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Titolo:
Application of antioxidants and other agents to prevent cisplatin ototoxicity
Autore:
Rybak, LP; Whitworth, C; Somani, S;
Indirizzi:
So Illinois Univ, Sch Med, Dept Surg, Springfield, IL 62794 USA So Illinois Univ Springfield IL USA 62794 Surg, Springfield, IL 62794 USA So Illinois Univ, Sch Med, Dept Pharmacol, Springfield, IL 62794 USA So Illinois Univ Springfield IL USA 62794 acol, Springfield, IL 62794 USA
Titolo Testata:
LARYNGOSCOPE
fascicolo: 11, volume: 109, anno: 1999,
pagine: 1740 - 1744
SICI:
0023-852X(199911)109:11<1740:AOAAOA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
SODIUM THIOSULFATE; 4-METHYLTHIOBENZOIC ACID; INDUCED NEPHROTOXICITY; REDUCED GLUTATHIONE; PROTECTION; DIETHYLDITHIOCARBAMATE; SYSTEM; ASSAY; RATS; MECHANISM;
Keywords:
cisplatin; ototoxicity; free radicals; antioxidants; glutathione;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Rybak, LP So Illinois Univ, Sch Med, Dept Surg, POB 19638, Springfield, IL62794 USA So Illinois Univ POB 19638 Springfield IL USA 62794 IL 62794 USA
Citazione:
L.P. Rybak et al., "Application of antioxidants and other agents to prevent cisplatin ototoxicity", LARYNGOSCOP, 109(11), 1999, pp. 1740-1744

Abstract

Objective/Hypothesis: To review the recent data from experiments performedin this laboratory to test the hypothesis that cisplatin ototoxicity is related to depletion of glutathione and antioxidant enzymes in the cochlea and that the use of antioxidants or protective agents would protect the cochlea against cisplatin damage and prevent hearing loss. Study Design/Methods:Data were reviewed from experiments performed in this laboratory. Control rats were treated intraperitoneally with cisplatin 16 mg/kg. Experimental rats were given cisplatin in combination with one of the following protective agents: diethyldithiocarbamate, 4-methylthiobenzoic acid, ebselen, or lipoic acid. Animals in each group underwent auditory brainstem response (ABR)threshold testing before and 3 days after treatment. Cochleae were removedafter final ABR testing and analyzed for glutathione and activities of theenzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and malondialdehyde, Results: Rats in the control group receiving cisplatin were found to have significant ABR threshold shifts. This wasaccompanied by a reduction of glutathione and the activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase) and an elevation of malondialdehyde, Experimental animals had preservation of ABR thresholds and levels of glutathione, antioxidant enzyme activity, and malondialdehyde that were similar to untreated animals,Conclusion: Cisplatin ototoxicity appears to be initiated by free-radical production, which causes depletion of glutathione and antioxidant enzymes in the cochlea, and Lipid peroxidation, manifested by an increase in malondialdehyde, These effects were blocked by each of a series of antioxidant compounds given in combination with cisplatin, A mechanism for cisplatin ototoxicity is elaborated with a proposed plan of chemoprevention using agents with different mechanisms of action. These substances could be used alone orin combination to reduce the severity of cisplatin ototoxicity in patients.

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Documento generato il 10/07/20 alle ore 00:17:46