Linked Life Data

10966522

Source:http://linkedlifedata.com/resource/pubmed/id/10966522

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-10-13
pubmed:abstractText
Cadmium (Cd) is an environmental pollutant of increasing importance, due to industrialization, smoking, and the lack of effective therapy for Cd poisoning. The general population is exposed to Cd principally through food and water. The metal accumulates slowly in the liver and kidney, the target organs of acute and chronic Cd toxicity, respectively. We showed recently that liver is also a target organ for chronic Cd toxicity. Gap junctional intercellular communication (GJIC) is a means of maintaining cellular homeostasis in multicellular organisms. It involves the transfer of small, water-soluble molecules through intercellular channels (gap junctions), composed of proteins called connexins. The major connexins of liver (hepatocytes) are connexin 32 (Cx32) and connexin 26 (Cx26). Cd disrupts cellular homeostasis in the liver through its induction of necrosis, apoptosis, and cellular proliferation. It is to be expected, therefore, that Cd must exert some effect on GJIC. This study investigates Cd-induced alterations in GJIC, Cx32, and Cx26 expression, and in cytoskeletal actin, and relates the changes to apoptosis and cell proliferation induced by Cd in vivo. Mice were injected ip with 30 micromol Cd/kg, and were observed for up to 48 h. Other groups of mice were injected with 5-60 micromol Cd/kg and observed for 9 h. Blood and liver were harvested and used for analysis of GJIC, connexin expression, cytoskeletal actin, serum enzymes, and liver pathology. Cd produced a time- and dose-dependent inhibition of GJIC in liver, along with parallel decreases in the expression of Cx32 and Cx26. Cd also produced disruption and loss of cytoskeletal actin in liver in a time- and dose-dependent manner. These observations are discussed in relation to the toxicity of Cd, and possible mechanisms of induction of the GJIC-related alterations are presented.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1096-6080
pubmed:author
pubmed:issnType
Print
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
156-66
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Cadmium decreases gap junctional intercellular communication in mouse liver.
pubmed:affiliation
Center for Environmental and Occupational Health, Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, 2018 Breidenthal Building, 3901 Rainbow Boulevard, Kansas City, Kansas 66160-7417, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't