Linked Life Data

9096284

Source:http://linkedlifedata.com/resource/pubmed/id/9096284

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-4-28
pubmed:abstractText
Various pesticides and transition metals induce oxidative deterioration of biological macromolecules. Protein kinase C (PKC) may mediate these effects. However, no information is available regarding whether these xenobiotics can modulate PKC which is a critical event signaling the increase in endothelial permeability and cell proliferation. Female Sprague-Dawley rats were treated p.o. with two 0.25 LD50 doses of selected pesticides and transition metal salts at 0 and 21 h, and killed at 24 h. PKC activities were measured in liver and brain tissues. Cultured PC-12 cells were incubated for 24 h with 50, 100 or 200 nM concentrations of these pesticides, while 0.20, 0.40 or 0.60 microM concentrations of cadmium chloride (Cd(II)) and sodium dichromate (Cr(VI)) salts were employed. PKC activations were observed in the hepatic and brain cytosol fractions by all xenobiotics. Approximately 1.4- to 2.0-fold and 1.6- to 3.5-fold increases in PKC activity in the hepatic and brain cytosol fractions were observed, respectively. In the hepatic tissues, the greatest increases in activities were observed with TCDD, chlorpyrifos, endrin and Cd(II), while chlorpyrifos and fenthion exerted the greatest increases in the brain tissues. In cultured PC-12 cells, the greatest activation of PKC was observed primarily with 100-nM concentrations of the pesticides. The maximum effects were induced by chlorpyrifos, fenthion, Cd(II) and Cr(VI) salt. The results clearly indicate that pesticides as well as Cd(II) and Cr(VI) salts can modulate a vital component of the cell signaling pathway, namely PKC activity. PKC may be a target of free radicals and oxidative stress, leading to altered cell proliferation and differentiation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0378-4274
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9096284-Animals, pubmed-meshheading:9096284-Brain, pubmed-meshheading:9096284-Cadmium Chloride, pubmed-meshheading:9096284-Cell Division, pubmed-meshheading:9096284-Cell Survival, pubmed-meshheading:9096284-Chromates, pubmed-meshheading:9096284-Endothelium, pubmed-meshheading:9096284-Enzyme Activation, pubmed-meshheading:9096284-Female, pubmed-meshheading:9096284-Herbicides, pubmed-meshheading:9096284-Hydrocarbons, Chlorinated, pubmed-meshheading:9096284-Insecticides, pubmed-meshheading:9096284-Lethal Dose 50, pubmed-meshheading:9096284-Liver, pubmed-meshheading:9096284-Male, pubmed-meshheading:9096284-Organothiophosphorus Compounds, pubmed-meshheading:9096284-PC12 Cells, pubmed-meshheading:9096284-Protein Kinase C, pubmed-meshheading:9096284-Rats, pubmed-meshheading:9096284-Rats, Sprague-Dawley, pubmed-meshheading:9096284-Signal Transduction, pubmed-meshheading:9096284-Tetrachlorodibenzodioxin
pubmed:year
1997
pubmed:articleTitle
Comparative in vitro and in vivo protein kinase C activation by selected pesticides and transition metal salts.
pubmed:affiliation
Department of Pharmaceutical and Administrative Sciences, Creighton University, Omaha, NE 68178, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't