Alterations of Arachidonate Metabolism in Cardiovascular System by Cigarette Smoking

Tai, Hsin‐Hsiung; Chang, Wen-Chang; Liu, Ying; Fukuda, Shoshi

doi:10.1007/978-1-4684-5829-9_21

Cited by 8 publications

(7 citation statements)

References 30 publications

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“…The toxicity of inhaled tobacco could by caused by a variety of compounds including reactive oxygen species, eg, causing DNA damage, 36 inhibition of the transcription nuclear factor kappa B (NFB) in human monocytes 37 and production of platelet activator factor, 38 nitric oxide modified substances, 39 glycotoxines, 40 endotoxins, 41 and substances stimulating the production of isoeicosanoids. 42 Smokers with reduced lung function comprise another group at risk for cardiovascular disease. It has been documented in prospective studies that ISP influences this risk.…”

Section: Discussionmentioning

confidence: 99%

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Lind

Engström

Stavenow

et al. 2004

ATVB

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Background-The extent to which differences in cardiovascular risk between smokers with similar daily tobacco consumption may be related to plasma levels of inflammation-sensitive proteins (ISP) and whether these proteins are associated with levels of carboxyhemoglobin (COHb%) have not been clarified. Methods and Results-In a population-based cohort of 1489 never smokers, 1685 former smokers, and 2901 current smokers, aged 28 to 61 years, plasma levels of orosomucoid (␣ 1 -acid glycoprotein), ␣ 1 -antitrypsin, haptoglobin, fibrinogen, and ceruloplasmin were measured. COHb% levels were available for 2098 of them. Incidence of myocardial infarction, stroke, and death were monitored over 18.7Ϯ4.7 years. The proportion with high ISP levels (ie, Ն2 ISP in the top quartile) increased progressively with daily tobacco consumption (PϽ0.01) and COHb% (PϽ0.01). In all smoking categories, the incidence of stroke, cardiac events, and death was related to ISP. In heavy smokers, high ISP levels were associated with adjusted relative risks of 1.57 (1.05 to 2.35) and 1.50 (1.11 to 2.03) for cardiac events and death, respectively. Corresponding figures for moderate and light smokers were 1.59 (1.13 to 2.24) and 1.14 (0.87 to 1.49), respectively, and 1.32 (0.95 to 1.85) and 1.48 (1.10 to 1.98), respectively. Key Words: stroke Ⅲ myocardial infarction Ⅲ smoking Ⅲ inflammation Ⅲ plasma proteins Ⅲ epidemiology S moking is one of the major risk factors for arteriosclerosis and its complications. [1][2][3] Yet how smoking harms the vessel wall remains controversial. The biological mechanism linking smoking and atherothrombosis is complex and not fully understood 4 and include vascular endothelial dysfunction, 5 systemic coagulation disturbances, 6 and lipid disorders. 7 It has been demonstrated in several cohort studies that the incidence of myocardial infarction and stroke are associated with plasma level of interleukin-6 (IL-6), 8 tumor necrosis factor-␣ (TNF-␣), 9 soluble intracellular adhesion molecule type 1 (ICAM-1), 10 E-selectin, 11 P-selectin, 12 high sensitive C-reactive protein (CRP), 13,14 and other inflammatory-sensitive proteins (ISP), eg, fibrinogen, orosomucoid (␣ 1 -acid glycoprotein), ␣ 1 -antitrypsin, haptoglobin, and ceruloplasmin. 15,16 Plasma levels of inflammatory markers are generally higher in smokers compared with nonsmokers. 17,18 Between smokers with equal tobacco consumption there are, however, great variations of the cardiovascular risk. This may be related to the amount of harmful components in the tobacco smoke that is absorbed into the blood. Carboxyhemoglobin (COHb%), which in prospective studies has been identified as a predictor of cardiovascular disease in smokers, 19 may vary substantially within categories defined in terms of daily consumption. Whether and how the cardiovascular risk in smokers is related to the plasma levels of ISP and whether the amount of these proteins has any relationship with the level of COHb% is largely unknown. 20 The objectives in this prospective cohort study have been to...

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Section: Discussionmentioning

confidence: 99%

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Lind

Engström

Stavenow

et al. 2004

ATVB

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“…It is well known from epidemiologic studies that the PLA 2 /AA cascade is important in the mechanism by which cigarette smoking causes heart disease (9–12); however, little work has focused on identifying specific components of cigarette smoke that are responsible for this effect. This study is the first to identify specific PAHs present in high concentrations in cigarette smoke that stimulate PLA 2 ‐mediated release of membrane fatty acids.…”

Section: Discussionmentioning

confidence: 99%

“…The biochemical cascade resulting from phospholipase A 2 (PLA 2 ) hydrolysis of arachidonic acid (AA) gives rise to more than 100 biologically active metabolites known as eicosanoids. A substantial body of evidence implicates the PLA 2 /AA cascade in the acceleration of cardiovascular disease by smoking (9–12). Compared with nonsmokers, smokers preferentially metabolize AA to thrombogenic and vasoconstrictive metabolites, including thromboxane A2 (12).…”

