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Titolo:
Aristolochic acid impedes endocytosis and induces DNA adducts in proximal tubule cells
Autore:
Lebeau, C; Arlt, VM; Schmeiser, HH; Boom, A; Verroust, PJ; Devuyst, O;
Indirizzi:
Free Univ Brussels, Sch Med, Dept Pathophysiol, B-1070 Brussels, Belgium Free Univ Brussels Brussels Belgium B-1070 iol, B-1070 Brussels, Belgium Inst Canc Res, Sect Mol Carcinogenesis, Sutton, Surrey, England Inst Canc Res Sutton Surrey England cinogenesis, Sutton, Surrey, England CHU St Antoine, INSERM, U538, Paris, France CHU St Antoine Paris FranceCHU St Antoine, INSERM, U538, Paris, France German Canc Res Ctr, Div Mol Toxicol, D-6900 Heidelberg, Germany German Canc Res Ctr Heidelberg Germany D-6900 D-6900 Heidelberg, Germany Univ Catholique Louvain, Sch Med, Div Nephrol, B-1200 Brussels, Belgium Univ Catholique Louvain Brussels Belgium B-1200 B-1200 Brussels, Belgium
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 4, volume: 60, anno: 2001,
pagine: 1332 - 1342
SICI:
0085-2538(200110)60:4<1332:AAIEAI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHINESE HERBS NEPHROPATHY; INTERSTITIAL RENAL FIBROSIS; OPOSSUM KIDNEY; ORGANIC ANION; ALBUMIN REABSORPTION; EPITHELIAL-CELLS; LINE; TRANSPORT; OK; IDENTIFICATION;
Keywords:
cadmium chloride; Chinese herbs nephropathy; megalin; low molecular weight protein excretion; nephrotoxicity; proteinuria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Lebeau, C Free Univ Brussels, Sch Med, Dept Pathophysiol, Campus Erasme,Bldg E2 RoomE2-4-114,808 Route Len, B-1070 Brussels, Belgium Free Univ Brussels Campus Erasme,Bldg E2 Room E2-4-114,808 Route Len Brussels Belgium B-1070
Citazione:
C. Lebeau et al., "Aristolochic acid impedes endocytosis and induces DNA adducts in proximal tubule cells", KIDNEY INT, 60(4), 2001, pp. 1332-1342

Abstract

Background. Aristolochic acid (AA), present in Aristolochia plants, appears to be the toxin responsible for Chinese herbs nephropathy (CHN), a rapidly progressive tubulointerstitial nephritis. One of the earliest sign of CHNis the urinary excretion of low-molecular-weight proteins (LMWP), suggesting that AA is toxic to proximal tubules (PT). Methods. The effects of AA on PT functions including reabsorption of LMWP were investigated on the well-established opossum kidney (OK) cell line, a model for PT. and compared with those of the classical PT toxin cadmium chloride (CdCl2). Results. OK cell monolayers internalized albumin and beta2-microglobulin by receptor-mediated endocytosis, both proteins apparently competing for thesame receptor, a complex of megalin and cubulin. The process was significantly impaired by 24-hour preincubation with AA (10 or 20 mu mol/L) or CdCl2(15 mu mol/L). Furthermore, 24-hour exposure to AA followed by its removalduring one to six days led to a persistent inhibition of the uptake of albumin, in contrast to the substantial recovery observed after CdCl2 removal. Neither AA nor CdCl2 affected cell viability, Na+-glucose cotransport or total rate of protein synthesis. A A significantly decreased megalin expression and formed specific DNA adducts in OK cells, similar to those found in kidneys from CHN patients. Conclusions. The present data support the involvement of AA in the early PT dysfunction found in CHN; furthermore, they suggest a causal relationshipbetween DNA adduct formation. decreased megalin expression, and inhibitionof receptor-mediated endocytosis of LMWP.

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Documento generato il 04/07/20 alle ore 05:16:22