File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Apoptosis and p53 gene expression in male reproductive tissues of cadmium exposed rats

TitleApoptosis and p53 gene expression in male reproductive tissues of cadmium exposed rats
Authors
KeywordsApoptosis
Cadmium
p53 gene expression
Rat
RT-PCR
Testes
Issue Date1999
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0966-0844
Citation
Biometals, 1999, v. 12 n. 2, p. 131-139 How to Cite?
AbstractReverse transcription (RT) PCR technique was used to investigate the mechanism of apoptosis induced by Cd and the change of its related genes in testes and prostate of rats. Adult male rats were given a single (s.c.) injection of CdCl 2 0, 2.5, 5.0, 10 μmol/kg. 48 h and 72 h after administration of Cd, animals were sacrificed. The results indicated that Cd can induce apoptosis in testes via p53-independent pathway. No apoptosis occurred in prostate in any of the Cd-exposed groups. There was a clearly negative relationship in testes between p53 gene expression and Cd exposure and this dose-response relationship was observed both at 48 h and 72 h. There was a very small increase of this gene expression in the dorsolateral lobe of the prostate in Cd exposed groups. The other apoptosis related gene, bcl-x, was not detectable in either control or Cd-exposed group in testes and dorsal prostate. Although the MT-I gene was expressed in testes or dorsal prostate both in control and exposed groups, no overexpression of MT-I gene was found after administration of Cd. The expression of MT-I in the ventral prostate was not detected in the control group, but a weak expression was found after Cd exposure. Since p53 is a tumor suppressor gene which can inhibit tumorigenesis, the consequence of a Cd-induced decrease of p53 in testes may have a relation to the known risk of Cd tumorigenesis in this tissue.
Persistent Identifierhttp://hdl.handle.net/10722/170018
ISSN
2023 Impact Factor: 4.1
2023 SCImago Journal Rankings: 0.618
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Gen_US
dc.contributor.authorZhou, Gen_US
dc.contributor.authorJin, Ten_US
dc.contributor.authorZhou, Ten_US
dc.contributor.authorHammarström, Sen_US
dc.contributor.authorBergh, Aen_US
dc.contributor.authorNordberg, Gen_US
dc.date.accessioned2012-10-30T06:04:47Z-
dc.date.available2012-10-30T06:04:47Z-
dc.date.issued1999en_US
dc.identifier.citationBiometals, 1999, v. 12 n. 2, p. 131-139en_US
dc.identifier.issn0966-0844en_US
dc.identifier.urihttp://hdl.handle.net/10722/170018-
dc.description.abstractReverse transcription (RT) PCR technique was used to investigate the mechanism of apoptosis induced by Cd and the change of its related genes in testes and prostate of rats. Adult male rats were given a single (s.c.) injection of CdCl 2 0, 2.5, 5.0, 10 μmol/kg. 48 h and 72 h after administration of Cd, animals were sacrificed. The results indicated that Cd can induce apoptosis in testes via p53-independent pathway. No apoptosis occurred in prostate in any of the Cd-exposed groups. There was a clearly negative relationship in testes between p53 gene expression and Cd exposure and this dose-response relationship was observed both at 48 h and 72 h. There was a very small increase of this gene expression in the dorsolateral lobe of the prostate in Cd exposed groups. The other apoptosis related gene, bcl-x, was not detectable in either control or Cd-exposed group in testes and dorsal prostate. Although the MT-I gene was expressed in testes or dorsal prostate both in control and exposed groups, no overexpression of MT-I gene was found after administration of Cd. The expression of MT-I in the ventral prostate was not detected in the control group, but a weak expression was found after Cd exposure. Since p53 is a tumor suppressor gene which can inhibit tumorigenesis, the consequence of a Cd-induced decrease of p53 in testes may have a relation to the known risk of Cd tumorigenesis in this tissue.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0966-0844en_US
dc.relation.ispartofBioMetalsen_US
dc.subjectApoptosis-
dc.subjectCadmium-
dc.subjectp53 gene expression-
dc.subjectRat-
dc.subjectRT-PCR-
dc.subjectTestes-
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCadmium - Toxicityen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshGenes, P53en_US
dc.subject.meshMaleen_US
dc.subject.meshMetallothionein - Geneticsen_US
dc.subject.meshProstate - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReproducibility Of Resultsen_US
dc.subject.meshTestis - Drug Effects - Metabolism - Pathologyen_US
dc.titleApoptosis and p53 gene expression in male reproductive tissues of cadmium exposed ratsen_US
dc.typeArticleen_US
dc.identifier.emailZhou, G:wormoscz@gmail.comen_US
dc.identifier.authorityZhou, G=rp00527en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1023/A:1009273711068en_US
dc.identifier.pmid10406082-
dc.identifier.scopuseid_2-s2.0-0033066279en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033066279&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume12en_US
dc.identifier.issue2en_US
dc.identifier.spage131en_US
dc.identifier.epage139en_US
dc.identifier.isiWOS:000081592300004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridXu, G=10340314600en_US
dc.identifier.scopusauthoridZhou, G=23394245100en_US
dc.identifier.scopusauthoridJin, T=7202994127en_US
dc.identifier.scopusauthoridZhou, T=7402989477en_US
dc.identifier.scopusauthoridHammarström, S=7102117831en_US
dc.identifier.scopusauthoridBergh, A=7101766838en_US
dc.identifier.scopusauthoridNordberg, G=7005720784en_US
dc.identifier.issnl0966-0844-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats