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Cardiovascular Diseases & Diagnosis

ISSN: 2329-9517

Open Access

The Role of Mercury in Cardiovascular Disease

Abstract

Mark C. Houston

Mercury toxicity is highly correlated with hypertension, coronary heart disease (CHD), myocardial infarction (MI), stroke and other cardiovascular disease. Mercury has a high affinity for sulfhydryl (-SH) groups, which inactivates numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants [NAC (n-acetyl cysteine, ALA (alpha lipoic acid), GSH (glutathione)], with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitutes for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation. Selenium and fish containing omega 3 fatty acids or omega 3 fatty acids supplements with DHA and EPA antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress, inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction and hypertrophy, endothelial dysfunction, dyslipidemia, immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, cardiac arrhythmias, reduced heart rate variability, increased carotid IMT and carotid artery obstruction, CVA, generalized atherosclerosis, renal dysfunction, renal insufficiency and proteinuria. Pathological and biochemical findings correlate with the clinical manifestations of mercury toxicity. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates COMT (catecholamine 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, CHD, MI, CVD, CVA or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine and serum should be done with both baseline and provocation methods.

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