Analysis of Oxidative Stress Enzymes and Structural and Functional Proteins on Human Aortic Tissue from Different Aortopathies

被引:37
作者
Elena Soto, Maria [1 ]
Soria-Castro, Elizabeth [2 ]
Guarner Lans, Veronica [3 ]
Muruato Ontiveros, Eleazar [4 ]
Hernandez Mejia, Benjamin Ivan [4 ]
Martinez Hernandez, Humberto Jorge [4 ]
Barragan Garcia, Rodolfo [4 ]
Herrera, Valentin [4 ]
Perez-Torres, Israel [2 ]
机构
[1] Natl Inst Cardiol Ignacio Chavez, Dept Immunol, Mexico City 14080, DF, Mexico
[2] Natl Inst Cardiol Ignacio Chavez, Dept Pathol, Mexico City 14080, DF, Mexico
[3] Natl Inst Cardiol Ignacio Chavez, Dept Physiol, Mexico City 14080, DF, Mexico
[4] Natl Inst Cardiol Ignacio Chavez, Cardiovasc Surg Dept, Mexico City 14080, DF, Mexico
关键词
MANGANESE SUPEROXIDE-DISMUTASE; NITRIC-OXIDE SYNTHASE; ENDOGENOUS ANTIOXIDANT ENZYMES; ENDOTHELIAL DYSFUNCTION; TAKAYASUS-ARTERITIS; FREE-RADICALS; VASCULAR INFLAMMATION; ANEURYSM FORMATION; XANTHINE-OXIDASE; DENSITY-LIPOPROTEIN;
D O I
10.1155/2014/760694
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The role of oxidative stress in different aortopathies is evaluated. Thirty-two tissue samples from 18 men and 14 women were divided into: 4 control (C) subjects, 11 patients with systemic arterial hypertension (SAH), 4 with variants of Marfan's syndrome (MV), 9 with Marfan's syndrome (M), 2 with Turner's syndrome, and 2 with Takayasu's arteritis (TA). Aorta fragments were homogenized. Lipoperoxidation (LPO), copper-zinc and manganese superoxide dismutase (Mn and Cu-Zn-SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), endothelial nitric oxide synthase (eNOS), nitrates and nitrites (NO3-/NO2-), and type IV collagen, and laminin were evaluated. There was an increase in Mn- and Cu-Zn-SOD activity in SAH, MV, M, and Turner's syndrome. There was also an increase in CAT activity in M and Turner' syndrome. GPx and GST activity decreased and LPO increased in all groups. eNOS was decreased in SAH, MV, and M and NO3-/NO2- were increased in SAH and TA. Type IV collagen was decreased in Turner's syndrome and TA. Laminin gamma-1 was decreased in MV and increased in M. In conclusion, similarities and differences in oxidative stress in the different aortopathies studied including pathologies with aneurysms were found with alterations in SOD, CAT, GPx, GST, and eNOS activity that modify subendothelial basement membrane proteins.
引用
收藏
页数:13
相关论文
共 97 条
[1]   The Role of the Endogenous Antioxidant Enzymes and Malondialdehyde in Essential Hypertension [J].
Ahmad, Aquil ;
Singhal, Usha ;
Hossain, Mohd Mobark ;
Islam, Najmul ;
Rizvi, Imran .
JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH, 2013, 7 (06) :987-990
[2]  
[Anonymous], 2002, NURS ETHICS, V9, P105
[3]  
AREND WP, 1990, ARTHRITIS RHEUM, V33, P1129
[4]   Mitochondrial integrity and function in atherogenesis [J].
Ballinger, SW ;
Patterson, C ;
Knight-Lozano, CA ;
Burow, DL ;
Conklin, CA ;
Hu, ZY ;
Reuf, J ;
Horaist, C ;
Lebovitz, R ;
Hunter, GC ;
McIntyre, K ;
Runge, MS .
CIRCULATION, 2002, 106 (05) :544-549
[5]   Nitric oxide modulates vascular inflammation and intimal hyperplasia in insulin resistance and the metabolic syndrome [J].
Barbato, JE ;
Zuckerbraun, BS ;
Overhaus, M ;
Raman, KG ;
Tzeng, E .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 289 (01) :H228-H236
[6]   Effect of 8-isoprostaglandin F2α on the newborn rat pulmonary arterial muscle and endothelium [J].
Belik, J ;
Jankov, RP ;
Pan, J ;
Yi, M ;
Pace-Asciak, CR ;
Tanswell, AK .
JOURNAL OF APPLIED PHYSIOLOGY, 2003, 95 (05) :1979-1985
[7]   A TECHNIQUE FOR COMPLETE REPLACEMENT OF ASCENDING AORTA [J].
BENTALL, H ;
DEBONO, A .
THORAX, 1968, 23 (04) :338-&
[8]  
BEUTLER E, 1988, BLOOD CELLS, V14, P69
[9]   MARKED REDUCTION OF FREE-RADICAL GENERATION AND CONTRACTILE DYSFUNCTION BY ANTIOXIDANT THERAPY BEGUN AT THE TIME OF REPERFUSION - EVIDENCE THAT MYOCARDIAL STUNNING IS A MANIFESTATION OF REPERFUSION INJURY [J].
BOLLI, R ;
JEROUDI, MO ;
PATEL, BS ;
ARUOMA, OI ;
HALLIWELL, B ;
LAI, EK ;
MCCAY, PB .
CIRCULATION RESEARCH, 1989, 65 (03) :607-622
[10]  
Bonomini F, 2008, HISTOL HISTOPATHOL, V23, P381, DOI 10.14670/HH-23.381