Bilirubin is highly effective in preventing in vivo delta-aminolevulinic acid-induced oxidative cell damage.
Biochim Biophys Acta
; 1638(2): 173-8, 2003 Jul 14.
Article
en En
| MEDLINE
| ID: mdl-12853123
Delta-aminolevulinic acid (ALA), precursor of heme, accumulates in a number of organs, particularly in liver of patients with acute porphyrias or lead intoxication. This study characterizes the involvement of bilirubin as an antioxidant in a chronic intoxication with ALA. Female Wistar rats were injected intraperitoneally a daily dose of 40 mg ALA/body wt., during 10 days. A marked increase in lipid peroxidation and a decrease in GSH content were observed 24 h after the last injection of ALA. The activities of liver antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase were also diminished. ALA synthase (ALA-S) and heme oxygenase-1 were induced. Both ALA dehydratase (ALA-D) and porphobilinogenase (PBG-ase) activities were inhibited. Administration of bilirubin (5 mmol/kg body wt.) 2 h before ALA treatment entirely prevented the effects of ALA. Co-administration of ALA and Sn-protoporphyrin IX (Sn-PPIX; 100 microg/body wt., i.p.), a potent inhibitor of heme oxygenase, completely abolished its induction and provoked a marked decrease in liver GSH levels as well as an increase in lipid peroxidation. These results add further support to the proposal assigning bilirubin a key protective role against oxidative damage here induced by ALA.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Bilirrubina
/
Estrés Oxidativo
/
Ácido Aminolevulínico
/
Hígado
/
Antioxidantes
Límite:
Animals
Idioma:
En
Revista:
Biochim Biophys Acta
Año:
2003
Tipo del documento:
Article
País de afiliación:
Argentina
Pais de publicación:
Países Bajos