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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

Volcanoes, medicine, and monasticism: Investigating mercury exposure in medieval Iceland

TL;DR: The conclusion is that a variety of factors from medical treatment to scholarly work lead to mercury exposure at Skriðuklaustur, whereas at Skeljastaðir, volcanogenic emissions are implicated.
Journal ArticleDOI

Plasma microRNAs expression profile in female workers occupationally exposed to mercury

TL;DR: Plasma miR-92a-3p and mi-486-5p might prove to be potential biomarkers to indicate responses to mercury exposure, however, further studies are necessary to prove the causal association between miRNAs changes and mercury Exposure, and to determine whether these two mi RNAs are clear biomarkersto mercury exposure.
Journal ArticleDOI

Amelioration of acute mercury toxicity by a novel, non-toxic lipid soluble chelator N,N′bis-(2-mercaptoethyl)isophthalamide: effect on animal survival, health, mercury excretion, and organ accumulation

TL;DR: A chelator, N,N′-bis(2-mercaptoethyl)isophthalamide (NBMI), is reported on and it is shown that it prevented the toxic effects associated with acute exposure induced by injected mercury chloride.
Journal ArticleDOI

Mercury Toxicity and Detection Using Chromo-Fluorogenic Chemosensors.

TL;DR: The chromo-fluorogenic chemosensors possess the attractive analytical parameters of low-cost, enhanced detection ability with high sensitivity, simplicity, rapid on-site monitoring ability, etc..
Journal ArticleDOI

An “off–on” optical sensor for mercury ion detection in aqueous solution and living cells

TL;DR: In this article, a rhodamine-based optical sensor was developed for selective detection of Hg2+ in aqueous solution as well as in living cells, which showed marked sensitivity and selectivity with a chelation-induced “off-on” response in acetonitrile (ACN)/MOPS buffer (10mM, pH 7.3, v/v, 1:1).
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 - 
TL;DR: Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit and vitamin E had no benefit and its effects on fatal cardiovascular events require further exploration.
Journal ArticleDOI

Environmental Health Criteria

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Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (dart)

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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