Oxidant injury in coronary heart disease [Part-1]

Pandya, Dipak P.

doi:10.1007/s12019-001-0026-0

Cited by 17 publications

(12 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the presence of mt-Nd2 a , neither complex I nor complex III ROS production was elevated in the context of either ALR or NOD nuclear DNA. We hypothesize that this lowered ROS production is a key mechanistic effect provided by mt-Nd2 a in resistance to various pathological conditions (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)18). This hypothesis is supported by the finding that mice encoding mt-Nd2 c exhibit heightened susceptibility to alloxan-induced diabetes (39).…”

Section: Volume 283 • Number 16 • April 18 2008mentioning

confidence: 81%

“…Reactive oxygen species (ROS) 2 play an important role in the pathologies of many diseases such as atherosclerosis (1)(2)(3)(4)(5), myocardial infarction (6,7), and hypertension (8,9) due to the ability of ROS to damage lipids, protein, and DNA. ROS production has also been associated with the process of aging (10 -12).…”

mentioning

confidence: 99%

“…(22)(23)(24). Manganese superoxide dismutase converts O 2 . to H 2 O 2 , which is converted to the more deleterious hydroxyl radical via the Fenton reaction (25).…”

mentioning

confidence: 99%

See 2 more Smart Citations

mt-Nd2 Suppresses Reactive Oxygen Species Production by Mitochondrial Complexes I and III

Gusdon

Votyakova

Mathews

2008

Journal of Biological Chemistry

View full text Add to dashboard Cite

Reactive oxygen species (ROS) play a critical role in the pathogenesis of human diseases. A cytosine to adenine transversion in the mitochondrially encoded NADH dehydrogenase subunit 2 (mt-ND2, human; mt-Nd2, mouse) gene results in resistance against type 1 diabetes and several additional ROS-associated conditions. Our previous studies have demonstrated that the adeninecontaining allele (mt-Nd2 a ) is also strongly associated with resistance against type 1 diabetes in mice. In this report we have confirmed that the cytosine-containing allele (mt-Nd2 c ) results in elevated mitochondrial ROS production. Using inhibitors of the electron transport chain, we show that when in combination with nuclear genes from the alloxan-resistant (ALR) strain, mt-Nd2 c increases ROS from complex III. Furthermore, by using alamethicin-permeabilized mitochondria, we measured a significant increase inelectrontransportchain-dependentROSproductionfrom all mt-Nd2 c -encoding strains including ALR.mt NOD , non-obese diabetic (NOD), and C57BL/6 (B6). Studies employing alamethicin and inhibitors were able to again localize the heightened ROS production in ALR.mt NOD to complex III and identified complex I as the site of elevated ROS production from NOD and B6 mitochondria. Using submitochondrial particles, we confirmed that in the context of the NOD or B6 nuclear genomes, mt-Nd2 c elevates complex I-specific ROS production. In all assays mitochondria from mt-Nd2 a -encoding strains exhibited low ROS production. Our data suggest that lowering overall mitochondrial ROS production is a key mechanism of disease protection provided by mt-Nd2 a

show abstract

Section: Volume 283 • Number 16 • April 18 2008mentioning

confidence: 81%

mentioning

confidence: 99%

See 1 more Smart Citation

mt-Nd2 Suppresses Reactive Oxygen Species Production by Mitochondrial Complexes I and III

Gusdon

Votyakova

Mathews

2008

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Belch et al [29] have reported a negative correlation between left ventricular ejection fraction and oxidative stress, similar to the findings we report here. ROS may lead to the modification of several molecules including the oxidation of LDL-C. Ox-LDL may lead to endothelial dysfunction, increased vascular smooth muscle cell growth and monocyte migration and activation [30,31,32], and all of these processes may lead to myocardial dysfunction and deterioration in congestive heart failure patients [33]. …”

Section: Discussionmentioning

confidence: 99%

Prooxidant-Antioxidant Balance and Antioxidized LDL Antibody Level Values and Cardiac Function in Patients with Coronary Artery Disease

Rahsepar

Mirzaee²,

Moodi³

et al. 2012

Cardiology

View full text Add to dashboard Cite

Objectives: We studied the association between the prooxidant-antioxidant balance (PAB), anti-malondialdehyde-modified low-density lipoprotein (oxidized LDL, ox-LDL) IgG antibody and indices of cardiac function (systolic and diastolic function) in patients with coronary artery disease (CAD). Methods: Fifty-five patients with established CAD were selected, and serum levels of anti-ox-LDL IgG and PAB values were measured and compared with 40 matched healthy controls. Systolic and diastolic functions were determined for all patients. Results: PAB values were significantly higher in patients than in controls (p < 0.001), whilst serum anti-ox-LDL concentrations were not statistically different between the 2 groups (p = 0.821). However, after adjustment for high-density lipoprotein cholesterol, the patients had higher anti-ox-LDL levels (p = 0.04). Total PAB values were inversely associated with ejection fraction (r = –0.326, p = 0.031), but this was not the case for anti-ox-LDL in either group (p > 0.05). Conclusion: Serum concentrations of a marker of oxidative stress (PAB values) are inversely associated with cardiac function. PAB is a relatively simple index that could be incorporated into risk assessment in CAD patients. Anti-ox-LDL IgG antibody concentration does not appear to reflect total oxidative stress as assessed by PAB.

show abstract

“…Oxidative stress was shown to be involved in the development of vascular dysfunction and atherosclerosis [2,3]. Increased production of reactive oxygen species (ROS) leads to oxidation of low density lipoprotein (LDL), endothelial dysfunction, vascular smooth muscle cell growth and monocyte migration leading to atheroma formation [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrially Targeted Antioxidants for the Treatment of Cardiovascular Diseases

Subramanian

Kalyanaraman²,

Migrino³

2010

PRC

View full text Add to dashboard Cite

Oxidative stress resulting from imbalance between reactive oxygen species (ROS) generation and antioxidant mechanisms is important in the pathogenesis of cardiovascular diseases such as atherosclerosis, ischemic heart disease, heart failure, stroke, hypertension and diabetes. Paradoxically, antioxidant therapy such as vitamin E has not been shown on large randomized clinical trials to favorably affect clinical outcomes. Since mitochondria are involved not only with bioenergetics but also with oxidative damage through ROS generation and cell signaling leading to apoptosis, antioxidants targeted at the mitochondria are appealing novel agents to attenuate oxidative stress. In particular, antioxidants conjugated with triphenylphosphonium cation such as mitoquinone, mitovitamin E and mitophenyltertbutyline achieve concentrations in the mitochondrial matrix several-fold greater than those achieved in the cytosol because of the high negative membrane potential of the inner mitochondrial membrane. We review preliminary experiments and also some patents on cell and animal models of cardiovascular diseases where mitochondrially targeted antioxidants have been used and were shown to reduce ROS production and the effects of oxidative stress due to ROS, apoptosis and improve cardiac function. Although ongoing human clinical studies involve only non-cardiovascular applications at this time, preclinical studies show promise for eventual human trials for cardiovascular diseases.

show abstract

Oxidant injury in coronary heart disease [Part-1]

Cited by 17 publications

References 73 publications

mt-Nd2 Suppresses Reactive Oxygen Species Production by Mitochondrial Complexes I and III

mt-Nd2 Suppresses Reactive Oxygen Species Production by Mitochondrial Complexes I and III

Prooxidant-Antioxidant Balance and Antioxidized LDL Antibody Level Values and Cardiac Function in Patients with Coronary Artery Disease

Mitochondrially Targeted Antioxidants for the Treatment of Cardiovascular Diseases

Contact Info

Product

Resources

About