Linked Life Data

3697756

Source:http://linkedlifedata.com/resource/pubmed/id/3697756

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1986-6-13
pubmed:abstractText
The effects of bromocriptine on GH3 pituitary tumor cell [3H]thymidine incorporation were studied. Cells were grown in the presence of bromocriptine, then exposed to a short-term pulse of [3H]thymidine in serum-free medium containing deoxycytidine (10 microM) to prevent deoxythymidine triphosphate (dTTP) pooling. After 48 h exposure to bromocriptine, basal prolactin (PRL)-secretion during 45 min was inhibited by 50% by 10 microM bromocriptine and thyroid releasing hormone-induced PRL stimulation was suppressed. Incorporation of radiolabelled thymidine into acid-precipitable DNA increased progressively from 15 to 60 min and was abolished by simultaneous incubation with excess unlabelled thymidine (100 microM). Bromocriptine (10 microM) inhibited incorporation of 5-50 microM [3H]thymidine, but this was not reversed by simultaneous incubation with metoclopramide (10 microM). Aminopterin, an inhibitor of endogenous de novo DNA synthesis, stimulated [3H]thymidine incorporation twofold and this increased DNA salvage pathway activity was also blocked by bromocriptine. As incorporation of [3H]thymidine into acid-soluble cell nucleotides was also inhibited by bromocriptine, the data suggest that in these cells the drug inhibits thymidine kinase activity, a salvage pathway of DNA synthesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
369
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
83-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Bromocriptine inhibits incorporation of [3H]thymidine into rat pituitary tumor cells.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.