Toxic effects of mercury, lead and gadolinium on vascular reactivity

Vassallo, Dalton Valentim; Simões, Maylla Ronacher; Furieri, Lorena Barros; Fioresi, Mirian; Fiorim, Jonaína; Almeida, Edna Aparecida Silveira; Angeli, Jhuli Keli; Wiggers, Giulia Alessandra; Peçanhã, Franck Maciel; Salaíces, Mercedes

doi:10.1590/s0100-879x2011007500098

Cited by 53 publications

(28 citation statements)

References 51 publications

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“…The cardiovascular toxicity of mercury, cadmium and other divalent metal ions has long been known [19], [23], [24]. We observed that after one week of treatment with cadmium, the systolic blood pressure increased, and this increase was maintained until the end of the experimental period.…”

Section: Discussionmentioning

confidence: 74%

“…Both enzymes reduced the maximal response to phenylephrine to control levels, suggesting that cadmium exposure causes oxidative stress. Cadmium could increase oxidative stress by inducing the generation of ROS, damaging the antioxidant defense systems of cells by depleting GSH and inhibiting SH-dependent enzymes, or interfering with some essential metal(s) needed for antioxidant enzyme activities [19], [29]–[31].…”

Section: Discussionmentioning

confidence: 99%

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Chronic Cadmium Treatment Promotes Oxidative Stress and Endothelial Damage in Isolated Rat Aorta

et al. 2013

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Cadmium is a highly toxic metal that is present in phosphate fertilizers, and the incidence of cadmium poisoning in the general population has increased, mainly due to cigarette smoking. Once absorbed, cadmium accumulates in the tissues, causing harmful effects including high blood pressure, endothelial damage and oxidative stress. Oxidative stress is known to efficiently produce oxidized low-density lipoprotein and consequently atherosclerosis, mainly in the aorta. However, the mechanisms through which endothelial damage is induced by cadmium have not been elucidated. Thus, the aim of this study was to investigate the effects of this metal in the isolated aorta and the possible role of oxidative stress. Rats received 100 mg.L−1 cadmium chloride (CdCl2) in the drinking water or distilled water alone for four weeks. The pressor effect of cadmium was followed throughout the exposure period by tail plethysmography. At the end of the fourth week, the blood cadmium content was established, and the vascular reactivity of the isolated aorta to phenylephrine, acetylcholine and sodium nitroprusside was analyzed in the context of endothelium denudation and incubation with L-NAME, apocynin, losartan, enalapril, superoxide dismutase (SOD) or catalase. We observed an increased response to phenylephrine in cadmium-treated rats. This increase was abolished by catalase and SOD incubation. Apocynin treatment reduced the phenylephrine response in both treatment groups, but its effect was greater in cadmium-treated rats, and NOX2 expression was greater in the cadmium group. These results suggested that cadmium in blood concentrations similar to those found in occupationally exposed populations is able to stimulate NOX2 expression, contributing to oxidative stress and reducing NO bioavailability, despite enhanced eNOS expression. These findings suggest that cadmium exposure promotes endothelial damage that might contribute to inflammation, vascular injury and the development of atherosclerosis.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Chronic Cadmium Treatment Promotes Oxidative Stress and Endothelial Damage in Isolated Rat Aorta

et al. 2013

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“…The fact that the endothelium is affected by low concentrations of heavy metals below the reference values highlights the importance and the need to better understand the mechanisms by which these metals promote development of cardiovascular diseases [8], [27]. Mercury induces toxicological consequences as a result of exposure to mercury vapour [2], the release of mercury from or during removal of amalgam fillings [29] and the ingestion of contaminated fish [4].…”

Section: Discussionmentioning

confidence: 99%

“…However, if short periods of exposure and if low concentrations of mercury also affect conductance arteries it is still unclear [13], [26]. The fact that the endothelium is affected by low concentrations of heavy metals below the reference values highlights the importance and the need to better understand the mechanisms by which these metals promote development of cardiovascular diseases [27]–[28]. Therefore, the current study aimed to explore the acute effect of low-concentration mercury exposure on endothelial function in the isolated aortic rings of rats and the possible role of oxidative stress and prostanoids generation.…”

