scholarly journals The Influence of Arsenic, Lead, and Mercury on the Development of Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Peter Jennrich
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Cardiovascular Effects ◽  
Hazardous Substances ◽  
Priority List ◽  
Heart Study ◽  
Potential Toxic Metals ◽  
Environmental Toxin ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

As a group, cardiovascular disease (CVD) is the leading cause of death worldwide. It killed twice as many people as infectious and parasitic disease and three times as many people as all forms of cancer. There are other crucial risk factors next to the major risk factors identified by the Framingham Heart Study. In the last few years, detailed studies showed the correlation between environmental pollution and the development of CVD. The question, which environmental toxin is particularly harmful, is answered by CERCLA Priority List of Hazardous Substances with the following toxins: arsenic, lead, and mercury. The effect of these potential toxic metals on the development of cardiovascular diseases includes pathomechanisms as the accumulation of free radicals, damage of endothelial nitric oxide synthase, lipid peroxidation, and endocrine influences. This leads to the damage of vascular endothelium, atherosclerosis, high blood pressure, and an increased mortality from cardiovascular diseases. The cardiovascular effects of arsenic, lead, and mercury exposure and its impact on cardiovascular mortality need to be included in the diagnosis and the treatment of CVD.

scholarly journals Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 377
Author(s):  
Yunna Lee ◽  
Eunok Im
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Natural Antioxidants ◽  
Sirtuin 1 ◽  
Potential Benefits ◽  
New Perspective ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial dysfunction. Recently, considerable evidence has highlighted an important role played by the synergistic interaction between endothelial nitric oxide synthase (eNOS) and sirtuin 1 (SIRT1) in the maintenance of endothelial function. To provide a new perspective on the role of natural antioxidants against CVDs, we focused on microRNAs (miRNAs), which are important posttranscriptional modulators in human diseases. Several miRNAs are regulated via the consumption of natural antioxidants and are related to the regulation of oxidative stress by targeting eNOS and/or SIRT1. In this review, we have discussed the specific molecular regulation of eNOS/SIRT1-related endothelial dysfunction and its contribution to CVD pathologies; furthermore, we selected nine different miRNAs that target the expression of eNOS and SIRT1 in CVDs. Additionally, we have summarized the alteration of miRNA expression and regulation of activities of miRNA through natural antioxidant consumption.

scholarly journals Crystallization and preliminary X-ray crystallographic analysis of the ArsM arsenic(III)S-adenosylmethionine methyltransferase

2010 ◽  
Vol 66 (9) ◽  
pp. 1050-1052 ◽  
Author(s):  
Kavitha Marapakala ◽  
A. Abdul Ajees ◽  
Jie Qin ◽  
Banumathi Sankaran ◽  
Barry P. Rosen
Keyword(s):  
Crystallographic Analysis ◽  
Hazardous Substances ◽  
Diffusion Method ◽  
Monoclinic Space Group ◽  
Hanging Drop ◽  
Unit Cell Parameters ◽  
Priority List ◽  
X Ray ◽  
Cell Parameters ◽  
Environmental Toxin

Arsenic is the most ubiquitous environmental toxin and carcinogen and consequently ranks first on the Environmental Protection Agency's Superfund Priority List of Hazardous Substances. It is introduced primarily from geochemical sources and is acted on biologically, creating an arsenic biogeocycle. A common biotransformation is methylation to monomethylated, dimethylated and trimethylated species. Methylation is catalyzed by the ArsM (or AS3MT) arsenic(III)S-adenosylmethionine methyltransferase, an enzyme (EC 2.1.1.137) that is found in members of every kingdom from bacteria to humans. ArsM from the thermophilic algaCyanidioschyzonsp. 5508 was expressed, purified and crystallized. Crystals were obtained by the hanging-drop vapor-diffusion method. The crystals belonged to the monoclinic space groupC2, with unit-cell parametersa= 84.85,b= 46.89,c= 100.35 Å, β = 114.25° and one molecule in the asymmetric unit. Diffraction data were collected at the Advanced Light Source and were processed to a resolution of 1.76 Å.

scholarly journals Effects of Endothelial Nitric Oxide Synthase, Interleukin-6 Gene Polymorphisms and Asymmetric Dimethylarginine Levels on Risk Factors and Lesion Sites in Peripheral Artery Disease

