Toxic effects of mercury, lead and gadolinium on vascular reactivity

• Main Authors: D.V. Vassallo, M.R. Simões, L.B. Furieri, M. Fioresi, J. Fiorim, E.A.S. Almeida, J.K. Angeli, G.A. Wiggers, F.M. Peçanha, M. Salaices
• Format: Article
• Language: English
• Published: Associação Brasileira de Divulgação Científica 2011-09-01
• Series: Brazilian Journal of Medical and Biological Research
• Subjects: Heavy metal toxicity; Vascular reactivity; Mercury; Lead; Gadolinium
• Online Access: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000900016

Heavy metals have been used in a wide variety of human activities that have significantly increased both professional and environmental exposure. Unfortunately, disasters have highlighted the toxic effects of metals on different organs and systems. Over the last 50 years, the adverse effects of chronic lead, mercury and gadolinium exposure have been underscored. Mercury and lead induce hypertension in humans and animals, affecting endothelial function in addition to their other effects. Increased cardiovascular risk after exposure to metals has been reported, but the underlying mechanisms, mainly for short periods of time and at low concentrations, have not been well explored. The presence of other metals such as gadolinium has raised concerns about contrast-induced nephropathy and, interestingly, despite this negative action, gadolinium has not been defined as a toxic agent. The main actions of these metals, demonstrated in animal and human studies, are an increase of free radical production and oxidative stress and stimulation of angiotensin I-converting enzyme activity, among others. Increased vascular reactivity, highlighted in the present review, resulting from these actions might be an important mechanism underlying increased cardiovascular risk. Finally, the results described in this review suggest that mercury, lead and gadolinium, even at low doses or concentrations, affect vascular reactivity. Acting via the endothelium, by continuous exposure followed by their absorption, they can increase the production of free radicals and of angiotensin II, representing a hazard for cardiovascular function. In addition, the actual reference values, considered to pose no risk, need to be reduced.