Copper is essential for homeostasis and regulation of body functions, but in excess, it is a cardiovascular risk factor since it increases oxidative stress. The objective of this study was to evaluate the effects of exposure to the recommended daily dose (13 µg/kg/day), upper tolerable dose (0.14 mg/kg/day) and twice the upper tolerable dose (0.28 mg/kg/day) via i.p. over 4 weeks on the vascular reactivity of aortic rings and the contraction of LV papillary muscles. It was also determined whether the antioxidant peptide from egg white hydrolysate (EWH) prevents these effects. Copper exposure at the doses evaluated did not change weight gain, the reactivity of the aortic rings or the cardiac mass. The dose of 0.13 µg/kg/day did not reduce the force of contraction, but it impaired the time derivatives of force. Doses of 0.14 and 0.28 mg/kg/day reduced the force of contraction, the inotropic response to calcium and isoproterenol, the postrest contraction and the peak and plateau of tetanized contractions. EWH treatment antagonized these effects. These results suggest that copper, even at the dose described as upper tolerable, can impair cardiac contraction without altering vascular reactivity. Antioxidative stress therapy with EWH reversed these harmful effects, suggesting a possible strategy for the amelioration of these effects.
Mercury has been shown to be a significant health risk factor and is positively associated with cardiovascular diseases. Evidence reveals that men are more likely to develop cardiovascular diseases than women during reproductive age.However, the effects of mercury in females remain poorly investigated, despite the finding that female hormones demonstrate a cardioprotective role. In the present study, we evaluated whether chronic mercury chloride exposure could alter blood pressure and vascular function of the female rat aorta.Ten-week-old female Wistar rats were divided into two groups: control (vehicle) and mercury treated (first dose of 4.6 μg/kg, subsequent daily doses of 0.07 μg/kg), im. Mercury treatment did not modify systolic blood pressure (SBP) but increased vascular reactivity due to the reduction of nitric oxide bioavailability associated with the increase in reactive oxygen species from endothelial nitric oxide synthase (eNOS) uncoupling. Furthermore, increased participation of the cyclooxygenase-2 pathway occurred through an imbalance in thromboxane 2 and prostacyclin 2. However, the oestrogen signalling pathway was not altered in either group. These results demonstrated that chronic exposure to mercury in females induced endothelial dysfunction and, consequently, increased aortic vascular reactivity, causing vascular damage to the female rat aorta and representing a risk of cardiovascular diseases.endothelial dysfunction, eNOS uncoupling, female rats, mercury chloride, vascular reactivity
| INTRODUCTIONMercury has been recognized by the Agency for Toxic Substances and Disease Registry 1 as ranking third, behind arsenic and lead, on the priority list of substances that pose potential threats to human health due to its high toxicity and ability to biomagnify and bioaccumulate in the food chain. 2 Studies have shown that acute and chronic mercury exposure lead to adverse effects, such as the development of atherosclerosis, coronary artery disease, hypertension, changes in the oestrous cycle and features of polycystic ovary syndrome. [3][4][5][6][7]
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