Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1991-4-15
pubmed:abstractText
Effects of a single administration of hepatotoxic chemicals on the major gap-junction protein of liver (connexin 32) were studied in rats. The connexin-32 content was analyzed by immunoblotting and immunohistochemistry using an affinity-purified monoclonal antibody against connexin 32. The connexin-32 content decreased dramatically to less than 10% of the control value 24 h after injection of 25 mg/kg dimethylnitrosamine and returned to the normal level 240 h later. Injection of CCl4 at a dose of 1 ml/kg also caused a transient reduction of connexin-32 content in the liver, as seen after the dimethylnitrosamine injection. The decrease in hepatic connexin-32 content was inversely correlated to the increase in plasmic alanine-aminotransferase activity which has been used as an index of acute liver injury. The changes in connexin 32 were essentially similar to those observed in regenerating liver after partial hepatectomy. However, incorporation of [3H]thymidine into liver DNA after dimethylnitrosamine injection was significantly less than that obtained after partial hepatectomy. The 5'-nucleotidase activity of the plasma-membrane fraction of the liver was not significantly altered by the injection of dimethylnitrosamine. These results suggest that liver gap-junction protein is specifically reduced by acute liver injury and that this kind of decrease in connexin 32 is not simply related to cell proliferation, unlike the decrease after partial hepatectomy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-2956
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
196
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-42
pubmed:dateRevised
2007-7-23
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Single administration of hepatotoxic chemicals transiently decreases the gap-junction-protein levels of connexin 32 in rat liver.
pubmed:affiliation
Department of Medical Biochemistry, Ehime University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't