Reactive Oxygen Species Are Involved in Smoking-Induced Dysfunction of Nitric Oxide Biosynthesis and Upregulation of Endothelial Nitric Oxide Synthase

Barua, Rajat S.; Ambrose, John A.; Srivastava, Sudhesh; DeVoe, Mary C.; Eales-Reynolds, Lesley-Jane

doi:10.1161/01.cir.0000066691.52789.be

Cited by 205 publications

(97 citation statements)

References 28 publications

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“…After “validating” our model, we first sought to investigate the impact of e‐cigarettes on thrombogenesis, as it is the major cause of tobacco‐induced CVD,38 including thrombosis‐based diseases 17, 77, 78, 79, 80, 81, 82, 83. Our findings revealed, for the first time, a drastic reduction in the time for carotid artery occlusion, indicating a prothrombotic phenotype, even after only a week of whole‐body exposure to e‐cigarettes.…”

Section: Discussionmentioning

confidence: 99%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

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BackgroundCardiovascular disease is the main cause of death in the United States, with smoking being the primary preventable cause of premature death, and thrombosis being the main mechanism of cardiovascular mortality in smokers. Due to the perception that electronic/e‐cigarettes are “safer/less harmful” than conventional cigarettes, their usage—among a variety of ages—has increased tremendously during the past decade. Notably, there are limited studies regarding the negative effects of e‐cigarettes on the cardiovascular system, which is also the subject of significant debate.Methods and ResultsWe employed a passive e‐VapeTM vapor inhalation system and developed an in vivo whole‐body e‐cigarette mouse exposure protocol that mimics real‐life human exposure scenarios/conditions and investigated the effects of e‐cigarettes and clean air on platelet function and thrombogenesis. Our results show that platelets from e‐cigarette–exposed mice are hyperactive, with enhanced aggregation, dense and α granule secretion, activation of the αIIbβ3 integrin, phosphatidylserine expression, and Akt and ERK activation, when compared with clean air–exposed platelets. E‐cigarette–exposed platelets were also found to be resistant to inhibition by prostacyclin, relative to clean air. Furthermore, the e‐cigarette–exposed mice exhibited a shortened thrombosis occlusion and bleeding times.ConclusionsTaken together, our data demonstrate for the first time that e‐cigarettes alter physiological hemostasis and increase the risk of thrombogenic events. This is attributable, at least in part, to the hyperactive state of platelets. Thus, the negative health consequences of e‐cigarette exposure should not be underestimated and warrant further investigation.

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Section: Discussionmentioning

confidence: 99%

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Qasim

Karim

Silva‐Espinoza

et al. 2018

JAHA

100

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“…19 Studies have shown altered endothelial function by changes in nitric oxide biosynthesis when exposed to smoking and confirmed that oxidative stress has a central role in smoking-mediated dysfunction of nitric oxide biosynthesis in endothelial cells. 22 Alcohol intake, on the other hand, reduces glutathione production, causing increased levels of H 2 O 2 , which in turn reacts with transition metals in the mitochondria of the cells and contributes to oxidative stress. Glutathione in the mitochondria is the only protection available to metabolize H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

et al. 2011

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Many mechanisms, including oxidative stress, contribute to hypertension. This study investigated the possible associations between oxidative stress, blood pressure and arterial stiffness in black South Africans. Ambulatory blood pressure measurements were taken for 101 black South African men and 99 women. The stiffness indices included ambulatory arterial stiffness index (AASI) and pulse pressure (PP). Reactive oxygen species (ROS) levels (Po0.0001) were higher in the African women compared with men. ROS levels were also higher in hypertensive compared with normotensive men. The 24 h systolic blood pressure (SBP; Po0.01), 24 h diastolic blood pressure (DBP; Po0.0001) and pulse wave velocity (PWV; Po0.01) were significantly higher in African men compared with women. There were unadjusted positive associations of 24 h SBP (r ¼ 0.33; P ¼ 0.001), 24 h DBP (r ¼ 0.26; P ¼ 0.008) and 24 h PP (r ¼ 0.29; P ¼ 0.003) with ROS in African men only. A positive association between AASI and ROS existed only in hypertensive men (r ¼ 0.27; P ¼ 0.035), but became nonsignificant (B ¼ 0.0014; P ¼ 0.14) after adjustments. Adjusted, positive associations of 24 h SBP (B ¼ 0.181; P ¼ 0.018) and 24 h PP (B ¼ 0.086; P ¼ 0.050) with ROS were again only evident in African men. ROS is positively associated with SBP and PP in African men, suggesting that increased ROS levels may contribute to hypertension in this population group.

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“…25 Human endothelial cells exposed to sera from smokers have decreased nitric oxide availability despite increased nitric oxide synthase expression, with scavenging of nitric oxide by increased reactive oxygen species generation. 26,27 Smokingassociated endothelial dysfunction can be ameliorated by 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A (CoA) reductase inhibitor therapy independently of changes in lipid levels, 28 by supplementation with tetrahydrobiopterin, 26 and by xanthine oxidase inhibition with allopurinol. 29 Monocytes isolated from smokers demonstrate increased adherence to endothelial cells, which is corrected by vitamin C therapy.…”

Section: Smoking-related Vascular Inflammation and Oxidative Stressmentioning

confidence: 99%

Smoking, Metalloproteinases, and Vascular Disease

Perlstein

Lee

2006

ATVB

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Abstract-Smoking causes up to 11% of total global cardiovascular deaths. Smoking has numerous effects that may promote atherosclerosis through vascular inflammation and oxidative stress, but the pathogenesis of smoking-related cardiovascular disease remains incompletely understood. The matrix metalloproteinases, a family of endopeptidases that can degrade extracellular matrix components in both physiological and pathophysiological states, play an important role in smoking-associated chronic obstructive pulmonary disease, the second leading cause of smoking attributable mortality. Emerging evidence indicates that the matrix metalloproteinases may also contribute to smoking-related vascular disease. Here we discuss the potential relationship between smoking, matrix metalloproteinases, and acceleration of vascular disease.

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Reactive Oxygen Species Are Involved in Smoking-Induced Dysfunction of Nitric Oxide Biosynthesis and Upregulation of Endothelial Nitric Oxide Synthase

Cited by 205 publications

References 28 publications

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

Smoking, Metalloproteinases, and Vascular Disease

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