Oxidative Stress and Cardiovascular Injury

Griendling, Kathy K.; FitzGerald, Garret A.

doi:10.1161/01.cir.0000093661.90582.c4

Cited by 739 publications

(488 citation statements)

References 147 publications

(120 reference statements)

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“…On the other hand, there are many documented evidences for main role of oxidative stress plays in the pathogenesis and development of cardiovascular diseases such as hypertension, hypercholesterolemia, diabetes mellitus, atherosclerosis, myocardial infarction, angina pectoris, and heart failure (30)(31)(32). Antioxidants are pivotal in maintaining redox balance by either preventing the formation of free radicals, detoxifying them, or by scavenging the reactive species or their precursors.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Koohsari

Shaki

Jahani

2016

Braz. arch. biol. technol.

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Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METHinduced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Koohsari

Shaki

Jahani

2016

Braz. arch. biol. technol.

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“…Furthermore, AT 1 receptor stimulation elicits vascular production of reactive oxygen species, including superoxide, which, in turn, induces arteriosclerotic vascular lesions. 39 Thus, enhanced tissue ACE expression and oxidative stress through AT 1 receptor may contribute, at least in part, to the long-term vascular effects of ADMA, irrespective of the presence or absence of eNOS.…”

Section: Involvement Of Renin-angiotensin System In Long-term Vasculamentioning

confidence: 99%

Asymmetric Dimethylarginine Produces Vascular Lesions in Endothelial Nitric Oxide Synthase–Deficient Mice

Suda

Tsutsui

Morishita

et al. 2004

ATVB

174

124

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Objective-Asymmetric dimethylarginine (ADMA) is widely believed to be an endogenous nitric oxide synthase (eNOS) inhibitor. However, in this study, we examined our hypothesis that the long-term vascular effects of ADMA are not mediated by inhibition of endothelial NO synthesis. Methods and Results-ADMA was infused in wild-type and eNOS-knockout (KO) mice by osmotic minipump for 4 weeks. In wild-type mice, long-term treatment with ADMA caused significant coronary microvascular lesions. Importantly, in eNOS-KO mice, treatment with ADMA also caused an extent of coronary microvascular lesions that was comparable to that in wild-type mice. These vascular effects of ADMA were not prevented by supplementation of L-arginine, and vascular NO production was not reduced by ADMA treatment. Treatment with ADMA caused upregulation of angiotensin-converting enzyme (ACE) and an increase in superoxide production that were comparable in both strains and that were abolished by simultaneous treatment with temocapril (ACE inhibitor) or olmesartan (AT 1 receptor antagonist), which simultaneously suppressed vascular lesion formation. Key Words: asymmetric dimethylarginine Ⅲ arteriosclerosis Ⅲ nitric oxide Ⅲ endothelial nitric oxide synthase Ⅲ mice E ndothelium-derived nitric oxide (NO), synthesized from L-arginine by endothelial NO synthase (eNOS), has several important antiatherogenic actions. 1-5 Indeed, reduction of endothelial NO synthesis (endothelial dysfunction) predisposes the blood vessel to arteriosclerosis, 1-5 and the eNOS-deficient (eNOS-KO) mice exhibit accelerated vascular lesion formation. 6,7 As pharmacological tools to inhibit endothelial NO synthesis, synthetic L-arginine analogues have been used in vitro and in vivo. Among them, N -nitro-L-arginine methyl ester (L-NAME) is the most frequently used agent. [1][2][3][4][5] Long-term treatment with L-NAME is known to cause arteriosclerotic coronary lesions, especially at microvascular levels, in experimental animals. 8,9 This model with L-NAME is regarded as a useful animal model for examining the protective roles of endothelium-derived NO in the pathogenesis of arteriosclerosis. 8,9 See cover However, it is controversial whether these vascular effects of L-NAME are caused primarily by the inhibition of endothelial NO synthesis for the following reasons: first, the importance of endothelium-derived NO decreases as the vessel size becomes smaller, 10 whereas L-NAME-induced vascular lesions are prominent at microvascular levels; 8 second, long-term treatment with L-NAME does not reduce eNOS activity; 11 third, multiple actions of L-NAME other than simple inhibition of NO synthesis have been reported. 12,13 The most appropriate way to address this issue is to use mice that are deficient in the eNOS gene and to examine whether long-term treatment with L-NAME causes coronary vascular lesions in those mice. We have recently shown that treatment with L-NAME causes a comparable extent of Conclusions-These

