6533b823fe1ef96bd127eac2
RESEARCH PRODUCT
Differential proto-oncogene mRNA induction from rats treated with peroxisome proliferators
Mustapha Cherkaoui MalkiMustapha Cherkaoui MalkiYu Chun LoneMarisol Corral-debrinskiNorbert LatruffeNorbert Latruffesubject
MaleSomatic cellGenes mycBiophysicsBiologyKidneyMicrobodiesBiochemistryClofibric AcidProto-OncogenesmedicineAnimalsAcyl-CoA oxidaseClofibrateRNA MessengerMolecular BiologyHypolipidemic AgentsKidneyMessenger RNAClofibrateOncogeneFibric AcidsCell BiologyPeroxisomeMolecular biologyRats Inbred F344RatsGenes rasmedicine.anatomical_structureGene Expression RegulationLiverOrgan SpecificityAcyl-CoA OxidaseCiprofibrateOxidoreductasesmedicine.drugdescription
After experimental treatment of rats with clofibrate or ciprofibrate, two peroxisomes proliferators with hypolipidemic activity, RNAs were prepared from liver, kidney, heart and brain; hybridization was done with DNA probes for c-myc and c-Ha-ras oncogenes and for cyanide insensitive Acyl CoA oxidase, a peroxisomal protein. c-myc mRNA is highly abundant in liver and at a lower extent in kidney, especially after treatment with ciprofibrate; clofibrate also allows a c-myc mRNA increase, but at a lower extent. c-Ha-ras, which is already expressed in all tested tissues from control animals, is stimulated by clofibrate and ciprofibrate treatments. Comparatively these compounds stimulate the cyanide insensitive Acyl CoA oxidase expression as well as they increase the somatic index of liver and kidney. From these experiments we suggest that hepatocarcinogenesis triggered by some hyolipidemic agents could be mediated by proto-oncogene mRNA level increase.
year | journal | country | edition | language |
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1990-12-31 | Biochemical and Biophysical Research Communications |