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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1992-4-17
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pubmed:abstractText |
Dimethylarsinic acid (DMAA) administration induced the preferential increase of the heterochromatic area forming the inside of the interphase nucleus. A histopathological study of the lung and liver in mice after DMAA administration was carried out by transmission electron microscopy. Ultrastructural alterations in the endothelial nuclei of the alveolar wall were observed 12-48 h after administration. Heterochromatin tended to collect in a dense, compact mass lining the inner walls of the nucleus. A significant increase in heterochromatin induced by DMAA administration was observed by morphometric analysis. However, no substantial differences appeared in the sinusoidal endothelium of the liver. This study suggests that the much greater induction of morphological alterations, such as increased heterochromatin, in lung endothelial nuclei than in the liver might explain the high risk of lung cancer by arsenics, and that there may be a close relationship between heterochromatin alteration and DNA damages.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0143-3334
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
391-3
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:1547528-Animals,
pubmed-meshheading:1547528-Cacodylic Acid,
pubmed-meshheading:1547528-Endothelium, Vascular,
pubmed-meshheading:1547528-Heterochromatin,
pubmed-meshheading:1547528-Liver,
pubmed-meshheading:1547528-Lung,
pubmed-meshheading:1547528-Male,
pubmed-meshheading:1547528-Mice,
pubmed-meshheading:1547528-Mice, Inbred ICR,
pubmed-meshheading:1547528-Microscopy, Electron
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pubmed:year |
1992
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pubmed:articleTitle |
Preferential increase of heterochromatin in venular endothelium of lung in mice after administration of dimethylarsinic acid, a major metabolite of inorganic arsenics.
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pubmed:affiliation |
Department of Chemicobiological Interaction, Chiba University, Japan.
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pubmed:publicationType |
Journal Article
|