LDL oxidation by arterial wall macrophages depends on the oxidative status in the lipoprotein and in the cells: Role of prooxidants vs. antioxidants

1998 ◽  
pp. 149-159
Author(s):  
Michael Aviram ◽  
Bianca Fuhrman
Keyword(s):  
Arterial Wall ◽  
Oxidative Status ◽  
Ldl Oxidation

scholarly journals Essential Role of the Redox-Sensitive Kinase p66shc in Determining Energetic and Oxidative Status and Cell Fate in Neuronal Preconditioning

2010 ◽  
Vol 30 (15) ◽  
pp. 5242-5252 ◽  
Author(s):  
J. E. Brown ◽  
S. L. H. Zeiger ◽  
J. C. Hettinger ◽  
J. D. Brooks ◽  
B. Holt ◽  
...  
Keyword(s):  
Cell Fate ◽  
Essential Role ◽  
Oxidative Status

Abstract 12770: The Significant Role of Endothelium and Arterial Wall Properties in Patients With Pseudoexfoliative Glaucoma

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Georgia Siasou ◽  
Gerasimos Siasos ◽  
Marilita M Moschos ◽  
Nikolaos Gouliopoulos ◽  
Evangelos Oikonomou ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Endothelial Function ◽  
Significant Role ◽  
Vascular Function ◽  
Arterial Wall ◽  
Augmentation Index ◽  
Open Angle Glaucoma ◽  
Anterior Segment ◽  
Pseudoexfoliative Glaucoma

Introduction: Primary open-angle glaucoma (POAG) is one of the most prevalent causes of irreversible blindness and is associated with endothelial dysfunction and arterial stiffness. Pseudoexfoliative glaucoma (PEG) is another type of glaucoma observed in pseudoexfoliation syndrome. It is characterized by the deposition of pseudoexfoliative material not only to the anterior segment of the eye, but also to the vessels, heart and other organs. Hypothesis: Endothelial function and arterial stiffness are impaired in patients with POAG and PEG supporting the significant role of vascular function impairment in the progression of the disease. Methods: Forty four POAG patients, 22 PEG and 38 healthy subjects (Cl) were included in this study. All subjects were free of cardiovascular or inflammatory diseases. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections Results: Between the three study groups CL, POAG, PEG there was no difference in age (67±10years vs. 70±9years vs. 66±12yeras, p=0.12) or prevalence of male sex (70% vs. 57% vs. 50%, p=0.21). Importantly, there was a linear impairment of FMD (7.35±2.77% vs. 6.58±3.18% vs. 4.88±3.29%, p=0.006), PWV (7.98±1.56m/sec vs. 9.20±1.84m/sec vs. 9.22±2.16m/sec, p=0.004) and AIx (21.29±8.77% vs. 25.14±5.71% vs. 28.20±8.75%, p=0.002) from CL to POAG and PEG. Interestingly post hoc test after Scheffe correction revealed also that PEG subjects had not only significantly impaired FMD, compared to control subjects, but also compared to POAG subjects (4.88±3.29% vs. 6.58±3.18%, p=0.02). Conclusions: Endothelial function and arterial stiffness are significantly impaired in patients with pseudoexfoliative glaucoma. These findings shed some light in the pathophysiology of pseudoexfoliative glaucoma and support the theory that pseudoexfoliative fibrils may also accumulate and damage the arterial wall.

scholarly journals The Role of HO-1 and Its Crosstalk with Oxidative Stress in Cancer Cell Survival

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2401
Author(s):  
Shih-Kai Chiang ◽  
Shuen-Ei Chen ◽  
Ling-Chu Chang
Keyword(s):  
Oxidative Stress ◽  
Redox Regulation ◽  
Oxidative Status ◽  
Multiple Roles ◽  
Mitochondrial Enzymes ◽  
Heme Oxygenases ◽  
Downstream Effects ◽  
Cancer Cell Survival ◽  
And Oxidative Stress

Heme oxygenases (HOs) act on heme degradation to produce carbon monoxide (CO), free iron, ferritin, and biliverdin. Upregulation of cellular HO-1 levels is signature of oxidative stress for its downstream effects particularly under pro-oxidative status. Subcellular traffics of HO-1 to different organelles constitute a network of interactions compromising a variety of effectors such as pro-oxidants, ROS, mitochondrial enzymes, and nucleic transcription factors. Some of the compartmentalized HO-1 have been demonstrated as functioning in the progression of cancer. Emerging data show the multiple roles of HO-1 in tumorigenesis from pathogenesis to the progression to malignancy, metastasis, and even resistance to therapy. However, the role of HO-1 in tumorigenesis has not been systematically addressed. This review describes the crosstalk between HO-1 and oxidative stress, and following redox regulation in the tumorigenesis. HO-1-regulated signaling pathways are also summarized. This review aims to integrate basic information and current progress of HO-1 in cancer research in order to enhance the understandings and facilitate following studies.