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“…[1][2][3] Biomarkers of oxidative stress, such as serum malondialdehyde level measured as thiobarbituric acid-reactive substances, oxidized low-density lipoprotein, oxidation injury of DNA, 8-hydroxydeoxyguanosine and urinary excretion of 8-iso-prostaglandin-F2a, are generally measured in laboratories. [4][5][6][7] On the other hand, as indices of antioxidant potential, intracellular levels of superoxide dismutase and glutathione peroxidase have mainly been measured.…”

Section: Introductionmentioning

confidence: 99%

Significance of measuring oxidative stress in lifestyle-related diseases from the viewpoint of correlation between d-ROMs and BAP in Japanese subjects

et al. 2011

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In recent years, oxidative stress has been postulated to be an important factor in the pathogenesis and development of lifestyle-related diseases. In this study, we investigated the association between the derivatives of reactive oxygen metabolites (d-ROMs), as an index of products of reactive oxygen species (ROS), and biological antioxidant potential (BAP), as an index of antioxidant potential. We also investigated the associations between d-ROMs or BAP and the risk factors for lifestyle-related diseases or metabolic syndrome-associated factors to evaluate their usefulness in preventive medicine. There were 442 subjects who underwent health checkup examination in our facilities. In addition to standard medical checkup items, we analyzed d-ROMs, BAP, brachial-ankle pulse wave velocity, high-sensitivity C-reactive protein level and visceral fat area (VFA) visualized on a computed tomography scan. The mean d-ROM value in females was significantly higher than that in males. There was a positive correlation between the d-ROM and VFA levels. On correlation analysis, there was a negative correlation between the d-ROM and creatinine levels. As factors that influence d-ROMs, the level of VFA was selected, suggesting the significance of oxidative stress measurement with d-ROMs. In addition, there was a positive correlation between d-ROMs and BAP values. Further research is required to resolve whether increased production of ROS or the antioxidant potential that can compensate for such an increase of ROS is more important in vivo. INTRODUCTIONOxidative stress may be involved in various disorders and pathogeneses, especially in lifestyle-related diseases, and it causes the progression and acceleration of atherosclerosis. 1-3 Biomarkers of oxidative stress, such as serum malondialdehyde level measured as thiobarbituric acid-reactive substances, oxidized low-density lipoprotein, oxidation injury of DNA, 8-hydroxydeoxyguanosine and urinary excretion of 8-iso-prostaglandin-F2a, are generally measured in laboratories. [4][5][6][7] On the other hand, as indices of antioxidant potential, intracellular levels of superoxide dismutase and glutathione peroxidase have mainly been measured. [8][9] However, these assay methods are complex and are not suitable for analysis of a large number of subjects. Recently, simpler methods for detecting reactive oxygen species (ROS) using derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) were developed, and reports on studies using these methods have been increasing. [10][11][12][13][14][15][16][17][18][19][20] Thus, in the present study, we measured d-ROMS and BAP as indices for the production of ROS and antioxidant potential, respectively.

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Oxidative Stress and Cardiovascular Injury

Cited by 739 publications

References 147 publications

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Protective Effects of Edaravone against Methamphetamine-Induced cardiotoxicity

Asymmetric Dimethylarginine Produces Vascular Lesions in Endothelial Nitric Oxide Synthase–Deficient Mice

Significance of measuring oxidative stress in lifestyle-related diseases from the viewpoint of correlation between d-ROMs and BAP in Japanese subjects

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