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© 1993 Oxford University Press

research-article

Modulation of c-myc Gene Expression in Rat Livers by Aflatoxin B1 Exposure and Age1

P. S. LARSON*,2, G. MCMAHON{dagger} and G. N. WOGAN*

*Division of Toxicology, Whitaker College of Health Sciences and Technology, Department of Chemistry, Massachusetts Institute of Technology Cambridge, Massachusetts 02139 {dagger}Division of Oncology, Sandoz Research Institute East Hanover, New Jersey 07936

Received July 31, 1992; accepted November 4, 1992

A single dose of aflatoxin B1 (AFB1) caused a rapid and transient induction in c-myc mRNA levels in livers derived from adult male Fischer 344 rats. The inducibility of c-myc expression by AFB1 increased with age as c-myc mRNA levels from untreated livers declined from 18-fold in 29-day-old animals to 1-fold in 39-day-old animals, relative to untreated 43-day-old control animals. A dose-dependent increase in c-myc mRNA was found when 53- and 76-day-old rats were administered various AFB1 doses whereas 29-day-old animals exhibited essentially no change in c-myc mRNA levels for the doses examined. Rats were treated with multiple doses of AFB1 to induce hepatoccllular carcinomas. C-myc mRNA levels were measured in rat liver samples taken during and subsequent to chronic AFB1 exposure. Characterization of the c-myc induction response at the time of AFB1 exposure revealed that a transient elevation of c-myc mRNA occurred during each (5-day) dosing period for the first 3 weeks, consistent with the acute exposure studies. RNA prepared from hepatocellular carcinomas exhibited elevated levels of c-myc mRNA compared to vehicle-treated control animals. Examination of tumors isolated from the 28-day-old animals showed that the increased c-myc mRNA observed was not the result of gene amplification or gene rearrangement. A comparison of tumor data showed that the 28-day-old animals had a 100% liver tumor incidence while the 38-day-old rats had a 20% liver tumor incidence. The presence of elevated c-myc mRNA in young 28-day-old animals may signify a developmental susceptibility to the hepatocarcinogenic effects of AFB1.


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