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Titolo:
UP-REGULATION OF ADENOSINE RECEPTORS IN THE COCHLEA BY CISPLATIN
Autore:
FORD MS; NIE ZZ; WHITWORTH C; RYBAK LP; RAMKUMAR V;
Indirizzi:
SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL,POB 19230 SPRINGFIELD IL 62794 SO ILLINOIS UNIV,SCH MED,DEPT PHARMACOL SPRINGFIELD IL 62794 SO ILLINOIS UNIV,SCH MED,DEPT SURG SPRINGFIELD IL 62794
Titolo Testata:
Hearing research
fascicolo: 1-2, volume: 111, anno: 1997,
pagine: 143 - 152
SICI:
0378-5955(1997)111:1-2<143:UOARIT>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
OUTER HAIR-CELLS; GUINEA-PIG; ANTIOXIDANT ENZYMES; INDUCED OTOTOXICITY; SUPEROXIDE ANION; IN-VITRO; SYSTEM; PROTECTION; MECHANISM; DIETHYLDITHIOCARBAMATE;
Keywords:
ADENOSINE; ADENOSINE RECEPTOR; CISPLATIN; COCHLEA; ANTIOXIDANT ENZYME; CYTOPROTECTION; COMPOUND ACTION POTENTIAL; ENDOCOCHLEAR POTENTIAL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
M.S. Ford et al., "UP-REGULATION OF ADENOSINE RECEPTORS IN THE COCHLEA BY CISPLATIN", Hearing research, 111(1-2), 1997, pp. 143-152

Abstract

In a previous study, we have demonstrated the presence of two adenosine receptor (AR) subtypes, namely A(1) and A(3)AR, in the chinchilla cochlea. One or both of these receptors couple to activation of antioxidant enzymes, with resulting decreases in lipid peroxidation. The chemotherapeutic agent, cisplatin, was shown to produce ototoxicity withina few days of administration presumably by generating reactive oxygenspecies (ROS) and :hereby increasing lipid peroxidation. In this study, we focused on whether lipid peroxidation induces hearing loss by assessing the cochlear antioxidant defense system over a shorter time period (24 h) following cisplatin administration. Cisplatin was administered to anesthetized chinchillas by round window membrane application and hearing loss was determined by compound action potential (CAP) andendocochlear potential (EP) 24 and 72 h post-treatment. Elevations inCAP thresholds in response to click and to 2, 4, 8 and 16 kHz tones and decreases in EP were obtained within 24 h of cisplatin treatment. These changes persisted for at least up to 72 h. Measurements of antioxidant enzymes indicate no change in the activities of superoxide dismutase, catalase or glutathione peroxidase, either 24 or 72 h following cisplatin treatment. The levels of malondialdehyde obtained at these time points were equivalent to those obtained from the controls. Furthermore, no difference in cochlear morphology was detectable by scanningelectron microscopy at the basal, middle or apical turns of the cochlea within 24 h. By 72 h, however, losses in both inner and outer hair cells were observed in the basal and middle turns of the cochlea. A major finding of this study is that exposure to cisplatin led to a 5-fold up-regulation of [I-125]N-6-2-{4-amino-3-phenyl}ethyladenosine binding in the cochlea within 24 h, reflecting increases in expression of AR(s) in this tissue. These data indicate a dissociation between cisplatin acute (within 24 h) ototoxicity and lipid peroxidation. Furthermore, up-regulation of AR(s) may represent a rapid compensatory mechanismby the cochlea to counter the toxic effects of increased ROS generated by cisplatin.

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Documento generato il 10/07/20 alle ore 02:28:01