Adverse cardiovascular effects of exposure to cadmium and mercury alone and in combination on the cardiac tissue and aorta of Sprague-Dawley rats.

Autor: Arbi S; Department of Anatomy, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa., Bester MJ; Department of Anatomy, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa., Pretorius L; Department of Anatomy, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa., Oberholzer HM; Department of Anatomy, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa.
Jazyk: angličtina
Zdroj: Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering [J Environ Sci Health A Tox Hazard Subst Environ Eng] 2021; Vol. 56 (6), pp. 609-624. Date of Electronic Publication: 2021 Mar 15.
DOI: 10.1080/10934529.2021.1899534
Abstrakt: The aim of this study was to identify cardiovascular effects of relevant concentrations of Cd and Hg alone and in combination as a mixture in water. This was achieved by administering to male Sprague-Dawley rats via gavage 0.62 mg/kg Cd or 1.23 mg/kg Hg, or a combination of 0.62 mg/kg Cd and 1.23 mg/kg Hg in the co-exposure group for 28 days. Concentrations were the rat equivalence dosages of 1,000 times the World Health Organization's limits of 0.003 mg/L and 0.006 mg/L for Cd and Hg, respectively, for water. With termination, blood levels of the metals were increased. For all metal exposed groups, histological evaluation and transmission electron microscopy of the myocardium revealed myofibrillar necrosis, increased fibrosis, vacuole formation and mitochondrial damage. Cd caused the most mitochondrial damage while Hg to a greater degree induced fibrosis. In the aorta, both Cd and Hg also increased collagen deposition adversely altering the morphology of the fenestrated elastic fibers in the tunica media. Co-exposure resulted in increased cardiotoxicity with increased mitochondrial damage, fibrosis and distortion of the aortic wall as a result of increased collagen deposition, as well as altered elastin deposition, fragmentation and interlink formation. These are typical features of oxidative damage that correlates with a phenotype of premature ageing of the CVS that potentially can lead to hypertension and premature cardiac failure.
Databáze: MEDLINE