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Titolo:
Oxidant mechanisms in toxic acute renal failure
Autore:
Baliga, R; Ueda, N; Walker, PD; Shah, SV;
Indirizzi:
Univ Arkansas Med Sci, Dept Med, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Arkansas Med Sci, Dept Pathol, Little Rock, AR 72205 USA Univ Arkansas Med Sci Little Rock AR USA 72205 Little Rock, AR 72205 USA Univ Mississippi, Med Ctr, Jackson, MS 39216 USA Univ Mississippi JacksonMS USA 39216 ppi, Med Ctr, Jackson, MS 39216 USA Cent Arkansas Vet Healthcare Syst, Little Rock, AR 72205 USA Cent ArkansasVet Healthcare Syst Little Rock AR USA 72205 , AR 72205 USA
Titolo Testata:
DRUG METABOLISM REVIEWS
fascicolo: 4, volume: 31, anno: 1999,
pagine: 971 - 997
SICI:
0360-2532(1999)31:4<971:OMITAR>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED LIPID-PEROXIDATION; OXYGEN-FREE-RADICALS; CISPLATIN-INDUCED NEPHROTOXICITY; RAT-KIDNEY CORTEX; CYCLOSPORINE-A; HYDROGEN-PEROXIDE; HEME OXYGENASE; CORTICAL MITOCHONDRIA; TISSUE-INJURY; NONTRAUMATIC RHABDOMYOLYSIS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
84
Recensione:
Indirizzi per estratti:
Indirizzo: Shah, SV Univ Arkansas Med Sci, Dept Med, 4301 W Markham,Slot 501, Little Rock, AR 72205 USA Univ Arkansas Med Sci 4301 W Markham,Slot 501 Little Rock AR USA 72205
Citazione:
R. Baliga et al., "Oxidant mechanisms in toxic acute renal failure", DRUG METAB, 31(4), 1999, pp. 971-997

Abstract

Over the last decade, there is accumulating evidence for a role of reactive oxygen metabolites in the pathogenesis of a variety of renal diseases, including gentamicin, glycerol, cisplatin, and cyclosporine A models of toxicacute renal failure. Gentamicin has been shown both in in vitro and in vivo studies to enhance the generation of reactive oxygen metabolites. Iron isimportant in models of tissue injury, presumably because it is capable of catalyzing free-radical formation. Gentamicin has been shown to cause release of iron from renal cortical mitochondria. Scavengers of reactive oxygen metabolites as well as iron chelators provide protection in gentamicin-induced nephrotoxicity. In glycerol-induced acute renal failure, an animal model of rhabdomyolysis, there is enhanced generation of hydrogen peroxide, andscavengers of reactive oxygen metabolites and iron chelators provide protection. Although the dogma is that the myoglobin is the source of iron, recent studies suggest that cytochrome P450 may be an important source of iron in this model. In addition, there are marked alterations in antioxidant defenses, such as glutathione, as well as changes in heme oxygenase. Several recent in vitro and in vivo studies indicate an important role of reactive oxygen metabolites in cisplatin-induced nephrotoxicity. Thus, catalytic ironis increased both in vitro and in vivo by cisplatin, and iron chelators aswell as hydroxyl radical scavengers have been shown to be protective. Recent studies indicate that cytochrome P450 may also be an important source ofthe catalytic iron in cisplatin nephrotoxicity. Cyclosporine A has been shown to enhance generation of hydrogen peroxide in vitro and enhance lipid peroxidation in vitro and in vivo. Antioxidants have been shown to be protective in cyclosporine A nephrotoxicity. This collective body of evidence suggests an important role for reactive oxygen metabolites in toxic acute renal failure and may provide therapeutic opportunities of preventing or treating acute renal failure in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 13:07:44