Role of Elastic Tissue in Cholesterol Deposition in the Arterial Wall

1973 ◽  
Vol 15 (1-2) ◽  
pp. 46-58 ◽  
Author(s):  
B. Jacotot ◽  
J.L. Beaumont ◽  
G. Monnier ◽  
M. Szigeti ◽  
B. Robert ◽  
...  
Keyword(s):  
Arterial Wall ◽  
Elastic Tissue

scholarly journals Evidence for the role of high density lipoproteins in mediating the antioxidant effect of estrogens

2000 ◽  
pp. 79-83 ◽  
Author(s):  
W Abplanalp ◽  
MD Scheiber ◽  
K Moon ◽  
B Kessel ◽  
JH Liu ◽  
...  
Keyword(s):  
Density Lipoprotein ◽  
Antioxidant Effect ◽  
High Density ◽  
In Vivo Studies ◽  
Ldl Oxidation ◽  
High Density Lipoproteins ◽  
Oh Groups

Estrogens possess strong antioxidant effects in vitro, but in vivo studies in humans have yielded conflicting results. Little is known regarding factors that mediate the antioxidant effect of estrogens in vivo. In this study the potential role of high density lipoprotein (HDL) was examined. The antioxidant effect of estradiol-17beta (E2) added to low density lipoprotein (LDL) was lost after dialysis. In contrast, the antioxidant effect of E2 added to HDL was conserved after dialysis, suggesting that E2 was bound to HDL. Binding of E2 to LDL increased after esterification (especially to long chain fatty acids). In the presence of HDL, an increased amount of E2 was transferred to LDL. E2-17 ester was as potent as E2 in preventing LDL oxidation in vitro, but 3,17-diesters were not as effective (E2=E2-17 ester>E2-3 ester>E2-3,17 diester). This was also supported by experiments which showed that estrogens with masked 3-OH groups were not effective as antioxidants. These studies provide evidence that HDL could facilitate the antioxidant effect of E2 through initial association, esterification and eventual transfer of E2 esters to LDL. Therefore it is critical that HDL peroxidation parameters be evaluated in subjects receiving estrogen replacement therapy.

Endothelium-dependent arterial wall tone elasticity modulated by blood viscosity

2002 ◽  
Vol 282 (2) ◽  
pp. H389-H394 ◽  
Author(s):  
Edmundo I. Cabrera Fischer ◽  
Ricardo L. Armentano ◽  
Franco M. Pessana ◽  
Sebastián Graf ◽  
Luis Romero ◽  
...  
Keyword(s):  
Blood Viscosity ◽  
Muscle Activation ◽  
Arterial Wall ◽  
Mock Circulation ◽  
Significant Difference ◽  
Before And After ◽  
Strain Relationship ◽  
Instantaneous Pressure

The role of blood viscosity on arterial wall elasticity before and after deendothelization (DE) was studied. Seven ovine brachiocephalic arteries were studied in vitro under physiological pulsatile flow conditions achieved by a mock circulation loop. Instantaneous pressure and diameter signals were assessed in each arterial segment. Incremental elastic modulus ( E inc) was calculated using the slope of the pure elastic stress-strain relationship. There was no significant difference between E inc values before and after DE (3.11 vs. 3.16 107 dyn/cm2) at a blood viscosity of 2.00 mPa · s. Increases in blood viscosity (2.50, 3.00, 3.50, and 4.00 mPa · s) always resulted in decreases of E inc before DE; inversely, increases in blood viscosity resulted in increases of E inc after DE. These values of E inc, for identical levels of blood viscosity, were always significantly lower ( P< 0.05) before DE than those obtained after DE. Arterial wall elasticity assessed through E inc was strongly influenced by blood viscosity, probably due to presence or absence of endothelium relaxing factors or to direct shear smooth muscle activation when endothelial cells are removed.

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