Section: Introductionmentioning

confidence: 99%

Low Mercury Concentration Produces Vasoconstriction, Decreases Nitric Oxide Bioavailability and Increases Oxidative Stress in Rat Conductance Artery

et al. 2012

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Mercury is an environmental pollutant that reduces nitric oxide (NO) bioavailability and increases oxidative stress, having a close link with cardiovascular diseases, as carotid atherosclerosis, myocardial infarction, coronary heart disease and hypertension. One of the main sites affected by oxidative stress, which develops atherosclerosis, is the aorta. Under acute exposure to low mercury concentrations reactive oxygen species (ROS) production were only reported for resistance vessels but if low concentrations of mercury also affect conductance arteries it is still unclear. We investigated the acute effects of 6 nM HgCl2 on endothelial function of aortic rings measuring the reactivity to phenylephrine in rings incubated, or not, with HgCl2 for 45 min, the protein expression for cyclooxygenase 2 (COX-2) and the AT1 receptor. HgCl2 increased Rmax and pD2 to phenylephrine without changing the vasorelaxation induced by acetylcholine and sodium nitroprusside. Endothelial damage abolished the increased reactivity to phenylephrine. The increase of Rmax and pD2 produced by L-NAME was smaller in the presence of HgCl2. Enalapril, losartan, indomethacin, furegrelate, the selective COX-2 inhibitor NS 398, superoxide dismutase and the NADPH oxidase inhibitor apocynin reverted HgCl2 effects on the reactivity to phenylephrine, COX-2 protein expression was increased, and AT1 expression reduced. At low concentration, below the reference values, HgCl2 increased vasoconstrictor activity by reducing NO bioavailability due to increased ROS production by NADPH oxidase activity. Results suggest that this is due to local release of angiotensin II and prostanoid vasoconstrictors. Results also suggest that acute low concentration mercury exposure, occurring time to time could induce vascular injury due to endothelial oxidative stress and contributing to increase peripheral resistance, being a high risk factor for public health.

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“…At higher concentrations, mercury reduces tetanic tension development, myosin ATPase activity and induces a negative inotropism in the left ventricle [36], [37]. Additionally, low mercury concentrations produce a negative inotropic effect and reduces β-adrenergic response in perfused hearts.…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Low Doses of HgCl2 Avoids Calcium Handling Impairment in the Right Ventricle after Myocardial Infarction in Rats

et al. 2014

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Right ventricle systolic dysfunction is a major risk factor for death and heart failure after myocardial infarction (MI). Heavy metal exposure has been associated with the development of several cardiovascular diseases, such as MI. The aim of this study was to investigate whether chronic exposure to low doses of mercury chloride (HgCl2) enhances the functional deterioration of right ventricle strips after MI. Male Wistar rats were divided into four groups: Control (vehicle); HgCl2 (exposure during 4 weeks- 1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m. to cover daily loss); MI surgery induced and HgCl2-MI groups. One week after MI, the morphological and hemodynamic measurements and isometric tension of right ventricle strips were investigated. The chronic HgCl2 exposure did not worsen the injury compared with MI alone in the morphological or hemodynamic parameters evaluated. At basal conditions, despite similar maximum isometric force at L-max, relaxation time was increased in the MI group but unaffected in the HgCl2-MI compared to the Control group. Impairment of the sarcoplasmic reticulum (SR) function and reduction in the sarcolemmal calcium influx were observed in MI group associated with SERCA2a reduction and increased PLB protein expression. Induction of MI in chronic HgCl2 exposed rats did not cause any alteration in the developed force at L-max, lusitropic function or −dF/dt except for a tendency of a reduction SR function. These findings could be partially explained by the normalization in the sarcolemmal calcium influx and the increase in NCX protein expression observed only in this group. These results suggest that chronic exposure to low doses of HgCl2 prevents the impaired SR function and the reduced sarcolemmal calcium influx observed in MI likely by acting on NCX, PLB and SERCA2a protein expression.

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Toxic effects of mercury, lead and gadolinium on vascular reactivity

Cited by 53 publications

References 51 publications

Chronic Cadmium Treatment Promotes Oxidative Stress and Endothelial Damage in Isolated Rat Aorta

Chronic Cadmium Treatment Promotes Oxidative Stress and Endothelial Damage in Isolated Rat Aorta

Low Mercury Concentration Produces Vasoconstriction, Decreases Nitric Oxide Bioavailability and Increases Oxidative Stress in Rat Conductance Artery

Chronic Exposure to Low Doses of HgCl2 Avoids Calcium Handling Impairment in the Right Ventricle after Myocardial Infarction in Rats

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