Novel indices of oxidant stress in cardiovascular disease: specific analysis of F2-isoprostanes

Praticò, Domenico; Reilly, Michael P.; Ja, Lawson; Ga, FitzGerald

doi:10.1007/978-3-0348-7352-9_2

Cited by 7 publications

(7 citation statements)

References 48 publications

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“…1A). It is known that 8-isoprostanes are a family of eicosanoids of nonenzymatic origin produced in vivo by the random oxidation of tissue phospholipids by oxygen free radicals providing a reliable marker of in vivo oxidative stress (23). Importantly, a positive correlation was found between plasma homocysteine and F 2 -isoprostane concentrations in humans (33).…”

Section: Discussionmentioning

confidence: 95%

Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

Bagi¹,

Csekő²,

Toth³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Bagi, Zsolt, Csongor Csekő , Erika Tó th, and Akos Koller. Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment. Am J Physiol Heart Circ Physiol 285: H2277-H2283, 2003. First published July 17, 2003 10.1152/ajpheart.00448.2003.-We aimed to test the hypothesis that an enhanced level of reactive oxygen species (ROS) is primarily responsible for the impairment of nitric oxide (NO)-mediated regulation of arteriolar wall shear stress (WSS) in hyperhomocysteinemia (HHcy). Thus flow/WSS-induced dilations of pressurized gracilis muscle arterioles (basal diameter: ϳ170 m) isolated from control (serum Hcy: 6 Ϯ 1 M), methionine diet-induced HHcy rats (4 wk, serum Hcy: 30 Ϯ 6 M), and HHcy rats treated with vitamin C, a known antioxidant (4 wk, 150 mg ⅐ kg body wt Ϫ1 ⅐ day Ϫ1 ; serum Hcy: 32 Ϯ 10 M), were investigated. In vessels of HHcy rats, increases in intraluminal flow/WSS-induced dilations were converted to constrictions. Constrictions were unaffected by inhibition of NO synthesis by N -nitro-L-arginine methyl ester (L-NAME). Vitamin C treatment of HHcy rats reversed the WSS-induced arteriolar constrictions to L-NAME-sensitive dilations but did not affect control responses. Similar changes in responses were obtained for the calcium ionophore A-23187. In addition, diastolic and mean arterial blood pressure and serum 8-isoprostane levels (a marker of in vivo oxidative stress) were significantly elevated in rats with HHcy, changes that were normalized by vitamin C treatment. Taken together, our data show that in chronic HHcy long-term vitamin C treatment, by decreasing oxidative stress in vivo, enhanced NO bioavailability, restored the regulation of shear stress in arterioles, and normalized systemic blood pressure. Thus our study provides evidence that oxidative stress is an important in vivo mechanism that is primarily responsible for the development of endothelial dysregulation of WSS in HHcy.homocysteine; nitric oxide; thromboxane A2 power dissipation SEVERAL EPIDEMIOLOGICAL STUDIES have shown that hyperhomocysteinemia (HHcy) increases the risk for cardiovascular diseases, such as ischemic heart diseases; cerebrovascular, peripheral vascular diseases; and hypertension (1,6,7,9,29,32). Homocysteine is formed during the metabolism of the essential amino acid methionine, and its normal plasma concentration is between 5 and 15 M, but it can be increased due to genetic (e.g., cystathione-␤-synthase and methyltetrahydrofolate reductase) and nutritional alterations (deficiency of vitamins, e.g., folic acid, vitamin B 6 , and B 12 ), factors that participate in the metabolism of homocysteine and methionine (8).Although the underlying mechanisms responsible for the elevated risks have not yet been fully elucidated, there is increasing evidence to suggest that endothelial dysfunction of vessels contributes to the development of vascular diseases observed in both humans and animals with HHcy (19,34). Several studies have doc...

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Section: Discussionmentioning

confidence: 95%

Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

Bagi¹,

Csekő²,

Toth³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Oxidative damage may play an important role in the pathogenesis of several neurodegenerative diseases, and growing evidence points out the involvement of free radicals in mediating neuronal death in these disorders [1][2][3][4][5][6][7][8]32] . Thus, markers of oxidative damage reflecting the disease and potentially the disease stage and severity may be detectable in body fluids of affected patients.…”

Section: Discussionmentioning

confidence: 99%

8-OHdG in Cerebrospinal Fluid as a Marker of Oxidative Stress in Various Neurodegenerative Diseases

et al. 2009

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Background: The 8-hydroxy-2 deoxyguanosine (8-OHdG) is a product of nucleoside oxidation of DNA and a reliable marker of oxidative stress markers. Increased levels of oxidative stress have been reported in the cerebrospinal fluid (CSF) of patients with various neurodegenerative disorders. Objective: In search of a biochemical indicator of Parkinson’s disease (PD), we analyzed the levels 8-OHdG in the CSF of 99 patients, using ELISA to assess the differences between various neurodegenerative disorders. Results: Statistically significant higher CSF levels (p = 0.022) of 8-OHdG in non-demented PD patients as compared to the control group were observed. No differences between CSF 8-OHdG levels and age at the time of lumbar puncture, presence or severity of dementia, or gender were found. Conclusions: 8-OHdG levels could be potentially useful in the neurochemically supported diagnosis of PD.

