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Cardiovascular Research 2000 47(3):567-573; doi:10.1016/S0008-6363(00)00121-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Effect of vitamin E supplementation on antibody levels against malondialdehyde modified LDL in hyperlipidemic hamsters

Fernando G. de Oliveiraa, Cláudio L. Rossia, Marcelo G. de Oliveirab,*, Mário J.A. Saada and Lìcio A. Vellosoa

aFaculdade de Ciências Médicas, UNICAMP, Caixa Postal 6154, CEP 13083-970, Campinas, São Paulo, Brazil
bInstituto de Quìmica, UNICAMP, Caixa Postal 6154, CEP 13083-970, Campinas, São Paulo, Brazil

* Corresponding author mgo{at}iqm.unicamp.br

Objective: The aim of this work was to investigate the effect of vitamin E (VE) supplementation on the formation of autoantibodies against oxidized low density lipoproteins (LDL) in a hyperlipidemic animal model. Methods: Thirty-four male hamsters (Mesocricetus auratus), (4 weeks old) were divided into three groups: Group A (n=9) was fed with standard rodent chow; group B (n=13) was fed with a standard rodent chow plus 2% cholesterol and 10% butter and group C (n=12) was fed with the same diet plus 0.2% (w/w) VE. Blood samples were collected by intracardiac puncture and antibody levels were determined in each animal at 4 weeks of age and after 20 weeks of experimental diet. A modified ELISA technique was used to analyze the modulation of autoantibody titers against an epitope of oxidized LDL in serum samples. Antigens prepared for the ELISA tests were characterized using spectrofluorimetry. Serum VE levels were determined in the lipidic fractions by HPLC. Results: The groups fed with cholesterol-fat enriched diet presented a three-fold increase in total serum cholesterol and two-fold increase in serum triglycerides compared to the control group. VE supplementation played no role in serum cholesterol and serum triglyceride concentrations but led to a decreased autoantibody (anti-LDL–malondialdehyde) formation (P<0.05). Conclusions: Our results show that VE supplementation leads to a lower production of autoantibodies against oxidized LDL, suggesting a protective effect of VE against in vivo oxidation of LDL particles, in a dose-dependent manner.

KEYWORDS Atherosclerosis; Lipoproteins; Cholesterol; Free radicals


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