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Titolo:
IS THE INCREASE IN RENAL PAPILLARY PHOSPHOLIPID BIOSYNTHESIS A PROTECTIVE MECHANISM AGAINST INJURY
Autore:
SETTONAVRUJ CP; FERNANDEZTOME MD; NEGRI A; SCERBO A; ARRIZURIETA E; STERINSPEZIALE NB;
Indirizzi:
UNIV BUENOS AIRES,FAC FARM & BIOQUIM,DEPT QUIM BIOL,JUNIN 956 RA-1113BUENOS AIRES DF ARGENTINA UNIV BUENOS AIRES,FAC FARM & BIOQUIM,DEPT QUIM BIOL RA-1113 BUENOS AIRES DF ARGENTINA UNIV BUENOS AIRES,FAC MED,INST INVEST MED BUENOS AIRES DF ARGENTINA
Titolo Testata:
Kidney & blood pressure research
fascicolo: 1, volume: 19, anno: 1996,
pagine: 38 - 45
SICI:
1420-4096(1996)19:1<38:ITIIRP>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE TUBULAR NECROSIS; CADMIUM-METALLOTHIONEIN; METABOLISM; MERCURY; NEPHROTOXICITY; REGENERATION; ACCUMULATION; KIDNEY; DEGRADATION; CHLORIDE;
Keywords:
MERCURIC CHLORIDE; ACUTE RENAL FAILURE; THYROXINE; RENAL PAPILLA; RENAL MEDULLA; RENAL CORTEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
26
Recensione:
Indirizzi per estratti:
Citazione:
C.P. Settonavruj et al., "IS THE INCREASE IN RENAL PAPILLARY PHOSPHOLIPID BIOSYNTHESIS A PROTECTIVE MECHANISM AGAINST INJURY", Kidney & blood pressure research, 19(1), 1996, pp. 38-45

Abstract

Mercuric chloride (HgCl2) is a well-known renal toxic that causes acute renal failure. The effect of HgCl2 treatment and the protection by thyroxine were studied in rat renal papilla (P), outer medullary innerstripe (OMIS), outer medullary outer stripe (OMOS) and cortical phospholipids (PhLs). HgCl2 brought about an increase in the total phospholipid content in P and OMIS but a drop in OMOS and cortex. Only phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) accounted for such changes. Thyroxine, injected on HgCl2-treated rats, partiallyreversed the effect of the toxic metal in P and OMIS while completelyreversed the PtdCho drop in OMOS and cortex. However, the hormone failed to recover the sphingomyelin increase in P, the PtdEtn shortage inOMIS, OMOS and partially reversed the drop in the cortex. When thyroxine was injected whithout toxic treatment, no effect was observed in the phospholipid content of any kidney zone. Results obtained by using P-32 as a precursor to study the PhL de novo synthesis were consistentwith those of the phospholipid content. Thus, a radioactivity increase-associated with PtdCho and PtdEtn-was observed in the kidney zones where said endogenous PhLs had risen. But in OMOS and cortex, where PtdCho and PtdEtn had dropped, they were also accompanied by a decrease in radioactivity. The thyroxine-induced recovery phase also paralleled the phospholipid content results with those of the de novo synthesis. We suggest that the decrease in the renal phospholipid de novo synthesis may constitute one biochemical explanation of the selective renal toxic effect exerted by HgCl2 and that the increase observed in the renal phospholipid metabolism-induced by the toxic treatment in OMIS and P-may represent a protective mechanism of these zones against toxic injury. Moreover, recovery promoted by thyroxine treatment in OMOS and cortex was accompanied by the reversion of the corresponding PtdCho decrease induced by HgCl2.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 05:55:20