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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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References
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Journal ArticleDOI

Behavior of methylmercury in mammalian erythrocytes

TL;DR: Results of gel filtration using Sephadex G-15 and thin-layer chromatography suggest that the low molecular weight substance which is bound to methylmercury in erythrocytes is glutathione (GSH).
Journal ArticleDOI

Fish intake, mercury, long-chain n-3 polyunsaturated fatty acids and risk of stroke in northern Sweden

TL;DR: It is concluded that the relationship between stroke risk and fish intake seems to be different in men and women and increased levels of EPA and DHA do not decrease the risk for stroke and there is no association between strokerisk and Hg at these low levels.
Journal ArticleDOI

Reactivity of Hg(II) with superoxide: evidence for the catalytic dismutation of superoxide by Hg(II).

TL;DR: Hg(II), despite possessing little redox activity, enhances the rate of O2- dismutation, leading to increased production of H2O2 by renal mitochondria, which may contribute to the oxidative tissue-damaging properties of mercury compounds.
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Polymorphism in high density lipoprotein paraoxonase gene and risk of acute myocardial infarction in men: prospective nested case-control study.

TL;DR: A prospective study of the role of the Met54Leu polymorphism on the risk of acute myocardial infarction in healthy men from eastern Finland, carried out among participants in the Kuopio ischaemic heart disease risk factor study.
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Mortality from cardiovascular diseases and exposure to inorganic mercury

TL;DR: The study suggests a possible association between employment in mercury mining and refining and risk in some groups of cardiovascular diseases.
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