;
Indirizzi:
Univ Maryland, Sch Med, Div Otolaryngol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 Otolaryngol, Baltimore, MD 21201 USA Jackson Lab, Bar Harbor, ME 04609 USA Jackson Lab Bar Harbor ME USA 04609Jackson Lab, Bar Harbor, ME 04609 USA Albert Einstein Coll Med, Dept Otolaryngol & Neurosci, Bronx, NY 10467 USAAlbert Einstein Coll Med Bronx NY USA 10467 Neurosci, Bronx, NY 10467 USA
Titolo Testata:
ACTA OTO-LARYNGOLOGICA
fascicolo: 6, volume: 121, anno: 2001,
pagine: 666 - 672
SICI:
0001-6489(200109)121:6<666:OSIAIT>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED HEARING-LOSS; HAIR CELL LOSS; SUPEROXIDE-DISMUTASE; MICE; ANTIOXIDANT; SUSCEPTIBILITY; GLUTATHIONE; EXPRESSION; PROTECTION; GENETICS;
Keywords:
aging; C57B16/J mouse; oxidative stress; presbycusis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Staecker, H Univ Maryland, Sch Med, Div Otolaryngol, 16 S Eutaw Stress,Suite 500, Baltimore, MD 21201 USA Univ Maryland 16 S Eutaw Stress,Suite 500 Baltimore MD USA 21201
Citazione:
H. Staecker et al., "Oxidative stress in aging in the c57B16/J mouse cochlea.", ACT OTO-LAR, 121(6), 2001, pp. 666-672

Abstract

Presbycusis is a complex of high frequency hearing loss and disproportionate loss of speech discrimination that is seen concomitantly with physical signs of aging. Among the most extensively characterized strains of mice that show an early hearing loss is the C57B16/J strain, a strain that shows early onset of high frequency hearing loss at age 6 months and complete hearing loss by 1 year of age. The histopathology of this strain consists of loss of hair cells and spiral ganglion neurons in the basal turn, with a progression of loss of hair cells and ganglion neurons towards the apical portion of the cochlea as the animal ages. The process of aging has been extensively studied and although details differ in various organisms the consensus today is that oxidative stress, i.e. free radical-mediated tissue damage, is one of the core mechanisms of aging. Aerobic metabolism results in the creation of hydrogen peroxide and reactive oxygen species. These are normallydetoxified by a variety of enzymes and free radical scavengers, including superoxide dismutase (SOD), catalase and glutathione. To determine whether oxidative stress plays a role in the pathophysiology of hearing loss in this mouse model of presbycusis we determined the relative change in mRNA production for selected free radical detoxifying enzymes in the C57B16/J mouse cochlea. Using semi-quantitative RT-PCR with tubulin mRNA as a control, relative levels of antioxidant enzyme mRNAs were determined. There was an overall increase in SOD1 mRNA levels when comparing 1 and 9 month time points, and a transient increase in the expression level of catalase mRNA. B6.CAST(Ahl) mice, which carry the C57B16/J genome but receive their AN gene from CAST mice, do not show these alteractions in antioxidant enzyme production. Our results suggest that at an age of 9 months, at which point significanthearing loss has developed, the C57B16/J mouse cochlea is exposed to increased levels of free radicals and that the Ahl gene of the C57B16/J mouse mediates this decrease in protective enzymes and therefore increase in levelsof oxidative stress.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/07/20 alle ore 07:40:11