There is a vast body of research which demonstrates the effect that mercury has on the heart. One of the ways that this may be mediated is that cardiac function relies strongly on the use of selenium.  Mercury specifically binds selenium.

Marked Elevation of Myocardial Trace Elements in Idiopathic Dilated Cardiomyopathy Compared With Secondary Dysfunction

Frustaci, A., Magnavita, N., Chimenti, C., Caldarulo, M., Sabbioni, E., Pietra, R., Cellini, C., Possati, G.F. and Maseri, A. Department of Cardiology, Department of Occupational Medicine, and Department of Cardiac Surgery, Catholic University, Rome Italy and CEC 4Environmental Institute Joint  Research Center Ispra, Rome, Italy  Journal of the American College of Cardiology Vol. 33, No. 6, 1999, pp. 1578-1583

Objectives: We sought to investigate the possible pathogenic role of myocardial trace elements (TE) in patients with various forms of cardiac failure.

Background: Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy.

Methods: Myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE. One muscular and one left ventricular (LV) endomyocardial specimen from each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of LV dysfunction; 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function, and 3) LV endomyocardial biopsies from four normal subjects.

Results: A large increase (>10,000 times for mercury and antimony) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM. Patients with secondary cardiac dysfunction had mild increase (<5 times) of myocardial TE and normal muscular TE. In particular, in pts with IDCM mean mercury concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g), gold 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 ng/g) and cobalt 4 times (86.5 ng/g vs. 20 ng/g) higher than in control subjects.

Conclusions: A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.

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Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine.

Vassallo DV, Moreira CM, Oliveira EM, Bertollo DM, Veloso TC Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, ES, Brazil. Toxicol Appl Pharmacol 1999 Apr 15;156(2):113-8

The protective effects of dithiothreitol (DTT, 50 &mgr;M) and cysteine (CYS, 100 &mgr;M) against toxic effects of HgCl2 (1, 2.5, 5, and 10 &mgr;M) were studied in isolated, isometrically contracting rat papillary muscles. Force reduction promoted by Hg2+ was prevented by both DTT and CYS. Also, after both treatments, no significant changes in dF/dt were observed. A progressive reduction in the time to peak tension was observed when increased concentrations of HgCl2 were used after CYS and DTT treatment. This was an indication that the enhancement of calcium release from the sarcoplasmic reticulum produced by mercury was not affected by DTT and CYS. Tetanic contractions were also studied. After treatment with DTT or CYS tetanic tension did not change. No significant reduction of tetanic tension was observed during treatment with 1 &mgr;M Hg2+ but its reduction was observed after 5 &mgr;M Hg2+. Myosin ATPase activity was also affect by Hg2+, being completely blocked by 1 &mgr;M Hg2+ and reduced by 50% with 0.15 &mgr;M Hg2+. Full activity was restored by using 500 nM DTT. These findings suggest that several but not all toxic effects of Hg2+ on the mechanical activity of the heart muscle are prevented by protectors of SH groups such as DTT and CYS. The enhancement of the Ca2+ release from the sarcoplasmic reticulum by Hg2+ during activation was not affected by prior treatment with DTT and CYS, suggesting that interactions with SH groups may not be important for the activation of the Ca2+ channel of the sarcoplasmic reticulum. Copyright 1999 Academic Press.

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The chamber exposure of laboratory rats to metal oxides originating from metal producing industry.

Kovacikova Z, Chorvatovicova D    Physiol Res 1997;46(1):41-5

Institute of Preventive and Clinical Medicine, Slovak Academy of Sciences, Bratislava, Slovak Republic.

Laboratory rats were exposed to the inhalation of dust from an agglomeration unit which is the greatest contributor to dust pollution in the vicinity of a mercury producing plant. The exposure lasted for 6 months (4 hours daily, 5 days per week), the concentration of aerosol in the chamber was 10 mg x m(-3). After finishing the exposure, the animals were examined and compared with the controls which were held under standard laboratory conditions. The number of alveolar macrophages was highly elevated (P< 0.001) in the exposed animals, Mg2+ ATPase activity in the heart muscle was decreased. The alanine aminotransferase activity in the serum was not changed, the aspartate aminotransferase was slightly enhanced. No differences in the frequency of abnormal sperm and in the frequency of polychromatic erythrocytes in bone marrow were detected.