2009 ◽  
Vol 37 (4) ◽  
pp. 1003-1010
Author(s):  
AK Tuygun ◽  
M Keser ◽  
A Tuygun ◽  
B Ketenci ◽  
Y Şensöz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Gene Polymorphisms ◽  
Asymmetric Dimethylarginine ◽  
Peripheral Artery ◽  
Artery Disease ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

This study investigated risk factors for atherosclerosis and their relationship with lesion sites. Patients ( n = 160) with peripheral artery disease (PAD) completed a questionnaire regarding risk factors for PAD. Endothelial nitric oxide synthase (eNOS) and interleukin (IL)-6 gene polymorphisms and asymmetric dimethylarginine (ADMA) levels were measured. Patients with coronary artery disease had significantly higher ratios of eNOS T/C and C/C genotypes, which include the C allele, than the T/T genotype. The IL-6 gene polymorphism distribution ratios for patients with over four risk factors were significantly different compared with other patients, with a higher rate of the C/C genotype. ADMA levels did not show any significant relationship to risk factors or polymorphism. Levels were, however, slightly higher in femoral lesion sites. The results support a model in which the C/C genotype of eNOS and IL-6 gene polymorphisms promote PAD development. The eNOS C/C genotype may have an independent effect, whereas the effects of the IL-6 C/C genotype are seen in conjunction with other risk factors.

scholarly journals New Therapeutic Implications of Endothelial Nitric Oxide Synthase (eNOS) Function/Dysfunction in Cardiovascular Disease

2019 ◽  
Vol 20 (1) ◽  
pp. 187 ◽  
Author(s):  
Andreas Daiber ◽  
Ning Xia ◽  
Sebastian Steven ◽  
Matthias Oelze ◽  
Alina Hanf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Risk Factors ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Enos Activity ◽  
Life Style Changes ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The Global Burden of Disease Study identified cardiovascular risk factors as leading causes of global deaths and life years lost. Endothelial dysfunction represents a pathomechanism that is associated with most of these risk factors and stressors, and represents an early (subclinical) marker/predictor of atherosclerosis. Oxidative stress is a trigger of endothelial dysfunction and it is a hall-mark of cardiovascular diseases and of the risk factors/stressors that are responsible for their initiation. Endothelial function is largely based on endothelial nitric oxide synthase (eNOS) function and activity. Likewise, oxidative stress can lead to the loss of eNOS activity or even “uncoupling” of the enzyme by adverse regulation of well-defined “redox switches” in eNOS itself or up-/down-stream signaling molecules. Of note, not only eNOS function and activity in the endothelium are essential for vascular integrity and homeostasis, but also eNOS in perivascular adipose tissue plays an important role for these processes. Accordingly, eNOS protein represents an attractive therapeutic target that, so far, was not pharmacologically exploited. With our present work, we want to provide an overview on recent advances and future therapeutic strategies that could be used to target eNOS activity and function in cardiovascular (and other) diseases, including life style changes and epigenetic modulations. We highlight the redox-regulatory mechanisms in eNOS function and up- and down-stream signaling pathways (e.g., tetrahydrobiopterin metabolism and soluble guanylyl cyclase/cGMP pathway) and their potential pharmacological exploitation.

scholarly journals Modulating endothelial nitric oxide synthase: a new cardiovascular therapeutic strategy

2011 ◽  
Vol 301 (3) ◽  
pp. H634-H646 ◽  
Author(s):  
Yixuan Zhang ◽  
Stefan P. Janssens ◽  
Kirstin Wingler ◽  
Harald H. H. W. Schmidt ◽  
An L. Moens
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Diseases ◽  
Endothelial Nitric Oxide Synthase ◽  
Therapeutic Strategy ◽  
No Synthase ◽  
Superoxide Formation ◽  
No Signaling ◽  
No Bioavailability ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The pathogenesis of many cardiovascular diseases is associated with reduced nitric oxide (NO) bioavailability and/or increased endothelial NO synthase (eNOS)-dependent superoxide formation. These findings support that restoring and conserving adequate NO signaling in the heart and blood vessels is a promising therapeutic intervention. In particular, modulating eNOS, e.g., through increasing the bioavailability of its substrate and cofactors, enhancing its transcription, and interfering with other modulators of eNOS pathway, such as netrin-1, has a high potential for effective treatments of cardiovascular diseases. This review provides an overview of the possibilities for modulating eNOS and how this may be translated to the clinic in addition to describing the genetic models used to study eNOS modulation.

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