Soy isoflavones reduce electronegative low-density lipoprotein (LDL(-)) and anti-LDL (-) autoantibodies in experimental atherosclerosis.

BACKGROUND: Isoflavones present in soybean may contribute to soy atheroprotective effects. AIM OF THE STUDY: To investigate the effect of soy isoflavones supplementation on the formation of electronegative LDL (LDL(-)) and its autoantibodies in blood plasma and aortic atheromas of rabbits fed an atherogenic casein-based diet enriched with isoflavones. METHODS: New Zealand male rabbits (n = 15) were fed an atherogenic diet (27% casein) supplemented with isoflavones (0.73 or 7.3 mg of isoflavones/kg/day, Low and High Iso groups, respectively) for 180 days. Monthly, blood samples were collected after 12-15 h fasting and at 180 days of treatment all animals were sacrificed. Isoflavones were analyzed in plasma and urine samples by HPLC. LDL(-) in plasma and atheromas was detected by ELISA and immunohistochemistry, respectively, with a monoclonal antibody reactive to LDL(-). Autoantibodies reactive to LDL(-) were analyzed in plasma and aorta by ELISA. RESULTS: Low and High Iso groups had decreased LDL-cholesterol, increased HDL-cholesterol and lower levels of LDL(-) in blood plasma and aortic atherosclerotic lesions than the non-supplemented Control group. IgG autoantibodies reactive to LDL(- )were higher in plasma of the Control group in comparison with the High and Low Iso groups. In contrast, the aortas from animals that consumed isoflavones showed higher levels of IgG reactive to LDL(- )than the Control group. CONCLUSION: Soy isoflavones showed hypolipidemic effects and decreased the pro-inflammatory LDL(-) subfraction in blood plasma and aorta of hypercholesterolemic rabbits.

Minimally modified electronegative LDL and its autoantibodies in acute and chronic coronary syndromes.

OBJECTIVES: To determine the minimally modified electronegative LDL (LDL-) and its autoantibodies in coronary syndromes. DESIGN AND METHODS: LDL(-) and its autoantibodies were determined by ELISA in patients with acute (ACS, unstable angina; AMI, acute myocardial infarction) and chronic coronary syndromes (stable angina, SA) and compared to subjects without coronary disease (controls). Results are expressed as median of LDL- (microg/mL) and anti-LDL(-) IgG (OD405 nm). RESULTS: The concentrations of LDL(-) were higher in patients with coronary disease (ACS: 40.7 microg/mL; SA: 35.0 microg/mL) as compared to controls (21.6 microg/mL). The highest LDL- concentrations were found in patients with AMI (41.8 microg/mL). Anti-LDL(-) IgG was elevated in ACS (1.143) in relation to CCS (0.527) and controls (0.467). A positive correlation was observed between anti-LDL- IgG and CRP levels (r = 0.34, p <0.01) in the studied groups. CONCLUSIONS: LDL(-) and anti-LDL(-) autoantibodies may be useful markers to follow patients with high risk for coronary events.

Detection of electronegative low density lipoprotein (LDL-) in plasma and atherosclerotic lesions by monoclonal antibody-based immunoassays.

OBJECTIVES: To produce a monoclonal antibody (MAb) against electronegative LDL (LDL-) for detecting this modified lipoprotein in blood plasma and tissues. DESIGN AND METHODS: LDL- was isolated from human blood plasma and used as an antigen for immunization of Balb/c mice. Lymphocytes of immunized mice were fused with myeloma cells (SP2/0) to obtain the hybridomas. LDL- was detected in blood plasma and atherosclerotic lesions of humans and rabbits by MAb-based ELISA and immunohistochemistry, respectively. RESULTS: LDL- concentrations were higher (P < 0.05) in the blood plasma of hypercholesterolemic subjects (HC, 248 +/- 77 mg/dL of total cholesterol) than in normolipidemic subjects (NL, 173 +/- 82 mg/dL of total cholesterol) and rabbits (HC, 250 +/- 15 mg/dL of cholesterol versus NL, 81 +/- 12 mg/dL of cholesterol). Moreover, LDL- was detected in the atherosclerotic lesions of humans and rabbits. CONCLUSION: These MAb-based immunoassays are adequate to detect LDL- in biological samples and represent an important tool for investigating the role of LDL- in atherosclerosis.