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Mercury effects on the contractile activity of isolated heart muscle.

Oliveira EM, Vassallo DV, Sarkis JJ, Mill JG Toxicol Appl Pharmacol 1994 Sep;128(1):86-91 Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.

The toxic effects of HgCl2 (1, 2.5, 5, and 10 microM) were studied in isolated, isometrically contracting rat papillary muscles and frog ventricular strips. In rat papillary muscles 1 microM Hg2+ produced a small increase in the force of contraction. Higher concentrations of HgCl2 produced a dose-dependent decrease in contractile force. The rate of force development was affected differently, increasing at 1 and 2.5 microM Hg2+ and decreasing to control levels at 5 and 10 microM Hg2+. This was the result of a progressive reduction in the time to peak tension observed when HgCl2 concentrations increased. This effect probably reflects the binding of Hg2+ to SH groups inducing Ca2+ release from the sarcoplasmic reticulum. The relative potentiation of postrest contractions was used as an index of sarcoplasmic reticulum activity. It was measured after pauses of increasing duration and was reduced at concentrations of 1 microM Hg2+ when compared to that of the control. A further decrement in the relative potentiation was observed with higher Hg2+ concentrations, indicating that the activity of the sarcoplasmic reticulum was depressed by mercury in a dose-dependent manner. Tetanic contractions were also studied in the rat myocardium. The tetanic tension did not change during treatment with 1 microM Hg2+ but decreased with 5 microM Hg2+, suggesting a toxic effect on the contractile proteins only at high Hg2+ concentrations. Frog ventricular strips were studied using the same HgCl2 concentrations and no effects on either force or relative potentiation were observed. These findings suggest that Hg2+ promotes dose-dependent toxic effects on heart muscle via actions on the sarcolemma, the sarcoplasmic reticulum, and contractile proteins.

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Mercury compounds: lipophilicity and toxic effects on isolated myocardial tissue.

Halbach S   Arch Toxicol 1990;64(4):315-9

Gesellschaft fur Strahlen- und Umweltforschung, Institut fur Toxikologie, Neuherberg, Federal Republic of Germany.

Lipophilicity is suggested to modulate the diffusion and the cytotoxic effects of mercury compounds. To investigate this, the positive inotropic effect of four Hg compounds (HgCl2, CH3HgCl, chlormerodrin, bromomercurihydroxypropane) was studied in catecholamine-depleted isolated heart muscle preparations. The rate of development of the positive effect was inversely correlated to the concentration in the case of HgCl2 and chlormerodrin, i.e. the product of concentration (c) and time to half-maximal effect (t50) remained constant. This was in accordance with the assumption of a permeation-controlled rate of action, as was shown earlier for p-chloromercuriphenyl-sulfonic acid. In addition, the c X t50 values of the individual mercurials decreased hyperbolically with the increase in lipophilicity as measured by the octanol/water partition. The results support the view that the toxicity of mercurials increases with their lipid solubility. In conjunction with the previously reported negative inotropic effect of Hg compounds, a model is proposed allocating thiol groups responsible for the negative inotropic action to lipid compartments within the cell membrane, while SH groups conveying the increase in contraction force are thought to be situated at the internal surface of the sarcolemma.

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The relationship between mercury from dental amalgam and the cardiovascular system.

Siblerud RL Sci Total Environ 1990 Dec 1;99(1-2):23-35

Department of Physiology, College of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins 80523.

The findings presented here suggest that mercury poisoning from dental amalgam may play a role in the etiology of cardiovascular disorders. Comparisons between subjects with and without amalgam showed amalgam-bearing subjects had significantly higher blood pressure, lower heart rate, lower hemoglobin, and lower hematocrit. Hemoglobin, hematocrit, and red blood cells were significantly lower when correlated to increased levels of urine mercury. The amalgam subjects had a greater incidence of chest pains, tachycardia, anemia, fatigue, tiring easily, and being tired in the morning. The data suggest that inorganic mercury poisoning from dental amalgam does affect the cardiovascular system.

