Oxygen Free Radicals, Lipid Metabolism, and Whole Blood and Plasma Viscosity in the Prevention and Treatment of Human Cardiovascular Diseases

Mózsik, Gy.; Fiegler, M.; Juricskay, I.; Mezey, B.; Toth, K M

doi:10.1159/000421440

Cited by 4 publications

(3 citation statements)

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“…Free radicals are generated continuously; however, protective mechanisms in the body regulate their concentration leading to a well-balanced equilibrium [ 18 ]. Once this balance is compromised, an oxidative stress state occurs which associates with various pathophysiological conditions including autoimmune diseases, hypertension, cancer, diabetes, atherosclerosis, coronary heart disease, and heart failure [ 19 , 20 ]. This is not surprising as ROS production is intimately associated with aberrant inflammatory signalling, elevated platelet activation, and increased leukocyte recruitment to the site of inflammation [ 21 – 23 ].…”

Section: Introductionmentioning

confidence: 99%

Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

Kobeissy

Shaito

Kaplan

et al. 2017

Oxidative Medicine and Cellular Longevity

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Cigarette smoking (S) is a risk factor for progressive chronic kidney disease, renal dysfunction, and renal failure. In this study, the effect of smoking on kidney function was investigated in a mouse model of myocardial infarction (MI) using 4 groups: control (C), smoking (S), MI, and S+MI. Histological analysis of S+MI group showed alterations in kidney structure including swelling of the proximal convoluted tubules (PCTs), thinning of the epithelial lining, focal loss of the brush border of PCTs, and patchy glomerular retraction. Molecular analysis revealed that nephrin expression was significantly reduced in the S+MI group, whereas sodium-hydrogen exchanger-1 (NHE-1) was significantly increased, suggesting altered glomerular filtration and kidney functions. Moreover, S+MI group, but not S alone, showed a significant increase in the expression of connective tissue growth factor (CTGF) and fibrotic proteins fibronectin (FN) and α-smooth muscle actin (SMA), in comparison to controls, in addition to a significant increase in mRNA levels of IL-6 and TNF-α inflammatory markers. Finally, reactive oxygen species (ROS) production was significantly accentuated in S+MI group concomitant with a significant increase in NOX-4 protein levels. In conclusion, smoking aggravates murine acute renal damage caused by MI at the structural and molecular levels by exacerbating renal dysfunction.

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Section: Introductionmentioning

confidence: 99%

Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

Kobeissy

Shaito

Kaplan

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…While some suggestions have been advanced in this regard, e.g. oxygen free radicals, environmental stress, metabolic dysfunctions [1–3], to date no mechanism has been universally accepted. A particular opportunity to further understand the pathophysiology lies in the observation that often a shift in rheological properties of blood is accompanied by co-morbidities that are not necessarily directly derived from blood rheological mechanisms and a compromised blood perfusion that may be linked to them.…”

Section: Introductionmentioning

confidence: 99%

Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome. Early forms of autodigestion

Mazor

Schmid‐Schönbein

2016

BIR

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Abnormal blood rheological properties seldom occur in isolation and instead are accompanied by other complications, often designated as co-morbidities. In the metabolic syndrome with complications like hypertension, diabetes and lack of normal microvascular blood flow, the underlying molecular mechanisms that simultaneously lead to elevated blood pressure and diabetes as well as abnormal microvascular rheology and other cell dysfunctions have remained largely unknown. In this review, we propose a new hypothesis for the origin of abnormal cell functions as well as multiple co-morbidities. Utilizing experimental models for the metabolic disease with diverse co-morbidities we summarize evidence for the presence of an uncontrolled extracellular proteolytic activity that causes ectodomain receptor cleavage and loss of their associated cell function. We summarize evidence for unchecked degrading proteinase activity, e.g. due to matrix metalloproteases, in patients with hypertension, Type II diabetes and obesity, in addition to evidence for receptor cleavage in the form of receptor fragments and decreased extracellular membrane expression levels. The evidence suggest that a shift in blood rheological properties and other co-morbidities may in fact be derived from a common mechanism that is due to uncontrolled proteolytic activity, i.e. an early form of autodigestion. Identification of the particular proteases involved and the mechanisms of their activation may open the door to treatment that simultaneously targets multiple co-morbidities in the metabolic syndrome.

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“…Harrison et al and others demonstrated an association between the intensity of oxidative stress and the extent and severity of coronary artery disease, vascular disease development, atherosclerosis and hypertension (Harrison et al, 2003; Vassalle et al, 2004). Furthermore, oxidative stress is also implicated in various other illnesses that include autoimmune diseases, malignancy, emphysema, and chronic obstructive lung disease (Mózsik et al, 1992; Brownlee, 2001). Various drinks and fruit juices can be a great source of different exogenous antioxidants due to their high content of polyphenols.…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoking-Induced Cardiac Hypertrophy, Vascular Inflammation and Injury Are Attenuated by Antioxidant Supplementation in an Animal Model

et al. 2016

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Background: Cardiovascular diseases are the leading causes of morbidity and mortality worldwide. Cigarette smoking remains a global health epidemic with associated detrimental effects on the cardiovascular system. In this work, we investigated the effects of cigarette smoke exposure on cardiovascular system in an animal model. The study then evaluated the effects of antioxidants (AO), represented by pomegranate juice, on cigarette smoke induced cardiovascular injury. This study aims at evaluating the effect of pomegranate juice supplementation on the cardiovascular system of an experimental rat model of smoke exposure.Methods: Adult rats were divided into four different groups: Control, Cigarette smoking (CS), AO, and CS + AO. Cigarette smoke exposure was for 4 weeks (5 days of exposure/week) and AO group received pomegranate juice while other groups received placebo. Assessment of cardiovascular injury was documented by assessing different parameters of cardiovascular injury mediators including: (1) cardiac hypertrophy, (2) oxidative stress, (3) expression of inflammatory markers, (4) expression of Bradykinin receptor 1 (Bdkrb1), Bradykinin receptor 2 (Bdkrb2), and (5) altered expression of fibrotic/atherogenic markers [(Fibronectin (Fn1) and leptin receptor (ObR))].Results: Data from this work demonstrated that cigarette smoke exposure induced cardiac hypertrophy, which was reduced upon administration of pomegranate in CS + AO group. Cigarette smoke exposure was associated with elevation in oxidative stress, significant increase in the expression of IL-1β, TNFα, Fn1, and ObR in rat's aorta. In addition, an increase in aortic calcification was observed after 1 month of cigarette smoke exposure. Furthermore, cigarette smoke induced a significant up regulation in Bdkrb1 expression level. Finally, pomegranate supplementation exhibited cardiovascular protection assessed by the above findings and partly contributed to ameliorating cardiac hypertrophy in cigarette smoke exposed animals.Conclusion: Findings from this work showed that cigarette smoking exposure is associated with significant cardiovascular pathology such as cardiac hypertrophy, inflammation, pro-fibrotic, and atherogenic markers and aortic calcification in an animal model as assessed 1 month post exposure. Antioxidant supplementation prevented cardiac hypertrophy and attenuated indicators of atherosclerosis markers associated with cigarette smoke exposure.

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Oxygen Free Radicals, Lipid Metabolism, and Whole Blood and Plasma Viscosity in the Prevention and Treatment of Human Cardiovascular Diseases

Cited by 4 publications

References 0 publications

Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome. Early forms of autodigestion

Cigarette Smoking-Induced Cardiac Hypertrophy, Vascular Inflammation and Injury Are Attenuated by Antioxidant Supplementation in an Animal Model

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