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Article: Cadmium-induced apoptosis and changes in expression of p53, c-jun and MT-I genes in testes and ventral prostate of rats

TitleCadmium-induced apoptosis and changes in expression of p53, c-jun and MT-I genes in testes and ventral prostate of rats
Authors
Issue Date1999
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
Citation
Toxicology, 1999, v. 142 n. 1, p. 1-13 How to Cite?
Abstract
Apoptosis and a change in the expression of p53, c-jun and MT-I genes occurred in rats exposed to cadmium in a way known to cause carcinogenesis in testes and ventral prostate. In situ end labelling (ISEL), DNA electrophoresis, and RT-PCR methods were used in present study. Adult male Wistar rats were given a single (s.c.) injection of 0, 5, 10, or 20 μmol/kg CdCl2. Then 12, 48 or 96 h after administration of cadmium, animals were sacrificed. It was observed that cadmium markedly induced apoptosis in the testes at the dose of 5 μmol/kg while 10 and 20 μmol/kg cadmium caused more necrosis than apoptosis. Apoptosis in the ventral prostate was markedly induced by all the doses of cadmium and there was an obvious time- and dose-dependent relationship between apoptotic index (AI) and cadmium treatment. Far fewer apoptotic cells appeared in liver, compared to the testes and ventral prostate. p53 mRNA expression was clearly enhanced in the ventral prostate but clearly suppressed in the testes by cadmium exposure, and the time- and dose-effect was very clear. The expression level of p53 in the liver was not affected by cadmium treatment. Cadmium-induced overexpression of c-jun gene appeared at 12 h in the liver, but not until 96 h in the testes and ventral prostate. Although the MT-I gene was found to be expressed in all tissues, marked induction by cadmium of the expression of MT-I gene was only observed in the liver. These results indicate: (1) that apoptosis is an early mechanism of acute tissue damage by cadmium in the testes and ventral prostate; (2) that p53 and c-jun genes may be involved in cadmium-induced cytotoxicity (apoptosis) and related carcinogenicity in male reproductive tissues; and (3) that the enhanced expression of MT-I in the liver could protect this organ from cadmium-induced cytotoxicity (apoptosis) and carcinogenicity. Copyright (C) 1999 Elsevier Science Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/170016
ISSN
2013 Impact Factor: 3.745
2013 SCImago Journal Rankings: 1.196
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Ten_US
dc.contributor.authorZhou, Gen_US
dc.contributor.authorSong, Wen_US
dc.contributor.authorEguchi, Nen_US
dc.contributor.authorLu, Wen_US
dc.contributor.authorLundin, Een_US
dc.contributor.authorJin, Ten_US
dc.contributor.authorNordberg, Gen_US
dc.date.accessioned2012-10-30T06:04:46Z-
dc.date.available2012-10-30T06:04:46Z-
dc.date.issued1999en_US
dc.identifier.citationToxicology, 1999, v. 142 n. 1, p. 1-13en_US
dc.identifier.issn0300-483Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170016-
dc.description.abstractApoptosis and a change in the expression of p53, c-jun and MT-I genes occurred in rats exposed to cadmium in a way known to cause carcinogenesis in testes and ventral prostate. In situ end labelling (ISEL), DNA electrophoresis, and RT-PCR methods were used in present study. Adult male Wistar rats were given a single (s.c.) injection of 0, 5, 10, or 20 μmol/kg CdCl2. Then 12, 48 or 96 h after administration of cadmium, animals were sacrificed. It was observed that cadmium markedly induced apoptosis in the testes at the dose of 5 μmol/kg while 10 and 20 μmol/kg cadmium caused more necrosis than apoptosis. Apoptosis in the ventral prostate was markedly induced by all the doses of cadmium and there was an obvious time- and dose-dependent relationship between apoptotic index (AI) and cadmium treatment. Far fewer apoptotic cells appeared in liver, compared to the testes and ventral prostate. p53 mRNA expression was clearly enhanced in the ventral prostate but clearly suppressed in the testes by cadmium exposure, and the time- and dose-effect was very clear. The expression level of p53 in the liver was not affected by cadmium treatment. Cadmium-induced overexpression of c-jun gene appeared at 12 h in the liver, but not until 96 h in the testes and ventral prostate. Although the MT-I gene was found to be expressed in all tissues, marked induction by cadmium of the expression of MT-I gene was only observed in the liver. These results indicate: (1) that apoptosis is an early mechanism of acute tissue damage by cadmium in the testes and ventral prostate; (2) that p53 and c-jun genes may be involved in cadmium-induced cytotoxicity (apoptosis) and related carcinogenicity in male reproductive tissues; and (3) that the enhanced expression of MT-I in the liver could protect this organ from cadmium-induced cytotoxicity (apoptosis) and carcinogenicity. Copyright (C) 1999 Elsevier Science Ireland Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicolen_US
dc.relation.ispartofToxicologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCadmium - Toxicityen_US
dc.subject.meshElectrophoresisen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshGenes, Jun - Drug Effectsen_US
dc.subject.meshGenes, P53 - Drug Effectsen_US
dc.subject.meshLiver - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMetallothionein - Geneticsen_US
dc.subject.meshProstate - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTestis - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.titleCadmium-induced apoptosis and changes in expression of p53, c-jun and MT-I genes in testes and ventral prostate of 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.doi10.1016/S0300-483X(99)00115-8en_US
dc.identifier.pmid10647914en_US
dc.identifier.scopuseid_2-s2.0-0032704482en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032704482&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume142en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage13en_US
dc.identifier.isiWOS:000084524900001-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridZhou, T=7402989477en_US
dc.identifier.scopusauthoridZhou, G=23394245100en_US
dc.identifier.scopusauthoridSong, W=14219501800en_US
dc.identifier.scopusauthoridEguchi, N=36779881500en_US
dc.identifier.scopusauthoridLu, W=35122822100en_US
dc.identifier.scopusauthoridLundin, E=36923022200en_US
dc.identifier.scopusauthoridJin, T=7202994136en_US
dc.identifier.scopusauthoridNordberg, G=7005720784en_US

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