Exposure of rats to low concentration of cigarette smoke increases myocardial sensitivity to ischaemia/reperfusion

Jaarsveld, H. van; Kuyl, J. M.; Alberts, David W.

doi:10.1007/bf00796524

Cited by 40 publications

(19 citation statements)

References 20 publications

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“…191 Rats exposed to low concentrations of passive smoke exhibited impaired mitochondrial oxidative function and increased sensitivity of hearts to ischemia/reperfusion injury. 192 Similarly, exposure to passive cigarette smoke impaired oxidative phosphorylation, diminished cytochrome oxidase activity, increased mitochondrial F 1 -ATPase protein levels, and decreased coenzyme Q levels in rabbit cardiomyocytes. 193 Acute tobacco smoke exposure, as might occur in social settings, increases the susceptibility of rat cardiac mitochondria to calcium and promotes mitochondrial permeability transition.…”

Section: Cigarette Smokingmentioning

confidence: 98%

Mitochondrial Dysfunction in Atherosclerosis

Madamanchi

Runge

2007

Circulation Research

638

492

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Abstract-Increased production of reactive oxygen species in mitochondria, accumulation of mitochondrial DNA damage, and progressive respiratory chain dysfunction are associated with atherosclerosis or cardiomyopathy in human investigations and animal models of oxidative stress. Moreover, major precursors of atherosclerosis-hypercholesterolemia, hyperglycemia, hypertriglyceridemia, and even the process of aging-all induce mitochondrial dysfunction.

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Section: Cigarette Smokingmentioning

confidence: 98%

Mitochondrial Dysfunction in Atherosclerosis

Madamanchi

Runge

2007

Circulation Research

638

492

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“…The adverse effects of cigarette smoke on mitochondrial homeostasis in lung tissue and myocardium have long been recognized and likely involve multiple components of tobacco smoke (57,160). Cigarette smoking intake reduces inner mitochondrial membrane fluidity, inhibits respiration, and reduces ATP production through a switch from mitochondrial state 3 to state 4 respiration (50,75).…”

Section: Smoking and Mitochondrial Rosmentioning

confidence: 99%

Regulation of Endothelial Function by Mitochondrial Reactive Oxygen Species

Widlansky

Gutterman

2011

Antioxidants & Redox Signaling

168

152

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Mitochondria are well known for their central roles in ATP production, calcium homeostasis, and heme and steroid biosynthesis. However, mitochondrial reactive oxygen species (ROS), including superoxide and hydrogen peroxide, once thought to be toxic byproducts of mitochondrial physiologic activities, have recently been recognized as important cell-signaling molecules in the vascular endothelium, where their production, conversion, and destruction are highly regulated. Mitochondrial reactive oxygen species appear to regulate important vascular homeostatic functions under basal conditions in a variety of vascular beds, where, in particular, they contribute to endothelium-dependent vasodilation. On exposure to cardiovascular risk factors, endothelial mitochondria produce excessive ROS in concert with other cellular ROS sources. Mitochondrial ROS, in this setting, act as important signaling molecules activating prothrombotic and proinflammatory pathways in the vascular endothelium, a process that initially manifests itself as endothelial dysfunction and, if persistent, may lead to the development of atherosclerotic plaques. This review concentrates on emerging appreciation of the importance of mitochondrial ROS as cell-signaling molecules in the vascular endothelium under both physiologic and pathophysiologic conditions. Future potential avenues of research in this field also are discussed. Antioxid. Redox Signal. 15, 1517-1530.

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“…4 -6 A role for RS in atherogenesis is supported by epidemiological evidence of links between common risk factors for coronary artery disease and increased levels of RS. [7][8][9] Among the extensively studied intracellular systems capable of generating RS in vascular cells are the NADH/NADPH oxidase, xanthine oxidase, lipoxygenase, and cyclooxygenase systems. 6,10 -12 Mitochondria are biologically important sources and targets for RS.…”

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confidence: 99%

Mitochondrial Integrity and Function in Atherogenesis

et al. 2002

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Background-Coronary atherosclerotic disease remains the leading cause of death in the Western world. Although the exact sequence of events in this process is controversial, reactive oxygen and nitrogen species (RS) likely play an important role in vascular cell dysfunction and atherogenesis. Oxidative damage to the mitochondrial genome with resultant mitochondrial dysfunction is an important consequence of increased intracellular RS. Methods and Results-We examined the contribution of mitochondrial oxidant generation and DNA damage to the progression of atherosclerotic lesions in human arterial specimens and atherosclerosis-prone mice. Mitochondrial DNA damage not only correlated with the extent of atherosclerosis in human specimens and aortas from apolipoprotein E Ϫ/Ϫ mice but also preceded atherogenesis in young apolipoprotein E Ϫ/Ϫ mice. Apolipoprotein E Ϫ/Ϫ mice deficient in manganese superoxide dismutase, a mitochondrial antioxidant enzyme, exhibited early increases in mitochondrial DNA damage and a phenotype of accelerated atherogenesis at arterial branch points. Key Words: atherosclerosis Ⅲ muscle, smooth Ⅲ antioxidants R eactive species (RS) define a collective grouping of reactive oxygen and nitrogen species that can alter the biological functions of essential molecules such as lipids, proteins, and DNA. Numerous studies have linked excess RS generation with vascular lesion formation and functional defects. [1][2][3] This association has been reported for various RS models and species. 4 -6 A role for RS in atherogenesis is supported by epidemiological evidence of links between common risk factors for coronary artery disease and increased levels of RS. [7][8][9] Among the extensively studied intracellular systems capable of generating RS in vascular cells are the NADH/NADPH oxidase, xanthine oxidase, lipoxygenase, and cyclooxygenase systems. 6,10 -12 Mitochondria are biologically important sources and targets for RS. 13,14 However, their role as mediators of oxidative disease processes such as atherogenesis has not been examined. We recently reported that exposure of vascular cells to RS in vitro results in preferential mitochondrial DNA (mtDNA) damage and dysfunction and that mtDNA damage is a very sensitive marker for RS-mediated cellular effects. 15 In addition to the potential role of mtDNA damage as a marker of ambient oxidative stress, oxidative damage to the mitochondrion can lead to decreased oxidative energetic capacity (via impaired oxidative phosphorylation) and increased generation of intracellular RS. 15-17 Thus, we hypothesized that mitochondrial dysfunction accentuates atherosclerosis by modulating the phenotype of vascular cells and that measurements of mtDNA damage reflect RS-mediated atherosclerosis risk. Conclusions-MitochondrialUsing human aortic specimens and a murine model of early atherogenesis (the apolipoprotein E null, apoE Ϫ/Ϫ ), we examined the correlation between mtDNA damage and atherogenesis and sought to determine whether mtDNA damage is a cause or an effect in this pr...

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Exposure of rats to low concentration of cigarette smoke increases myocardial sensitivity to ischaemia/reperfusion

Cited by 40 publications

References 20 publications

Mitochondrial Dysfunction in Atherosclerosis

Mitochondrial Dysfunction in Atherosclerosis

Regulation of Endothelial Function by Mitochondrial Reactive Oxygen Species

Mitochondrial Integrity and Function in Atherogenesis

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