LIPID-PEROXIDATION PRODUCTS AND ANTIOXIDANT ENZYMES IN RED-BLOOD-CELLS DURING NORMAL AND DIABETIC PREGNANCY

被引:52
作者
CARONE, D
LOVERRO, G
GRECO, P
CAPUANO, F
SELVAGGI, L
机构
[1] UNIV BARI, POLICLIN, FAC MED, INST MED BIOCHEM & CHEM, I-70124 BARI, ITALY
[2] UNIV BARI, POLICLIN, FAC MED, INST OBSTET & GYNECOL 1, I-70124 BARI, ITALY
关键词
LIPOPEROXIDATION; ANTIOXIDANT ENZYMES; PREGNANCY; DIABETIC PREGNANCY;
D O I
10.1016/0028-2243(93)90021-4
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Oxygen free radicals produced during normal aerobic metabolism have been implicated in several pathophysiological mammalian processes. The importance of free radical-mediated fatty acid oxidation has received much attention. The generation of active oxygen species may lead to lipid peroxidation and formation of reactive products, which may be involved in severe damage of cell molecules and structures. Free radical metabolism in pregnancy and in diabetes mellitus is still unclear. To add new insights to the question, changes in lipid peroxidation products and activities of three antioxidant enzymes: catalase (CAT), glutathione peroxidase (GPX) and superoxide dismutase (SOD) in maternal red blood cells haemolysates were evaluated in pregnant women with insulin-dependent diabetes mellitus (IDDM-PW) and in healthy pregnant women (HPW). Healthy non-pregnant women were the control group for IDDM-PW and HPW, respectively. Pregnancy provoked an increase of lipoperoxidation products and an high SOD activity since early pregnancy, while CAT and GPX activities did not change during gestation. IDDM-PW showed higher content of lipoperoxidation breakdown products and lower SOD activity at each trimester, if compared with HPW; moreover, a slight increase of CAT and SOD acvitity is reported during late diabetic pregnancy. IDDM-PW were in very good metabolic control at time of sampling. The variations reported suggest an easier membrane lipoperoxidability and, consequently, an easier membrane damage during diabetic gestation.
引用
收藏
页码:103 / 109
页数:7
相关论文
共 24 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   LIPID-PEROXIDATION SYSTEM IN HUMAN PLACENTAL TISSUE - GENERAL-PROPERTIES AND THE INFLUENCE OF GESTATIONAL-AGE [J].
DIAMANT, S ;
KISSILEVITZ, R ;
DIAMANT, Y .
BIOLOGY OF REPRODUCTION, 1980, 23 (04) :776-781
[3]  
DULIN WE, 1983, DIABETES MELLITUS TH, P361
[4]   MICROSOMAL LIPID PEROXIDATION IN HUMAN PREGNANT UTERUS AND PLACENTA [J].
FALKAY, G ;
HERCZEG, J ;
SAS, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1977, 79 (03) :843-851
[5]   CUZN SUPEROXIDE-DISMUTASE, MN SUPEROXIDE-DISMUTASE, CATALASE AND GLUTATHIONE-PEROXIDASE IN LYMPHOCYTES AND ERYTHROCYTES IN INSULIN-DEPENDENT DIABETIC CHILDREN [J].
HAGGLOF, B ;
MARKLUND, SL ;
HOLMGREN, G .
ACTA ENDOCRINOLOGICA, 1983, 102 (02) :235-239
[6]   LIPOPEROXIDES IN THROMBOSIS AND ATHEROSCLEROSIS - PROCEEDINGS, 5TH WORKSHOP OF THE EUROPEAN-THROMBOSIS-RESEARCH-ORGANIZATION (ETRO), SUBCOMMITTEE ON LIPIDS, PROSTANOIDS AND THROMBOSIS, BAD-ISCHL, AUSTRIA, SEPTEMBER 15-16TH 1986 [J].
HORNSTRA, G ;
PARNHAM, MJ .
AGENTS AND ACTIONS, 1987, 22 (3-4) :330-332
[7]   LIPID-PEROXIDATION IN PREGNANCY - NEW PERSPECTIVES ON PREECLAMPSIA [J].
HUBEL, CA ;
ROBERTS, JM ;
TAYLOR, RN ;
MUSCI, TJ ;
ROGERS, GM ;
MCLAUGHLIN, MK .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1989, 161 (04) :1025-1034
[8]  
KAGAN VE, 1988, LIPID PEROXIDATION B, V13, P146
[9]  
Kappus H., 1985, OXIDATIVE STRESS, P273, DOI [10.1016/b978-0-12-642760-8.50016-8, DOI 10.1016/B978-0-12-642760-8.50016-8]
[10]   THE RELATIONSHIP BETWEEN PLASMA TRIGLYCERIDES, CHOLESTEROL, TOTAL LIPIDS AND LIPID-PEROXIDATION PRODUCTS DURING HUMAN ATHEROSCLEROSIS [J].
LEDWOZYW, A ;
MICHALAK, J ;
STEPIEN, A ;
KADZIOLKA, A .
CLINICA CHIMICA ACTA, 1986, 155 (03) :275-283