Plasma levels of lipid and cholesterol oxidation products and cytokines in diabetes mellitus and cigarette smoking: Effects of vitamin E treatment

被引:108
作者
Mol, MJTM
deRijke, YB
Demacker, PNM
Stalenhoef, AFH
机构
[1] Department of Medicine, Div. of General Internal Medicine, University Hospital Nijmegen, 6500 HB Nijmegen
关键词
atherosclerosis; diabetes mellitus; smoking; LDL oxidation; antioxidants; cytokines; vitamin E;
D O I
10.1016/S0021-9150(96)06022-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To evaluate the role of both oxidation and inflammation in atherosclerosis, we compared LDL oxidizability, in vivo lipid and cholesterol oxidation, and basal and lipopolysaccharide (LPS)-stimulated production of various cytokines in normolipidemic patients with diabetes mellitus (DM; n = 11), cigarettes smokers (n = 12) and controls (n = 14). In addition, the effects of vitamin E (600 I.U./day for 4 weeks) on these parameters were evaluated. Initial LDL oxidation characteristics before and after vitamin E were identical in the 3 groups. Plasma thiobarbituric acid reactive substances were higher in DM and smokers versus controls (0.77 +/- 0.22, 0.74 +/- 0.14 versus 0.62 +/- 0.10 mu mol malondialdehyde equivalents/l, respectively; P versus controls < 0.05) and normalized after vitamin E supplementation. Total plasma oxysterols were higher in smokers versus controls (354 +/- 104 versus 265 +/- 66 nmol/l, P < 0.05) and unaffected by vitamin E. The basal and LPS-stimulated levels of interleukin-1 beta and tumour necrosis factor alpha (TNF alpha) and the basal level of interleukin-1-receptor antagonist (IL-1RA) were identical for the 3 groups. LPS-stimulated IL-1RA was higher in DM versus controls (10.7 +/- 2.0 versus 8.1 +/- 1.7 pmol/l, P < 0.05). After vitamin E, TNF alpha dropped in controls and smokers, and IL-1RA in smokers only. Results suggest increased in vivo oxidative stress and inflammation in DM and smoking, which is partly overcome by vitamin E. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:169 / 176
页数:8
相关论文
共 67 条
[11]   CONTINUOUS MONITORING OF INVITRO OXIDATION OF HUMAN LOW-DENSITY LIPOPROTEIN [J].
ESTERBAUER, H ;
STRIEGL, G ;
PUHL, H ;
ROTHENEDER, M .
FREE RADICAL RESEARCH COMMUNICATIONS, 1989, 6 (01) :67-75
[12]  
FONG LG, 1991, J LIPID RES, V32, P1899
[13]   EFFECT OF VITAMIN-E ON ATHEROGENESIS IN LDL RECEPTOR-DEFICIENT RABBITS [J].
FRUEBIS, J ;
CAREW, TE ;
PALINSKI, W .
ATHEROSCLEROSIS, 1995, 117 (02) :217-224
[14]   A COMPARISON OF THE ANTIATHEROGENIC EFFECTS OF PROBUCOL AND OF A STRUCTURAL ANALOG OF PROBUCOL IN LOW-DENSITY-LIPOPROTEIN RECEPTOR-DEFICIENT RABBITS [J].
FRUEBIS, J ;
STEINBERG, D ;
DRESEL, HA ;
CAREW, TE .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (01) :392-398
[15]   ENHANCED SERUM LEVELS OF THIOBARBITURIC ACID-REACTIVE SUBSTANCES IN DIABETES-MELLITUS [J].
GRIESMACHER, A ;
KINDHAUSER, M ;
ANDERT, SE ;
SCHREINER, W ;
TOMA, C ;
KNOEBL, P ;
PIETSCHMANN, P ;
PRAGER, R ;
SCHNACK, C ;
SCHERNTHANER, G ;
MUELLER, MM .
AMERICAN JOURNAL OF MEDICINE, 1995, 98 (05) :469-475
[16]  
GUGLIUCCI A, 1994, BIOCHEM MOL BIOL INT, V32, P139
[17]   MALONDIALDEHYDE-ALTERED PROTEIN OCCURS IN ATHEROMA OF WATANABE HERITABLE HYPERLIPIDEMIC RABBITS [J].
HABERLAND, ME ;
FONG, D ;
CHENG, L .
SCIENCE, 1988, 241 (4862) :215-218
[18]  
HAMILTON TA, 1990, J IMMUNOL, V144, P2343
[19]   IMMUNE-MECHANISMS IN ATHEROSCLEROSIS [J].
HANSSON, GK ;
JONASSON, L ;
SEIFERT, PS ;
STEMME, S .
ARTERIOSCLEROSIS, 1989, 9 (05) :567-578
[20]   EFFECT OF VITAMIN-C AND VITAMIN-E SUPPLEMENTATION ON SUSCEPTIBILITY OF PLASMA-LIPOPROTEINS TO PEROXIDATION INDUCED BY ACUTE SMOKING [J].
HARATS, D ;
BENNAIM, M ;
DABACH, Y ;
HOLLANDER, G ;
HAVIVI, E ;
STEIN, O ;
STEIN, Y .
ATHEROSCLEROSIS, 1990, 85 (01) :47-54