Aortic Ascorbic Acid, Trace Elements, and Superoxide Dismutase Activity in Human Aneurysmal and Occlusive Disease

Dubick, Michael A.; Hunter, Glenn C.; Casey, Sharon M.; Keen, Carl L.

doi:10.3181/00379727-184-42457

Cited by 67 publications

(44 citation statements)

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“…The concentration of ascorbate used in these studies to inhibit LDL oxidation (40-60 MM) is well within the normal plasma range (23-85 gM) (44)(45)(46). In a recent study, it was shown that ascorbate levels were significantly lower in the aorta of patients with atherosclerotic vascular disease compared to controls (47). Also, smokers have an -40% reduction in plasma ascorbate levels, and patients with coronary artery disease have abnormally low plasma levels of ascorbate (48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Preservation of the endogenous antioxidants in low density lipoprotein by ascorbate but not probucol during oxidative modification.

Jialal

Grundy²

1991

J. Clin. Invest.

208

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Several lines of evidence indicate that the oxidative modification of low density lipoproteins (LDL) may provide an important link between plasma LDL and the genesis ofthe atherosclerotic lesion. Ascorbate is an important water-soluble, chainbreaking antioxidant in humans. Probucol, a lipid-soluble antioxidant drug has been shown to retard the progression of atherosclerosis. The aim of the present study was to compare the effects of probucol and physiologic levels of ascorbate on the oxidative modification of LDL in both a cell-free (2.5 ,M Cu++ in phosphate-buffered saline) and cellular system (human monocyte macrophages in Ham's F-10 medium). Both ascorbate and probucol inhibited the oxidative modification of LDL in both systems to a similar degree as evidenced by the thiobarbituric acid-reacting substance activity, electrophoretic mobility, and degradation by macrophages. However, whereas co-incubation with physiologic levels of ascorbate resulted in a substantial preservation of the a-tocopherol, y-tocopherol, and (3-carotene of the LDL, probucol in concentrations ranging from 10 to 80 ,M failed to protect these antioxidants. Thus, in addition to being as potent as probucol in inhibiting the oxidation of LDL, ascorbate in contrast preserves the endogenous antioxidants in the LDL. (J. Clin. Invest. 1991. 87:597401.)

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Section: Discussionmentioning

confidence: 99%

Preservation of the endogenous antioxidants in low density lipoprotein by ascorbate but not probucol during oxidative modification.

Jialal

Grundy²

1991

J. Clin. Invest.

208

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“…Early studies found reduced amounts of anti-oxidants (such as ascorbic acid, SOD, or GSH peroxidase) in AAA tissue samples compared with nonaneurysmal aorta (34,35). Later, increased ROS levels as well as increased expression of the NOX1/NOX2 subunits p47phox and p22phox were demonstrated as local features of AAA as opposed to nondiseased aortic segments (86).…”

Section: Abdominal Aortic Aneurysmsmentioning

confidence: 99%

Hemodynamic Regulation of Reactive Oxygen Species: Implications for Vascular Diseases

Raaz

Toh

Maegdefessel

et al. 2014

Antioxidants & Redox Signaling

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Significance: Arterial blood vessels functionally and structurally adapt to altering hemodynamic forces in order to accommodate changing needs and to provide stress homeostasis. This ability is achieved at the cellular level by converting mechanical stimulation into biochemical signals (i.e., mechanotransduction). Physiological mechanical stress helps maintain vascular structure and function, whereas pathologic or aberrant stress may impair cellular mechano-signaling, and initiate or augment cellular processes that drive disease. Recent Advances: Reactive oxygen species (ROS) may represent an intriguing class of mechanically regulated second messengers. Chronically enhanced ROS generation may be induced by adverse mechanical stresses, and is associated with a multitude of vascular diseases. Although a causal relationship has clearly been demonstrated in large numbers of animal studies, an effective ROS-modulating therapy still remains to be established by clinical studies. Critical Issues and Future Directions: This review article focuses on the role of various mechanical forces (in the form of laminar shear stress, oscillatory shear stress, or cyclic stretch) as modulators of ROS-driven signaling, and their subsequent effects on vascular biology and homeostasis, as well as on specific diseases such as arteriosclerosis, hypertension, and abdominal aortic aneurysms. Specifically, it highlights the significance of the various NADPH oxidase (NOX) isoforms as critical ROS generators in the vasculature. Directed targeting of defined components in the complex network of ROS (mechano-)signaling may represent a key for successful translation of experimental findings into clinical practice. Antioxid. Redox Signal. 20,[914][915][916][917][918][919][920][921][922][923][924][925][926][927][928]

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“…In 1987, Dubick et al reported that levels of ascorbic acid and Cu, Zn superoxide dismutase (SOD) activity were reduced in tissue samples from patients with AAA and atherosclerotic occlusive disease (AOD) as compared with nondiseased aorta from a different group of patients. 15 Subsequently, the same investigators showed that MnSOD, glutathione peroxidase, and glutathione reductase activities were reduced, while levels of lipid peroxidation products were increased, in AAA and AOD tissues as compared with nondiseased aorta. 16 In addition, Zhang et al showed evidence of increased expression of inducible nitric oxide synthase (iNOS) in the media and adventitia of human AAA tissues as compared with normal aorta.…”

Section: Evidence Of Increased Oxidative Stress In Human Aaamentioning

confidence: 99%

Role of Oxidative Stress in the Pathogenesis of Abdominal Aortic Aneurysms

McCormick

Gavrila

Weintraub

2007

ATVB

292

245

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Abstract-The role of inflammation in the pathogenesis of abdominal aortic aneurysms (AAA) is well established. The inflammatory process leads to protease-mediated degradation of the extracellular matrix and apoptosis of smooth muscle cells (SMC), which are the predominant matrix synthesizing cells of the vascular wall. These processes act in concert to progressively weaken the aortic wall, resulting in dilatation and aneurysm formation. Oxidative stress is invariably increased in, and contributes importantly to, the pathophysiology of inflammation. Moreover, reactive oxygen species (ROS) play a key role in regulation of matrix metalloproteinases and induction of SMC apoptosis. ROS may also contribute to the pathogenesis of hypertension, a risk factor for AAA. Emerging evidence suggests that ROS and reactive nitrogen species (RNS) are associated with AAA formation in animal models and in humans. Although experimental data are limited, several studies suggest that modulation of ROS production or activity may suppress AAA formation and improve experimental outcome in rodent models. Although a number of enzymes can produce injurious ROS in the vasculature, increasing evidence points toward a role for NADPH oxidase as a source of oxidative stress in the pathogenesis of AAA.

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Aortic Ascorbic Acid, Trace Elements, and Superoxide Dismutase Activity in Human Aneurysmal and Occlusive Disease

Cited by 67 publications

References 0 publications

Preservation of the endogenous antioxidants in low density lipoprotein by ascorbate but not probucol during oxidative modification.

Preservation of the endogenous antioxidants in low density lipoprotein by ascorbate but not probucol during oxidative modification.

Hemodynamic Regulation of Reactive Oxygen Species: Implications for Vascular Diseases

Role of Oxidative Stress in the Pathogenesis of Abdominal Aortic Aneurysms

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