The Vascular System as a Target of Metal Toxicity
Identifieur interne : 000079 ( Main/Exploration ); précédent : 000078; suivant : 000080The Vascular System as a Target of Metal Toxicity
Auteurs : Walter C. Prozialeck [États-Unis] ; Joshua R. Edwards [États-Unis] ; Daniel W. Nebert [États-Unis] ; James M. Woods [États-Unis] ; Aaron Barchowsky [États-Unis] ; William D. Atchison [États-Unis]Source :
- Toxicological Sciences [ 1096-6080 ] ; 2007-10-18.
Abstract
Vascular system function involves complex interactions among the vascular endothelium, smooth muscle, the immune system, and the nervous system. The toxic metals cadmium (Cd), arsenic (As), and lead (Pb) can target the vascular system in a variety of ways, ranging from hemorrhagic injury to subtle pathogenic remodeling and metabolic changes. Acute Cd exposure results in hemorrhagic injury to the testis, although some strains of animals are resistant to this effect. A comparison of Cd-sensitive with Cd-resistant mouse strains showed that expression of the Slc39a8 gene, encoding the ZIP8 transporter, in the testis vasculature endothelium is responsible for this difference. Endogenously, ZIP8 is a Mn2/HCO3symporter that may also contribute to Cd damage in the kidney. Chronic Cd exposure is associated with various cardiovascular disorders such as hypertension and cardiomyopathy and it is reported to have both carcinogenic and anticarcinogenic activities. At noncytotoxic concentrations of 10100nM, Cd can inhibit chemotaxis and tube formation of vascular endothelial cells. These angiostatic effects may be mediated through disruption of vascular endothelial cadherin, a Ca2-dependent cell adhesion molecule. With regard to As, ingestion of water containing disease-promoting concentrations of As promotes capillarization of the liver sinusoidal endothelium. Because capillarization is a hallmark precursor for liver fibrosis and contributes to an imbalance of lipid metabolism, this As effect on hepatic endothelial cells may be a pathogenic mechanism underlying As-related vascular diseases. With regard to Pb, perinatal exposure may cause sustained elevations in adult blood pressure, and genetically susceptible animals may show enhanced sensitivity to this effect. Taken together, these data indicate that the vascular system is a critical target of metal toxicity and that actions of metals on the vascular system may play important roles in mediating the pathophysiologic effects of metals in specific target organs.
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DOI: 10.1093/toxsci/kfm263
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Atchison</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Occupational and Environmental Health, University of Pittsburgh Graduate School of Public Heath, Pittsburgh</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Toxicological Sciences</title><idno type="ISSN">1096-6080</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2007-10-18">2007-10-18</date><biblScope unit="vol">102</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="207">207</biblScope><biblScope unit="page" to="218">218</biblScope></imprint><idno type="ISSN">1096-6080</idno></series><idno type="istex">FC2E36FB0E3029B918834582B1498449FA621A7F</idno><idno type="DOI">10.1093/toxsci/kfm263</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1096-6080</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Vascular system function involves complex interactions among the vascular endothelium, smooth muscle, the immune system, and the nervous system. The toxic metals cadmium (Cd), arsenic (As), and lead (Pb) can target the vascular system in a variety of ways, ranging from hemorrhagic injury to subtle pathogenic remodeling and metabolic changes. Acute Cd exposure results in hemorrhagic injury to the testis, although some strains of animals are resistant to this effect. A comparison of Cd-sensitive with Cd-resistant mouse strains showed that expression of the Slc39a8 gene, encoding the ZIP8 transporter, in the testis vasculature endothelium is responsible for this difference. Endogenously, ZIP8 is a Mn2/HCO3symporter that may also contribute to Cd damage in the kidney. Chronic Cd exposure is associated with various cardiovascular disorders such as hypertension and cardiomyopathy and it is reported to have both carcinogenic and anticarcinogenic activities. At noncytotoxic concentrations of 10100nM, Cd can inhibit chemotaxis and tube formation of vascular endothelial cells. These angiostatic effects may be mediated through disruption of vascular endothelial cadherin, a Ca2-dependent cell adhesion molecule. With regard to As, ingestion of water containing disease-promoting concentrations of As promotes capillarization of the liver sinusoidal endothelium. Because capillarization is a hallmark precursor for liver fibrosis and contributes to an imbalance of lipid metabolism, this As effect on hepatic endothelial cells may be a pathogenic mechanism underlying As-related vascular diseases. With regard to Pb, perinatal exposure may cause sustained elevations in adult blood pressure, and genetically susceptible animals may show enhanced sensitivity to this effect. Taken together, these data indicate that the vascular system is a critical target of metal toxicity and that actions of metals on the vascular system may play important roles in mediating the pathophysiologic effects of metals in specific target organs.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li><li>Michigan</li><li>Ohio</li><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Illinois"><name sortKey="Prozialeck, Walter C" sort="Prozialeck, Walter C" uniqKey="Prozialeck W" first="Walter C." last="Prozialeck">Walter C. Prozialeck</name></region><name sortKey="Atchison, William D" sort="Atchison, William D" uniqKey="Atchison W" first="William D." last="Atchison">William D. Atchison</name><name sortKey="Barchowsky, Aaron" sort="Barchowsky, Aaron" uniqKey="Barchowsky A" first="Aaron" last="Barchowsky">Aaron Barchowsky</name><name sortKey="Edwards, Joshua R" sort="Edwards, Joshua R" uniqKey="Edwards J" first="Joshua R." last="Edwards">Joshua R. Edwards</name><name sortKey="Nebert, Daniel W" sort="Nebert, Daniel W" uniqKey="Nebert D" first="Daniel W." last="Nebert">Daniel W. Nebert</name><name sortKey="Prozialeck, Walter C" sort="Prozialeck, Walter C" uniqKey="Prozialeck W" first="Walter C." last="Prozialeck">Walter C. Prozialeck</name><name sortKey="Woods, James M" sort="Woods, James M" uniqKey="Woods J" first="James M." last="Woods">James M. Woods</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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