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dc.contributor.authorLee, Kai-Fai
dc.contributor.authorLau, Kin-Mang
dc.contributor.authorHo, Shuk-Mei
dc.date2022-08-11T08:09:00.000
dc.date.accessioned2022-08-23T16:15:01Z
dc.date.available2022-08-23T16:15:01Z
dc.date.issued1999-01-12
dc.date.submitted2008-10-15
dc.identifier.citationToxicol Appl Pharmacol. 1999 Jan 1;154(1):20-7. <a href="http://dx.doi.org/10.1006/taap.1998.8556 ">Link to article on publisher's site</a>
dc.identifier.issn0041-008X (Print)
dc.identifier.doi10.1006/taap.1998.8556
dc.identifier.pmid9882588
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34001
dc.description.abstractHighly sensitive, sequence-specific competitive reverse transcriptase-polymerase chain reaction (RT-PCR) protocols were established for the detection and quantification of metallothionein (MT)-I and MT-II messages, in absolute values, in rat tissues. Detection limits for these protocols were in the range of 5 to 10 amol per microgram total RNA. Levels of MT-I and MT-II transcripts in the three major prostatic lobes, kidney, and testis were measured in untreated and cadmium (Cd)-treated rats. The dorsal prostate (DP), lateral prostate (LP), kidney, and testis expressed substantial levels of MT-I and MT-II mRNA while the ventral prostate (VP) had extremely low levels of the transcripts. Cd treatment induced higher levels of MT-I and/or MT-II mRNA expression in all tissues studied with the exception of LP. In the LP, Cd treatment caused reductions of MT-I and MT-II mRNA levels. The Cd-induced levels attained in the VP following Cd exposure were still markedly lower than those found in the kidney, testis, LP, and DP of untreated animals. These findings contradict previous claims that the MT genes in rat VP are unresponsive to Cd activation. The susceptibility of VP to Cd toxicity/carcinogenicity may therefore be explained by low levels of Cd-induced expression rather than lack of induction of MTs.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9882588&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1006/taap.1998.8556
dc.subjectAnimals; Binding, Competitive; Cadmium; Gene Expression; Kidney; Male; Metallothionein; Prostate; RNA, Messenger; Rats; Reverse Transcriptase Polymerase Chain Reaction; Testis
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of cadmium on metallothionein-I and metallothionein-II mRNA expression in rat ventral, lateral, and dorsal prostatic lobes: quantification by competitive RT-PCR
dc.typeJournal Article
dc.source.journaltitleToxicology and applied pharmacology
dc.source.volume154
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/654
dc.identifier.contextkey651124
html.description.abstract<p>Highly sensitive, sequence-specific competitive reverse transcriptase-polymerase chain reaction (RT-PCR) protocols were established for the detection and quantification of metallothionein (MT)-I and MT-II messages, in absolute values, in rat tissues. Detection limits for these protocols were in the range of 5 to 10 amol per microgram total RNA. Levels of MT-I and MT-II transcripts in the three major prostatic lobes, kidney, and testis were measured in untreated and cadmium (Cd)-treated rats. The dorsal prostate (DP), lateral prostate (LP), kidney, and testis expressed substantial levels of MT-I and MT-II mRNA while the ventral prostate (VP) had extremely low levels of the transcripts. Cd treatment induced higher levels of MT-I and/or MT-II mRNA expression in all tissues studied with the exception of LP. In the LP, Cd treatment caused reductions of MT-I and MT-II mRNA levels. The Cd-induced levels attained in the VP following Cd exposure were still markedly lower than those found in the kidney, testis, LP, and DP of untreated animals. These findings contradict previous claims that the MT genes in rat VP are unresponsive to Cd activation. The susceptibility of VP to Cd toxicity/carcinogenicity may therefore be explained by low levels of Cd-induced expression rather than lack of induction of MTs.</p>
dc.identifier.submissionpathgsbs_sp/654
dc.contributor.departmentDepartment of Surgery, Division of Urology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages20-7


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