Source:http://linkedlifedata.com/resource/pubmed/id/11578143
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2001-10-1
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| pubmed:abstractText |
Sensitivity to cadmium (Cd)-induced testicular injury varies greatly among mouse strains. For instance, 129/SvJ (129) mice are highly sensitive while C57BL/6J (C57) mice are refractory to Cd-induced testicular injury. Metallothionein (MT), a Cd-binding protein, is thought to be responsible for the strain susceptibility to Cd toxicity. In this study, MT-I/II knockout (MT-null) and wild-type 129 mice were used to determine the role of MT in Cd-induced testicular injury. Two additional strains of mice (C57 and the C57 x 129 F1cross) were also used to help define the role of genetic background in Cd toxicity. Mice were given 5-20 micromol/kg ip CdCl(2) and testicular injury was examined 24 h later by histopathology and testicular hemoglobin concentration. Cd produced dose-dependent testicular injury in all strains of mice, except for C57 mice, in which testicular injury could not be produced. MT-null mice were more sensitive than C57 x 129 mice but were equally sensitive as 129 mice to Cd-induced testicular injury. Fourteen days after 15 micromol/kg ip Cd administration, testicular atrophy was evident in MT-null, 129, and C57 x 129 mice but was absent in C57 mice. The resistance of C57 mice to Cd-induced testicular injury could not be attributed solely to a decreased uptake of (109)Cd nor to a greater amount of testicular MT. Microarray analysis revealed a higher expression of glutathione peroxidase in the testes of C57 mice, as well as genes encoding antioxidant components and DNA damage/repair, but their significance to Cd-induced injury is not immediately clear. Thus, this study demonstrates that it is genetic strain, not MT genotype, that is mechanistically important in determining susceptibility to Cd-induced testicular injury.
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| pubmed:grant | |
| 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 |
Oct
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| pubmed:issn |
0041-008X
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2001 Academic Press.
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| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
176
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1-9
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11578143-Animals,
pubmed-meshheading:11578143-Cadmium,
pubmed-meshheading:11578143-Crosses, Genetic,
pubmed-meshheading:11578143-DNA Damage,
pubmed-meshheading:11578143-DNA Repair,
pubmed-meshheading:11578143-Genetic Predisposition to Disease,
pubmed-meshheading:11578143-Genotype,
pubmed-meshheading:11578143-Glutathione Peroxidase,
pubmed-meshheading:11578143-Male,
pubmed-meshheading:11578143-Metallothionein,
pubmed-meshheading:11578143-Mice,
pubmed-meshheading:11578143-Mice, Inbred C57BL,
pubmed-meshheading:11578143-Mice, Knockout,
pubmed-meshheading:11578143-Necrosis,
pubmed-meshheading:11578143-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:11578143-Organ Size,
pubmed-meshheading:11578143-Phenotype,
pubmed-meshheading:11578143-Species Specificity,
pubmed-meshheading:11578143-Testicular Diseases,
pubmed-meshheading:11578143-Testis
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| pubmed:year |
2001
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| pubmed:articleTitle |
Genetic background but not metallothionein phenotype dictates sensitivity to cadmium-induced testicular injury in mice.
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| pubmed:affiliation |
Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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