Familial aggregation of LDL oxidation

被引:10
作者
Kujala, UM
Ahotupa, M
Vasankari, TJ
Kaprio, J
Tikkanen, MJ
机构
[1] UNIV TURKU,DEPT PHYSIOL,MCA,RES LAB,TURKU,FINLAND
[2] UNIV HELSINKI,DEPT PUBL HLTH,HELSINKI,FINLAND
[3] UNIV HELSINKI,DEPT MED,DIV CARDIOL,HELSINKI,FINLAND
关键词
families; heredity; LDL oxidation; twins;
D O I
10.1080/00365519709056382
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The ''oxidation hypothesis'' states that oxidative modification of low-density lipoprotein (LDL) is important in the pathogenesis of the atherosclerotic lesion. We studied 15 families (fathers, mothers and male twins of 16 to 18 years of age) to investigate the familial aggregation of LDL oxidation. As an indicator of LDL oxidation products we measured baseline levels of conjugated dienes extracted from LDL (LDL-BDC). For this analysis LDL was first isolated by rapid precipitation with buffered heparin. LDL-BDC was highest in fathers (mean 673 Delta Abs per mg LDL cholesterol, 95% confidence interval (CI) 547-800) followed by mothers (500, 95% CI 408-592) and twins (383, 95% CI 337-430). There was a high correlation in the LDL-BDC between the identical twins (r = 0.81, 95% CI 0.44-0.95), but no correlation between the parents (r = -0.36). The LDL-BDC of boys correlated positively with that of fathers (r = 0.49, 95% CI 0.16-0.72), but not with that of mothers (r = 0.00). Highly significant positive correlations were observed between LDL-BDC and serum lipid risk factors among parents, but among twins the correlations were usually weaker. Our study suggests that inherited factors contribute to interindividual variability in the oxidative modification of LDL.
引用
收藏
页码:141 / 146
页数:6
相关论文
共 14 条
[1]   Simple methods of quantifying oxidation products and antioxidant potential of low density lipoproteins [J].
Ahotupa, M ;
Ruutu, M ;
Mantyla, E .
CLINICAL BIOCHEMISTRY, 1996, 29 (02) :139-144
[2]  
GIDEZ LI, 1982, J LIPID RES, V23, P1206
[3]  
HODIS HN, 1994, J LIPID RES, V35, P669
[4]   MODIFICATION OF HUMAN-SERUM LOW-DENSITY-LIPOPROTEIN BY OXIDATION - CHARACTERIZATION AND PATHOPHYSIOLOGICAL IMPLICATIONS [J].
JURGENS, G ;
HOFF, HF ;
CHISOLM, GM ;
ESTERBAUER, H .
CHEMISTRY AND PHYSICS OF LIPIDS, 1987, 45 (2-4) :315-336
[5]  
KLEINVELD HA, 1992, CLIN CHEM, V38, P2066
[6]  
Roos E., 1995, Scandinavian Journal of Nutrition/Naringsforskning, V39, P55
[7]   ESTROGEN AND INHIBITION OF OXIDATION OF LOW-DENSITY LIPOPROTEINS IN POSTMENOPAUSAL WOMEN [J].
SACK, MN ;
RADER, DJ ;
CANNON, RO .
LANCET, 1994, 343 (8892) :269-270
[8]   AUTOANTIBODY AGAINST OXIDIZED LDL AND PROGRESSION OF CAROTID ATHEROSCLEROSIS [J].
SALONEN, JT ;
YLAHERTTUALA, S ;
YAMAMOTO, R ;
BUTLER, S ;
KORPELA, H ;
SALONEN, R ;
NYYSSONEN, K ;
PALINSKI, W ;
WITZTUM, JL .
LANCET, 1992, 339 (8798) :883-887
[9]   INITIATION OF ATHEROSCLEROTIC LESIONS IN CHOLESTEROL-FED RABBITS .2. SELECTIVE RETENTION OF LDL VS SELECTIVE INCREASES IN LDL PERMEABILITY IN SUSCEPTIBLE SITES OF ARTERIES [J].
SCHWENKE, DC ;
CAREW, TE .
ARTERIOSCLEROSIS, 1989, 9 (06) :908-918
[10]  
SING CF, 1987, MOL APPROACHES HUMAN, P99