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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

Experimentally induced lipid peroxidation after exposure to chromium, mercury or silver: interactions with carbon tetrachloride.

TL;DR: Exposure of mice to chromium, mercury, or silver and another stimulator of lipid peroxidation, carbon tetrachloride, showed synergism between inorganic mercury and CCl4, but pre-exposure to these metals at selected doses did not enhance CCl 4-toxicity as measured by organ content of MDA.
Journal ArticleDOI

Lipid peroxidation in liver of rats administrated with methyl mercuric chloride.

TL;DR: The results of this study implicate that the lipid peroxidation is one of the molecular mechanisms for cell injury in acute CH3HgCl poisoning.
Journal ArticleDOI

Effect of supplementation with organic selenium on mercury status as measured by mercury in pubic hair.

TL;DR: The study indicates that mercury accumulation in pubic hair can be reduced by dietary supplementation with small daily amounts of organic selenium in a short range of time.
Journal ArticleDOI

Mercury activates vascular endothelial cell phospholipase D through thiols and oxidative stress.

TL;DR: It is revealed that mercury induced the activation of PLD in the vascular ECs wherein cellular thiols and oxidative stress acted as signal mediators for the enzyme activation.
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