Roles of paraoxonase and oxidative stress in adolescents with uraemic, essential or obesity-induced hypertension

被引:25
作者
Barath, Akos [1 ]
Nemeth, Ilona [1 ]
Karg, Eszter [1 ]
Endreffy, Emoke [1 ]
Bereczki, Csaba [1 ]
Gellen, Balazs [1 ]
Haszon, Ibolya [1 ]
Turi, Sandor [1 ]
机构
[1] Univ Szeged, Albert Szent Gyorgyi Med & Pharmaceut Ctr, Dept Paediat, H-6721 Szeged, Hungary
关键词
essential hypertension; haemodialysis; oxidative stress; paraoxonase; adolescents;
D O I
10.1159/000095124
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Background/Aims: Paraoxonase 1 (PON1) is associated with high-density lipoproteins in the plasma, and is capable of hydrolysing oxidized lipids and preventing the oxidation of low-density lipoproteins. Oxidative stress and the POW (activity and Q192R polymorphism) were analysed in adolescent patients with essential (n = 49) or obesity-induced hypertension (n = 79), uraemic patients (n = 20), and also in obese normotensive patients (n = 60) and age-matched controls (n = 57). Methods: The POW activity was measured via paraoxon hydrolysis. The POW genotype was determined by real-time PCR. The levels of oxidized and reduced glutathione, the end-products of nitric oxide, cysteine, homocysteine and lipid peroxidation in the plasma were measured and related to the POW status. Results: There were no significant differences between the patient groups and the control group in the genotype distributions and the allele frequencies of the Q192R polymorphism. The PON activity was significantly lower (p < 0.001) in the uraemic hypertensive group than in the controls. The MDA concentration was significantly higher in the uraemic hypertensive (p < 0.001) and obese hypertensive (p < 0.05) patients. The plasma NOx concentrations were significantly lower (p < 0.001) and the ratio MDA/NO, were significantly higher in all four patient groups. The GSH levels were significantly lower in the patients with hypertension (p < 0.001) and obesity-induced hypertension (p < 0.05) than in the controls, while the GSSG level (p < 0.01) and the ratio GSSG/GSH (p < 0.05) was significantly higher in the uraemic hypertensive group. The plasma homocysteine level was significantly higher (p < 0.001) in the uraemic hypertensive patients as compared with the controls. Conclusions:We found no significant correlation between the biochemical parameters and neither genotypes nor enzyme activities. The POW status and the levels of certain biochemical parameters are independently associated with the hypertension in hypertensive and obese hypertensive patients, and the elevated levels of lipid peroxides and plasma homocysteine may contribute to the increased risk of cardiovascular complications in patients on haemodialysis. Copyright (c) 2006 S. Karger AG, Basel.
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收藏
页码:144 / 151
页数:8
相关论文
共 36 条
[11]   Endothelial dysfunction in human disease [J].
Drexler, H ;
Hornig, B .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (01) :51-60
[12]  
ECKERSON HW, 1983, AM J HUM GENET, V35, P214
[13]  
Gilfix BM, 1997, CLIN CHEM, V43, P687
[14]   THE MOLECULAR-BASIS OF THE HUMAN SERUM PARAOXONASE ACTIVITY POLYMORPHISM [J].
HUMBERT, R ;
ADLER, DA ;
DISTECHE, CM ;
HASSETT, C ;
OMIECINSKI, CJ ;
FURLONG, CE .
NATURE GENETICS, 1993, 3 (01) :73-76
[15]   Paraoxonase gene Gln192Arg (Q192R) polymorphism is associated with coronary artery spasm [J].
Ito, T ;
Yasue, H ;
Yoshimura, M ;
Nakamura, S ;
Nakayama, M ;
Shimasaki, Y ;
Harada, E ;
Mizuno, Y ;
Kawano, H ;
Ogawa, H .
HUMAN GENETICS, 2002, 110 (01) :89-94
[16]   Calcium-dependent human serum homocysteine thiolactone hydrolase -: A protective mechanism against protein N-homocysteinylation [J].
Jakubowski, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (06) :3957-3962
[17]   Homocysteine thiolactone and protein homocysteinylation in human endothelial cells - Implications for atherosclerosis [J].
Jakubowski, H ;
Zhang, L ;
Bardeguez, A ;
Aviv, A .
CIRCULATION RESEARCH, 2000, 87 (01) :45-51
[18]   Serum malondialdehyde and coronary artery disease in hemodialysis patients [J].
Jung, HH ;
Choi, DH ;
Lee, SH .
AMERICAN JOURNAL OF NEPHROLOGY, 2004, 24 (05) :537-542
[19]  
Kedziora-Kornatowska K, 2004, CELL MOL BIOL LETT, V9, P635
[20]  
Kuo K, 1997, CLIN CHEM, V43, P1653