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confidence: 99%

“…A substantial body of evidence implicates the PLA 2 /AA cascade in the acceleration of cardiovascular disease by smoking (9–12). Compared with nonsmokers, smokers preferentially metabolize AA to thrombogenic and vasoconstrictive metabolites, including thromboxane A2 (12). Furthermore, nonsteroidal anti‐inflammatory agents and diets high in omega‐3 fatty acids (fish oils), both of which inhibit the AA cascade, attenuate the incidence of myocardial infarction in smokers (9–11).…”

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confidence: 99%

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Polycyclic aromatic hydrocarbons present in cigarette smoke cause endothelial cell apoptosis by a phospholipase A₂dependent mechanism

et al. 2002

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Smoking is a major risk factor for endothelial cell injury and subsequent coronary artery disease. Epidemiological studies implicate the phospholipase A2/arachidonic acid cascade in the mechanism by which smoking causes heart disease. However, specific components of cigarette smoke that activate this pathway have not been identified. The purpose of this study was to investigate the effects of polycyclic aromatic hydrocarbons contained in cigarette smoke on phospholipase A2 (PLA2) activity and apoptosis of human coronary artery endothelial cells. 1-methylanthracene (1-MA), phenanthrene (PA), and benzo(a)pyrene (B(a)P) caused significant release of 3H-arachidonate from endothelial cells. 1-MA and PA, but not B(a)P, also caused significant release of 3H-linoleic acid. Release of fatty acids from membrane phospholipids preceded the onset of apoptosis. 3H-arachidonate release and apoptosis induced by 1-MA, B(a)P, and PA were inhibited by methylarachidonoyl-fluorophosphonate, an inhibitor of Groups IV and VI PLA2s. Bromoenol lactone, an inhibitor of Group VI enzymes, inhibited both 3H-arachidonate release and apoptosis induced by 1-MA and PA, but not B(a)P. MJ33, an inhibitor of the acidic calcium-independent PLA2, attenuated 3H-arachidonate release and apoptosis by PA, but not 1-MA or B(a)P. The presence of Groups IV and VI and the acidic iPLA2 in endothelial cells was demonstrated by reverse transcriptase-polymerase chain reaction and Western analysis. These data suggest that 1-MA, B(a)P and PA induce apoptosis of endothelial cells by a mechanism that involves activation of these three distinct isoforms of PLA2.

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“…Little work has been carried out on the role of individual PAHs on the apoptotic cascade (Tai et al . ) (i.e. arachidonic acid (AA) by phospholipase A 2 (PLA 2 )); however, in 2002, Tithof et al .…”

Section: Introductionmentioning

confidence: 99%

Polyaromatic hydrocarbons in pollution: a heart‐breaking matter

Marris

Kompella

Miller

et al. 2020

The Journal of Physiology

121

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Air pollution is associated with detrimental effects on human health, including decreased cardiovascular function. However, the causative mechanisms behind these effects have yet to be fully elucidated. Here we review the current epidemiological, clinical and experimental evidence linking pollution with cardiovascular dysfunction. Our focus is on particulate matter (PM) and the associated low molecular weight polycyclic aromatic hydrocarbons (PAHs) as key mediators of cardiotoxicity. We begin by reviewing the growing epidemiological evidence linking air pollution to cardiovascular dysfunction in humans. We next address the pollution‐based cardiotoxic mechanisms first identified in fish following the release of large quantities of PAHs into the marine environment from point oil spills (e.g. Deepwater Horizon). We finish by discussing the current state of mechanistic knowledge linking PM and PAH exposure to mammalian cardiovascular patho‐physiologies such as atherosclerosis, cardiac hypertrophy, arrhythmias, contractile dysfunction and the underlying alterations in gene regulation. Our aim is to show conservation of toxicant pathways and cellular targets across vertebrate hearts to allow a broad framework of the global problem of cardiotoxic pollution to be established. AhR; Aryl hydrocarbon receptor. Dark lines indicate topics discussed in this review. Grey lines indicate topics reviewed elsewhere.

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Alterations of Arachidonate Metabolism in Cardiovascular System by Cigarette Smoking

Cited by 8 publications

References 30 publications

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Polycyclic aromatic hydrocarbons present in cigarette smoke cause endothelial cell apoptosis by a phospholipase A₂dependent mechanism

Polyaromatic hydrocarbons in pollution: a heart‐breaking matter

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Alterations of Arachidonate Metabolism in Cardiovascular System by Cigarette Smoking

Cited by 8 publications

References 30 publications

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Risk of Myocardial Infarction and Stroke in Smokers Is Related to Plasma Levels of Inflammation-Sensitive Proteins

Polycyclic aromatic hydrocarbons present in cigarette smoke cause endothelial cell apoptosis by a phospholipase A2dependent mechanism

Polyaromatic hydrocarbons in pollution: a heart‐breaking matter

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Polycyclic aromatic hydrocarbons present in cigarette smoke cause endothelial cell apoptosis by a phospholipase A₂dependent mechanism