scispace - formally typeset
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
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.

read more

Content maybe subject to copyright    Report

Citations
More filters
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.
Journal ArticleDOI

Cycling of mercury in the environment: Sources, fate, and human health implications: A review

TL;DR: In this article, a review summarizes recent recent studies on Hg toxicity and its effects on the human health through the consumption of contaminated fish and rice since methylmercury is a potent neurotoxin and elemental Hg vapor is harmful for the central nervous system.
Journal ArticleDOI

Facile mercury detection and removal from aqueous media involving ligand impregnated conjugate nanomaterials

TL;DR: In this article, the conjugate nanomaterial (CNM) was prepared by sulfur donor containing organic ligand onto the silica substrate for simultaneous mercury (Hg(II)) ions detection and removal from water samples through a batch technique.
Journal ArticleDOI

Mercury exposure and heart diseases

TL;DR: An overview on the toxicity of mercury is reported and attention is focused on the toxic effects on the cardiovascular system.
Journal ArticleDOI

Toxicity of mercury: Molecular evidence.

TL;DR: A comprehensive review of mercurial toxic effects on wildlife and human is conducted, in particular synthesized key findings of molecular pathways involved inMercurial toxicity from the cells to human.
References
More filters
Journal ArticleDOI

The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners

TL;DR: The results of this study partly support the assumption that long-term occupational exposure to Hg0 enhances the formation of free radicals even several years after termination of occupational exposure, and could be one of the risk factors for increased lipid peroxidation.
Journal ArticleDOI

A preliminary study of mercury exposure and blood pressure in the Brazilian Amazon

TL;DR: The findings of this preliminary study add further support for Hg cardiovascular toxicity among a non-indigenous fish-eating population in the Brazilian Amazon.
Journal ArticleDOI

Low-level methylmercury exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction.

TL;DR: The results of the study indicate that a key event in the induction of T-cell apoptosis by mercuric compounds is depletion in the thiol reserve which predisposes cells to ROS damage and at the same time activates death signaling pathways.
Journal ArticleDOI

Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species, development of mitochondrial membrane permeability transition and loss of reductive reserve

TL;DR: The hypothesis that mercury potentiated reactive oxygen species (ROS) generation and that these species promoted apoptosis was tested and it was suggested that the low thiol reserve predisposes cells to ROS damage and at the same time activates death-signaling pathways.
Journal Article

Methylmercury-induced neurotoxicity in cerebral neuron culture is blocked by antioxidants and NMDA receptor antagonists.

TL;DR: Results indicate that both oxygen radicals and excitotixic amino acids are involved in the methylmercury-induced neurotoxicity of cerebral neuron cultures.
Related Papers (5)