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Titolo:
Susceptibility of MT-null mice to chronic CdCl2-induced ephrotoxicity indicates that renal injury is not mediated by the CdMT complex
Autore:
Liu, J; Liu, YP; Habeebu, SS; Klaassen, CD;
Indirizzi:
Univcupatas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Ctr Environm & Oc Univ Kansas Kansas City KS USA 66160 xicol & Therapeut, Ctr Environm & Oc
Titolo Testata:
TOXICOLOGICAL SCIENCES
fascicolo: 1, volume: 46, anno: 1998,
pagine: 197 - 203
SICI:
1096-6080(199811)46:1<197:SOMMTC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
CADMIUM-METALLOTHIONEIN; EXPOSED RATS; CHLORIDE; CELLS; NEPHROTOXICITY; NEPHROPATHY; TOXICITY; MOUSE; HEPATOTOXICITY; LETHALITY;
Keywords:
cadmium chloride; chronic exposure; nephrotoxicity; proteinuria; glucosuria; enzymuria; blood urea nitrogen; histopathology; metallothionein; CdMT complex; MT-null mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Klaassen, CD Univcupatas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, CtrEnvironm & Oc Univ Kansas Kansas City KS USA 66160 peut, Ctr Environm & Oc
Citazione:
J. Liu et al., "Susceptibility of MT-null mice to chronic CdCl2-induced ephrotoxicity indicates that renal injury is not mediated by the CdMT complex", TOXICOL SCI, 46(1), 1998, pp. 197-203

Abstract

Chronic human exposure to Cd results in kidney injury. It has been proposed that nephrotoxicity produced by chronic Cd exposure is via the Cd-metallothionein complex (CdMT) and not by inorganic forms of Cd. If this hypothesis is correct, then MT-null mice, which cannot form CdMT, should not developnephrotoxicity. Control and MT-null mice were injected sc with a wide range of CdCl2 doses, six times/week for up to 10 weeks, and their renal Cd burden, renal MT concentration, and nephrotoxicity were quantified. In controlmice, renal Cd burden increased in a dose- and time-dependent manner, reaching as high as 140 mu g Cd/g kidney, along with 150-fold increases in renal MT concentrations, reaching 800 mu g MT/g kidney. In MT-null mice, renal Cd concentration (10 mu g/g) was much lower, and renal MT was nonexistent. The maximum tolerated dose of Cd in MT-null mice was approximately one-eighth that of controls. MT-null mice were more susceptible than controls to Cd-induced renal injury, as evidenced by increased urinary excretion of protein, glucose, gamma-glutamyltransferase, and N-acetyl-beta-D-glucosaminidase, as well as by increased blood urea nitrogen levels. Kidneys of Cd-treatedmice were enlarged and histopathology showed various types of lesions, including proximal tubular degeneration, apoptosis, atrophy, interstitial inflammation, and glomerular swelling. These lesions were more severe in MT-null than in control mice, mirroring the biochemical analyses. These data indicate that Cd-induced renal injury is not necessarily mediated through the CdMT complex and that MT is an important intracellular protein in protectingagainst chronic Cd nephrotoxicity. (C) 1998 Society of Toxicology.

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Documento generato il 02/12/20 alle ore 15:20:18