Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

被引:53
作者
Abdilla, N.
Tormo, M. C.
Fabia, M. J.
Chaves, F. J.
Saez, G.
Redon, J.
机构
[1] Univ Valencia, Hosp Clin, Hypertens Clin, Valencia 46010, Spain
[2] Univ Valencia, Sch Med, Dept Biochem & Mol Biol, Valencia, Spain
[3] Univ Valencia, Fdn Hosp Clin, Res Unit, Valencia, Spain
关键词
essential hypertension; oxidative stress; metabolic syndrome; antioxidant mechanisms;
D O I
10.1038/sj.jhh.1002105
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
The objective of the present study was to analyze the impact of metabolic syndrome ( MS) and its individual components on oxidative stress ( OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehide, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase ( SOD) and catalase ( CAT) was measured in plasma and glutathione peroxidase 1 in hemolysad erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.
引用
收藏
页码:68 / 75
页数:8
相关论文
共 31 条
[21]   SUSCEPTIBILITY OF GLUTATHIONE-PEROXIDASE TO PROTEOLYSIS AFTER OXIDATIVE ALTERATION BY PEROXIDES AND HYDROXYL RADICALS [J].
PIGEOLET, E ;
REMACLE, J .
FREE RADICAL BIOLOGY AND MEDICINE, 1991, 11 (02) :191-195
[22]   Nitric oxide in hypertension: Relationship with renal injury and left ventricular hypertrophy [J].
Raij, L .
HYPERTENSION, 1998, 31 (01) :189-193
[23]   Antioxidant activities and oxidative stress byproducts in human hypertension [J].
Redón, J ;
Oliva, MR ;
Tormos, C ;
Giner, V ;
Chaves, J ;
Iradi, A ;
Sáez, GT .
HYPERTENSION, 2003, 41 (05) :1096-1101
[24]   Role of angiotensin and oxidative stress in essential hypertension [J].
Romero, JC ;
Reckelhoff, JF .
HYPERTENSION, 1999, 34 (04) :943-949
[25]   Factors related to the impact of anti hypertensive treatment in antioxidant activities and oxidative stress by-products in human hypertension [J].
Sáez, GT ;
Tormos, C ;
Giner, V ;
Chaves, A ;
Lozano, OV ;
Iradi, A ;
Redón, L .
AMERICAN JOURNAL OF HYPERTENSION, 2004, 17 (09) :809-816
[26]  
SALO DC, 1990, J BIOL CHEM, V265, P11919
[27]   Byproducts of oxidative protein damage and antioxidant enzyme activities in plasma of patients with different degrees of essential hypertension [J].
Simic, DV ;
Mimic-Oka, J ;
Pljesa-Ercegovac, M ;
Savic-Radojevic, A ;
Opacic, M ;
Matic, D ;
Ivanovic, B ;
Simic, T .
JOURNAL OF HUMAN HYPERTENSION, 2006, 20 (02) :149-155
[28]   Oxidative stress and renal dysfunction in salt-sensitive hypertension [J].
Trolliet, MR ;
Rudd, MA ;
Loscalzo, J .
KIDNEY & BLOOD PRESSURE RESEARCH, 2001, 24 (02) :116-123
[29]  
WONG SHY, 1987, CLIN CHEM, V33, P214
[30]   Increased methylglyoxal and oxidative stress in hypertensive rat vascular smooth muscle cells [J].
Wu, LY ;
Juurlink, BHJ .
HYPERTENSION, 2002, 39 (03) :809-814