Ascorbate as a substrate for glycolysis or gluconeogenesis: evidence for an interorgan ascorbate cycle.
Free Radic Biol Med
; 23(5): 804-8, 1997.
Article
en En
| MEDLINE
| ID: mdl-9296458
Ascorbate catabolism was investigated in murine and human cells unable to synthesize ascorbate due to the missing gulonolactone oxidase activity. In HepG2 cells the addition of ascorbate or dehydroascorbate resulted in high glucose production, while human erythrocytes, MCF7 cells and the cellular elements of the murine blood were able to metabolize ascorbate or dehydroascorbate to lactate. The oxidative agent menadione stimulated, while the transketolase inhibitor oxythiamine inhibited, the metabolism of dehydroascorbate in each of these three cell types. Our results suggest that ascorbate breakdown through the pentose phosphate pathway can reach the glycolytic/gluconeogenic route in different cells. In ascorbate synthesizing species the ascorbate-lactate route in peripheral cells may form a catabolic branch of an interorgan ascorbate cycle, where hepatocytes are responsible for ascorbate synthesis. The catabolic part of this cycle using exogenous ascorbate could be demonstrated even in humans cells.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Ácido Ascórbico
/
Glucólisis
Límite:
Animals
/
Humans
/
Male
Idioma:
En
Revista:
Free Radic Biol Med
Asunto de la revista:
BIOQUIMICA
/
MEDICINA
Año:
1997
Tipo del documento:
Article
País de afiliación:
Hungria
Pais de publicación:
Estados Unidos