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Titolo:
RENAL CORTICAL MITOCHONDRIAL ACONITASE IS REGULATED IN HYPOCITRATURIAAND HYPERCITRATURIA
Autore:
MELNICK JZ; PREISIG PA; MOE OW; SRERE P; ALPERN RJ;
Indirizzi:
NORTHWESTERN UNIV,SCH MED,DEPT PEDIAT,303 E CHICAGO AVE CHICAGO IL 60611 UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED DALLAS TX 00000 VET AFFAIRS MED CTR DALLAS TX 00000
Titolo Testata:
Kidney international
fascicolo: 1, volume: 54, anno: 1998,
pagine: 160 - 165
SICI:
0085-2538(1998)54:1<160:RCMAIR>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
BRUSH-BORDER MEMBRANE; URINARY CITRATE EXCRETION; METABOLIC-ACIDOSIS; COTRANSPORTER; DEPLETION; UROLITHIASIS; ADAPTATION; ANTIPORTER; TRANSPORT; RATS;
Keywords:
ACIDOSIS; ALKALOSIS; POTASSIUM DEFICIENCY; PROXIMAL TUBULE; NEPHROLITHIASIS; CITRATE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
J.Z. Melnick et al., "RENAL CORTICAL MITOCHONDRIAL ACONITASE IS REGULATED IN HYPOCITRATURIAAND HYPERCITRATURIA", Kidney international, 54(1), 1998, pp. 160-165

Abstract

Background.Chronic metabolic acidosis and K+ deficiency increase, while alkali feeding decreases proximal tubule citrate absorption and metabolism. The present studies examined the regulation of mitochondrial aconitase (m-aconitase), the first step in mitochondrial citrate metabolism, in these conditions. Methods. Rats were fed appropriate diets, and m-aconitase activity and protein abundance measured. Results. In chronic metabolic acidosis and chronic K+ deficiency. renal cortical m-aconitase activity was increased 17% and 43%, respectively. This was associated with respective 90% and 221% increases in renal cortical m-aconitase protein abundance. With chronic alkali feeding, there was a 12% decrease in renal cortical m-aconitase activity, associated with a 35% decrease in m-aconitase protein abundance. Hepatic m-aconitase activity was not regulated in a similar manner. There was no regulation of citrate: synthase, the enzyme responsible for mitochondrial citrate synthesis. Conclusion. These studies demonstrate tissue specific chronic regulation of renal cortical m-aconitase activity and protein abundance, which likely contributes to the hypocitraturia and hypercitraturia seen in these conditions. As m-aconitase is the only step in citrate transport and metabolism found to be regulated in alkali feeding, its regulation likely plays a significant role in mediating the hypercitraturia seen in this condition.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 13:41:07