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Journal ArticleDOI

Role of mercury toxicity in hypertension, cardiovascular disease, and stroke

Mark C. Houston
- 01 Aug 2011 - 
- Vol. 13, Iss: 8, pp 621-627
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TLDR
This poster presents a probabilistic procedure to assess the importance of baseline IgE levels in the decision-making process and shows clear patterns in response to known immune-inflammatory events.
Abstract
Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alpha-lipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.

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Journal ArticleDOI

Transcriptional Induction of Metallothionein by Tris(pentafluorophenyl)stibane in Cultured Bovine Aortic Endothelial Cells

TL;DR: The present data suggest that the original role of MT-1 is to protect cells from heavy metal toxicity and oxidative stress in the biological defense system, while that ofMT-2 is to regulate intracellular zinc metabolism.
Journal ArticleDOI

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies.

TL;DR: Heavy metals in small vessels are strongly associated with the development as well as the progression of CSVD, and Chelation therapy may be an effective strategy to reduce the toxic metal load and the associated complications.
Journal ArticleDOI

The effects of chemical mixtures on lipid profiles in the Korean adult population: threshold and molecular mechanisms for dyslipidemia involved

TL;DR: Mixed chemicals interacted with the PPARA gene and were linked with dyslipidemia, and the overall effect of the chemical mixture was significantly associated with HDL-C, triglycerides, total cholesterol, and total lipids.
Journal ArticleDOI

Relationship between Blood Mercury Level and Risk of Cardiovascular Diseases: Results from the Fourth Korea National Health and Nutrition Examination Survey (KNHANES IV) 2008-2009.

TL;DR: It is suggested that mercury in the blood may be associated with an increased risk of hypertension and myocardial infarction or angina in the general Korean population.
Journal ArticleDOI

Effect of Selenium on the Levels of Cytokines and Trace Elements in Toxin-Mediated Oxidative Stress in Male Rats.

TL;DR: A significant increase in the serum levels of inflammatory cytokines IL-6, TNF-α, and IL-10 after administration of Se seemed to counteract some of the damage, as indicated by differences in the plasma concentrations of major elements.
References
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Journal ArticleDOI

Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial

Roberto Marchioli
- 07 Aug 1999 - 
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Journal ArticleDOI

Environmental Health Criteria

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TL;DR: A modest intake of fatty fish (two or three portions per week) may reduce mortality in men who have recovered from MI.
Journal Article

The Environmental Protection Agency

TL;DR: A case study explores the background of the digitization project, the practices implemented, and the critiques of the project, which aims to provide access to a plethora of information to EPA employees, scientists, and researchers.
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