Estradiol enhances the resistance of LDL to oxidation by stabilizing apoB-100 conformation.
Biochemistry
; 39(45): 13897-903, 2000 Nov 14.
Article
en En
| MEDLINE
| ID: mdl-11076531
Among different proposed mechanisms to account for the protection exerted by estrogens against cardiovascular diseases, the antioxidant effect has attracted considerable attention. We confirmed that 17-beta-estradiol (E2), when added to human LDL at a 6:1 ratio to apoB-100, markedly delays the phase of massive LDL lipid peroxidation induced by Cu(2+). We also observed an increased oxidative resistance of E2-treated LDL by monitoring the early phase of oxidative degradation on the basis of increased LDL surface polarity by the generalized polarization of the lipophilic fluorescent probe 2-(dimethylamino)-6-lauroylnaphthalene (Laurdan). A scavenging of free radicals by E2 is ruled out since, consistent with its structure, its rate constant for the reduction of peroxy radicals is extremely low, i.e., 0.02% of that of vitamin E. Tryptophan fluorescence lifetime and circular dichroism measurements revealed that (i) apoB-100 undergoes a conformational modification and a progressive loss of secondary structure during lipid peroxidation; (ii) E2 increases apoB-100 secondary structure and modifies its conformation; and (iii) the apoB-100 conformational change induced by E2 makes this protein resistant to modifications brought about by lipid peroxidation. We propose that E2, by affecting apoB-100 secondary structure and conformation, modifies the interaction of this protein with the outer layer of the LDL particle thus increasing its overall oxidative resistance.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Apolipoproteínas B
/
Peroxidación de Lípido
/
Estradiol
/
Lipoproteínas LDL
/
2-Naftilamina
Límite:
Humans
Idioma:
En
Revista:
Biochemistry
Año:
2000
Tipo del documento:
Article
País de afiliación:
Italia
Pais de publicación:
Estados Unidos