Renal Anemia Induced by Chronic Ingestion of Depleted Uranium in Rats
Identifieur interne : 000137 ( France/Analysis ); précédent : 000136; suivant : 000138Renal Anemia Induced by Chronic Ingestion of Depleted Uranium in Rats
Auteurs : Hana Berradi [France] ; Jean-Marc Bertho [France] ; Nicolas Dudoignon [France] ; Andr Mazur [France] ; Line Grandcolas [France] ; Cdric Baudelin [France] ; Stphane Grison [France] ; Philippe Voisin [France] ; Patrick Gourmelon [France] ; Isabelle Dublineau [France]Source :
- Toxicological Sciences [ 1096-6080 ] ; 2008-03-28.
Abstract
Kidney disease is a frequent consequence of heavy metal exposure and renal anemia occurs secondarily to the progression of kidney deterioration into chronic disease. In contrast, little is known about effects on kidney of chronic exposure to low levels of depleted uranium (DU). Study was performed with rats exposed to DU at 40 mg/l by chronic ingestion during 9 months. In the present work, a 20% reduction in red blood cell (RBC) count was observed after DU exposure. Hence, three hypotheses were tested to determinate origin of RBC loss: (1) reduced erythropoiesis, (2) increased RBC degradation, and/or (3) kidney dysfunction. Erythropoiesis was not reduced after exposure to DU as revealed by erythroid progenitors, blood Flt3 ligand and erythropoietin (EPO) blood and kidney levels. Concerning messenger RNA (mRNA) and protein levels of spleen iron recycling markers from RBC degradation (DMT1 [divalent metal transporter 1], iron regulated protein 1, HO1, HO2 [heme oxygenase 1 and 2], cluster of differentiation 36), increase in HO2 and DMT1 mRNA level was induced after chronic exposure to DU. Kidneys of DU-contaminated rats had more frequently high grade tubulo-interstitial and glomerular lesions, accumulated iron more frequently and presented more apoptotic cells. In addition, chronic exposure to DU induced increased gene expression of ceruloplasmin (12), of DMT1 (2.5), and decreased mRNA levels of erythropoietin receptor (0.2). Increased mRNA level of DMT1 was associated to decreased protein level (0.25). To conclude, a chronic ingestion of DU leads mainly to kidney deterioration that is probably responsible for RBC count decrease in rats. Spleen erythropoiesis and molecules involved in erythrocyte degradation were also modified by chronic DU exposure.
Url:
DOI: 10.1093/toxsci/kfn052
Affiliations:
- France
- Auvergne (région administrative), Auvergne-Rhône-Alpes, Île-de-France
- Fontenay-aux-Roses, Saint-Genes Champanelle
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type="istex">AA97878069EF21DC10968DDAFCEC6D48E7371109</idno><idno type="DOI">10.1093/toxsci/kfn052</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1096-6080</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Kidney disease is a frequent consequence of heavy metal exposure and renal anemia occurs secondarily to the progression of kidney deterioration into chronic disease. In contrast, little is known about effects on kidney of chronic exposure to low levels of depleted uranium (DU). Study was performed with rats exposed to DU at 40 mg/l by chronic ingestion during 9 months. In the present work, a 20% reduction in red blood cell (RBC) count was observed after DU exposure. Hence, three hypotheses were tested to determinate origin of RBC loss: (1) reduced erythropoiesis, (2) increased RBC degradation, and/or (3) kidney dysfunction. Erythropoiesis was not reduced after exposure to DU as revealed by erythroid progenitors, blood Flt3 ligand and erythropoietin (EPO) blood and kidney levels. Concerning messenger RNA (mRNA) and protein levels of spleen iron recycling markers from RBC degradation (DMT1 [divalent metal transporter 1], iron regulated protein 1, HO1, HO2 [heme oxygenase 1 and 2], cluster of differentiation 36), increase in HO2 and DMT1 mRNA level was induced after chronic exposure to DU. Kidneys of DU-contaminated rats had more frequently high grade tubulo-interstitial and glomerular lesions, accumulated iron more frequently and presented more apoptotic cells. In addition, chronic exposure to DU induced increased gene expression of ceruloplasmin (12), of DMT1 (2.5), and decreased mRNA levels of erythropoietin receptor (0.2). Increased mRNA level of DMT1 was associated to decreased protein level (0.25). To conclude, a chronic ingestion of DU leads mainly to kidney deterioration that is probably responsible for RBC count decrease in rats. Spleen erythropoiesis and molecules involved in erythrocyte degradation were also modified by chronic DU exposure.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Auvergne (région administrative)</li><li>Auvergne-Rhône-Alpes</li><li>Île-de-France</li></region><settlement><li>Fontenay-aux-Roses</li><li>Saint-Genes Champanelle</li></settlement></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Berradi, Hana" sort="Berradi, Hana" uniqKey="Berradi H" first="Hana" last="Berradi">Hana Berradi</name></region><name sortKey="Baudelin, Cdric" sort="Baudelin, Cdric" uniqKey="Baudelin C" first="Cdric" last="Baudelin">Cdric Baudelin</name><name sortKey="Bertho, Jean Marc" sort="Bertho, Jean Marc" uniqKey="Bertho J" first="Jean-Marc" last="Bertho">Jean-Marc Bertho</name><name sortKey="Dublineau, Isabelle" sort="Dublineau, Isabelle" uniqKey="Dublineau I" first="Isabelle" last="Dublineau">Isabelle Dublineau</name><name sortKey="Dublineau, Isabelle" sort="Dublineau, Isabelle" uniqKey="Dublineau I" first="Isabelle" last="Dublineau">Isabelle Dublineau</name><name sortKey="Dudoignon, Nicolas" sort="Dudoignon, Nicolas" uniqKey="Dudoignon N" first="Nicolas" last="Dudoignon">Nicolas Dudoignon</name><name sortKey="Gourmelon, Patrick" sort="Gourmelon, Patrick" uniqKey="Gourmelon P" first="Patrick" last="Gourmelon">Patrick Gourmelon</name><name sortKey="Grandcolas, Line" sort="Grandcolas, Line" uniqKey="Grandcolas L" first="Line" last="Grandcolas">Line Grandcolas</name><name sortKey="Grison, Stphane" sort="Grison, Stphane" uniqKey="Grison S" first="Stphane" last="Grison">Stphane Grison</name><name sortKey="Mazur, Andr" sort="Mazur, Andr" uniqKey="Mazur A" first="Andr" last="Mazur">Andr Mazur</name><name sortKey="Voisin, Philippe" sort="Voisin, Philippe" uniqKey="Voisin P" first="Philippe" last="Voisin">Philippe Voisin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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