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“…8-Isoprostanes are stable products of membrane lipid peroxidation, and their tissue concentration correlates with the level of oxidative stress. 17 Ang II treatment resulted in a Ͼ3-fold increase in 8-isoprostane content in the abdominal aorta, which was markedly attenuated by dietary vitamin E supplementation (PϽ0.05; Figure 3). This observed decrease in 8-isoprostane formation is consistent with vitamin E providing antioxidant protection in the tissue where AAA develops.…”

Section: Vitamin E Decreased Formation Of 8-isoprostane In Abdominal mentioning

confidence: 99%

Vitamin E Inhibits Abdominal Aortic Aneurysm Formation in Angiotensin II–Infused Apolipoprotein E–Deficient Mice

Gavrila

McCormick

et al. 2005

ATVB

162

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Background-Abdominal aortic aneurysms (AAAs) in humans are associated with locally increased oxidative stress and activity of NADPH oxidase. We investigated the hypothesis that vitamin E, an antioxidant with documented efficacy in mice, can attenuate AAA formation during angiotensin II (Ang II) infusion in apolipoprotein E-deficient mice. Methods and Results-Six-month-old male apolipoprotein E-deficient mice were infused with Ang II at 1000 ng/kg per minute for 4 weeks via osmotic minipumps while consuming either a regular diet or a diet enriched with vitamin E (2 IU/g of diet). After 4 weeks, abdominal aortic weight and maximal diameter were determined, and aortic tissues were sectioned and examined using biochemical and histological techniques. Vitamin E attenuated formation of AAA, decreasing maximal aortic diameter by 24% and abdominal aortic weight by 34% (PϽ0.05, respectively). Importantly, animals treated with vitamin E showed a 44% reduction in the combined end point of fatalϩnonfatal aortic rupture (PϽ0.05). Vitamin E also decreased aortic 8-isoprostane content (a marker of oxidative stress) and reduced both aortic macrophage infiltration and osteopontin expression (PϽ0.05, respectively). Vitamin E treatment had no significant effect on the extent of aortic root atherosclerosis, activation of matrix metalloproteinases 2 or 9, serum lipid profile, or systolic blood pressure. Key Words: aneurysm Ⅲ vitamin E Ⅲ oxidative stress Ⅲ vascular inflammation Ⅲ NADPH oxidase Ⅲ osteopontin A bdominal aortic aneurysms (AAAs) occur in Ϸ3% of humans Ͼ65 years of age and are characterized by localized structural deterioration of the aortic wall, leading to progressive aortic dilation. The most dreaded complication of AAA is rupture, the likelihood of which is directly related to aneurysm diameter. 1 Although open surgical repair can improve outcomes in patients with large AAAs, the procedure is associated with significant operative risks and complications, particularly in the presence of comorbid conditions common in these patients. Percutaneous repair techniques (ie, stent grafting) have been developed, but not all patients are candidates, and these procedures are also associated with significant complications. 2 The development of effective medical therapy for AAA has been hampered by lack of understanding of the mechanisms responsible for aneurysm growth and rupture. Conclusions-VitaminStudies published over the past decade support the view that inflammation plays a key role in the pathogenesis of AAAs. [3][4][5][6][7] One of the known causes and consequences of inflammation is an increase in local levels of oxidative stress.Indeed, Miller et al have shown that human aneurysmal aorta displays clear evidence of increased oxidative damage and pro-oxidant enzyme expression/activity compared with adjacent nonaneurysmal tissue. 8 Whether oxidative stress is merely associated with AAAs, or whether it contributes to the pathogenesis of the disease, remains to be determined.In the present study, we examined the effects of ...

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Novel indices of oxidant stress in cardiovascular disease: specific analysis of F2-isoprostanes

Cited by 7 publications

References 48 publications

Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

8-OHdG in Cerebrospinal Fluid as a Marker of Oxidative Stress in Various Neurodegenerative Diseases

Vitamin E Inhibits Abdominal Aortic Aneurysm Formation in Angiotensin II–Infused Apolipoprotein E–Deficient Mice

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