Cadmium exposure is related to cardiovascular diseases, including hypertension, atherosclerosis, increased oxidative stress, endothelial dysfunction, and specific biochemical changes induced by this metal. Thus, we aimed to investigate whether cadmium exposure induces endothelial dysfunction, accelerates atherosclerotic plaque formation in the aorta, and enhances oxidative stress in apolipoprotein E knockout (ApoE) mice. Experiments were performed in 14-week-old male wild-type and ApoE mice. ApoE mice received cadmium (CdCl 100 mg/L in drinking water for 28 days) or vehicle (distilled water). After treatment, vascular reactivity to phenylephrine, acetylcholine, and sodium nitroprusside was analyzed using isolated aorta. Bone marrow cells were isolated to assess the production of nitric oxide and reactive oxygen and nitrogen species. ApoE cadmium-treated mice had higher cholesterol levels than non-exposed mice. Cadmium exposure decreased the vasodilatation response to acetylcholine in aortic ring of ApoE mice, though no changes in phenylephrine or sodium nitroprusside responses were observed. L-NAME reduced vasodilator responses to acetylcholine; this effect was lower in ApoE cadmium-treated mice, suggesting reduction in nitric oxide (NO) bioavailability. Moreover, in bone marrow cells, cadmium decreased cytoplasmic levels of NO and increased superoxide anions, hydrogen peroxide, and peroxynitrite in ApoE mice. Morphological analysis showed that cadmium exposure increased plaque deposition in the aorta by approximately 3-fold. Our results suggest that cadmium exposure induces endothelial dysfunction in ApoE mice. Moreover, cadmium increased total cholesterol levels, which may promote the early development of atherosclerosis in the aorta of ApoE mice. Our findings support the hypothesis that cadmium exposure might increase the risk of atherosclerosis.
Lead exposure has been considered to be a risk factor for hypertension and cardiovascular disease. Our purpose was to evaluate the effects of low plasma lead concentration on cardiac contractility in isolated papillary muscles. Wistar rats were divided in control group or group treated with 100 ppm of lead acetate in the drinking water for 15 days. Blood pressure (BP) was measured weekly. At the end of the treatment period, the animals were anesthetized and euthanized, and parameters related to isolated papillary muscle contractility were recorded. The lead concentrations in the blood reached 12.3 ± 2 μg/dL. The BP was increased in the group treated with 100 ppm of lead acetate. Lead treatment did not alter force and time derivatives of the force of left ventricular papillary muscles. In addition, the inotropic response induced by an increase in the extracellular Ca(2+) concentration was reduced in the Pb(2+) group. However, the uptake of Ca(2+) by the sarcoplasmic reticulum and the protein expression of SERCA and phospholamban remained unchanged. Postrest contraction was similar in the both groups, and tetanic peak and plateau tension were reduced in lead group. These results demonstrated that the reduction in the inotropic response to calcium does not appear to be caused by changes in the trans-sarcolemmal calcium flux but suggest that an impairment of the contractile machinery might be taking place. Our results demonstrate that even at a concentration below the limit considered to be safe, lead exerts deleterious effects on the cardiac contractile machinery.
Background: Cadmium is a worldwide spread toxicant that accumulates in tissues and affects many organs, mainly through oxidative damage. Oxidative stress is often associated with cardiovascular diseases and, when it affects vessels, it induces endothelial dysfunction, which, in turn, could precipitate atherosclerosis and hypertension. Therefore, it is reasonable to suggest antioxidant supplementation as a therapy against cadmium-induced endothelial dysfunction. Objective: This literature review aims to present the mechanisms involving oxidative stress by which cadmium induces endothelial dysfunction and the benefits of antioxidant supplementation as a therapeutic strategy against its harmful effects. Methods: On PubMed Central, articles that contemplated studies on cadmium intoxication and associated oxidative stress with endothelial dysfunction as well as articles that reported the use of antioxidant supplementation in an attempt to prevent or avoid endothelial dysfunction induced by cadmium exposure were selected. Results: Most of the studies that associated cadmium intoxication with endothelial dysfunction suggested oxidative stress as the major mechanism for this damage. Furthermore, experimental studies also revealed that the administration of substances with antioxidant properties, such as ascorbic acid and curcumin, has beneficial effects on the prevention of such dysfunction, reducing reactive oxygen species within the vessels, preventing a reduction in the amount of glutathione and the increase in blood pressure observed in animals exposed to cadmium. Conclusion: Antioxidant therapy demonstrated to be a potential treatment to reduce cardiovascular injuries provoked by cadmium, but more studies are encouraged to determine the best antioxidant substance and dose to treat or avoid this complication.
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