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Hemodynamic and electrophysiological effects of mercury in intact anesthetized rabbits and in isolated perfused hearts.

Rhee HM, Choi BH Exp Mol Pathol 1989 Jun;50(3):281-90

Department of Pharmacology, Oral Roberts University School of Medicine, Tulsa, Oklahoma 74171.

Using intact anesthetized rabbits and isolated perfused hearts, the hemodynamic and electrophysiological effects of mercury (Hg) were examined in order to assess the role of cardiovascular dysfunction in Hg intoxication. The most consistent and prominent cardiovascular effect was a significant reduction in blood pressure. This cardiodepressive action was probably brought about by the primary action of Hg on the heart rather than by altered sympathetic activity, as evidenced by normal renal nerve activity at times when the hemodynamic actions of Hg were clearly manifest. Although the principal target organ for the toxic actions of inorganic Hg is the kidney, chronic exposure to both inorganic and organic Hg frequently results in signs and symptoms of CNS dysfunction. The profound hemodynamic effects of Hg that we have observed emphasize the potential importance of Hg cardiotoxicity and indicate the need to differentiate between the primary and the secondary effects of Hg intoxication on CNS tissues for evaluation of the toxic effects of Hg compounds.

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Cardiovascular homeostasis in rats chronically exposed to mercuric chloride.

Carmignani M, Boscolo P Arch Toxicol Suppl 1984;7:383-8

Two groups of male Sprague-Dawley rats received from weaning 50 micrograms/ml of mercury as mercuric chloride (HgCl2) in drinking water for 320 and 350 days. Hg exposure increased cardiac inotropism, without chronotropic changes, in both groups, and induced arterial hypertension in the rats exposed for 350 days. In the exposed rats, cardiovascular responses to the stimulation of peripheral alpha and beta adrenoceptors were decreased and increased, respectively, possibly through a reduced intracellular availability of calcium ions for contractile mechanisms. Hg exposure did not affect either vagal or sympathetic activity or cardiovascular reactivity to several physiological agonists. On the other hand, Hg exposure induced baroreflex hyposensitivity and produced a drastic alteration of the levels of copper and zinc in brain and kidney.

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Mechanisms in cardiovascular regulation following chronic exposure of male rats to inorganic mercury.

Carmignani M, Finelli VN, Boscolo P Toxicol Appl Pharmacol 1983 Jul;69(3):442-50

In this study we verified the possibility that chronic exposure to inorganic mercury may induce hemodynamic changes in the rat by affecting some neurogenic and/or humoral mechanisms regulating cardiovascular function. For this reason, aortic blood pressure, maximum rate of rise of the left ventricular pressure, heart rate, and electrocardiogram were monitored under pentothal anesthesia in rats which received 50 micrograms/ml of mercury (as HgCL2) in drinking water for 320 days and in control rats. No pressor or electrocardiographic changes were found in mercury-treated animals, which showed increase of cardiac inotropism and decrease of the pressor and inotropic responses to bilateral carotid occlusion. Cardiovascular responses to bilateral vagotomy and iv hexamethonium under vagotomy were unchanged in the mercury-exposed rats. In these animals both pressor and inotropic responses to iv norepinephrine and to higher doses of epinephrine were reduced, while the vascular beta-adrenergic response to 0.125 micrograms/kg of iv epinephrine was potentiated. Cardiovascular responses to acetylcholine, angiotensin I, angiotensin II, bradykinin, histamine, and serotonin did not differ in the two groups of rats. These results indicated that chronic mercury exposure affects cardiovascular function by interfering with the baroreflex mechanisms and/or the reactivity to catecholamines. Higher amounts of mercury were found in kidney, but the metal was significantly accumulated also in urine, blood, and brain. Mercury exposure greatly increased the levels of copper and zinc, but not that of iron, in brain and kidney. The increased accumulation of copper and zinc in tissues may be related in part to the mercury-induced synthesis of metallothionein, a protein able to bind these essential metals. It may be suggested that zinc and copper interact with mercury in inducing cardiovascular changes.

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