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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

Association of urinary metal concentrations with blood pressure and serum hormones in Spanish male adolescents

TL;DR: It is suggested that combined exposure to toxic metals, especially As and Cd, may contribute to BP elevation in male adolescents and that exposure to Hg, As, Cc, Ni, Pb, and Cr may affect their hormone levels.
Journal ArticleDOI

Mercury exposure, cardiovascular disease, and mortality: A systematic review and dose-response meta-analysis.

TL;DR: Chronic exposure to Hg was associated with an increased risk of all-cause mortality and fatal/nonfatal IHD and a heterogeneous relationship was found between studies reporting fatal and nonfatal outcomes and between cohort and non-cohort studies.
Journal ArticleDOI

High selenium exposure lowers the odds ratios for hypertension, stroke, and myocardial infarction associated with mercury exposure among Inuit in Canada.

TL;DR: Evidence is provided that inuit living in the Arctic have high exposure to both Se and Hg through their marine mammal and fish rich traditional diet and that Se may exhibit a protective effect against Hg on cardiovascular disease.
Journal ArticleDOI

Effect of particulate matter-bound metals exposure on prothrombotic biomarkers: A systematic review.

TL;DR: Results support the hypothesis that exposure to inhalable metals, as elemental compounds in particulate matter, cause changes or activation of a number of human prothrombotic hemostatic biomarkers leading to venous thromboembolism.
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

Journal ArticleDOI

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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