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University of Illinois College of Medicine at Urbana-Champaign, Urbana, IL 61801
Isoenergetic diets containing 20% corn oil, 20% beef tallow, or an equal mixture of 10% corn oil and 10% beef tallow (mixed fat) were fed to 30 rats per diet for 28 weeks following weaning. DMBA [7,12-dimethylbenz(a)anthracene] was administered (1.75 mg/100 g body weight) in a single oral dose after 4 weeks of feeding. After 28 weeks, 70% of the rats fed corn oil had mammary tumors versus 47% for mixed fat and 30% for tallow. Diet had no effect on the number of tumors per tumor-bearing rat or the proportion of tumors that were adenocarcinomas. Other rats assigned to each of the three diets were killed at the time corresponding to DMBA administration for examination of hepatic mixed-function oxidase activity. NADPH cytochrome c reductase activity and cytochrome P-450 content were higher in rats fed corn oil or mixed fat rather than tallow. However, no significant differences in aryl hydrocarbon hydroxylase, glutathione transferase, and uridine-diphosphoglucuronide transferase activities were observed. The effects of dietary fat saturation on enzyme activity failed to show a clear association with DMBA carcinogenesis. In other rats assigned to the three dietary treatments for 4 or 16 weeks, lipid saturation did not change serum prolactin (PRL) concentrations during diestrus or proestrus. PRL secretion was examined following a provocative stimulus (perphenazine) in rats fed the experimental diets for 4 or 1022 weeks. Although perphenazine increased serum PRL and depleted the pituitary of PRL, differences in dietary lipid saturation caused no significant changes in these indices. These data show that the incidence of mammary tumors in rats fed high fat diets (20% by weight) was greater in those fed corn oil compared to beef tallow. The effect of dietary lipid source on tumorigenesis was not associated with changes in carcinogen-metabolizing enzyme activity or PRL secretion.
KEY WORDS: dietary fat corn oil beef tallow mixed-function oxidase breast cancer 7,12-dimethylbenz(a)anthracene serum prolactin perphenazine
1 Supported by Public Health Service, National Institutes of Health, National Cancer Institute grant numbers CA22326 and CA28629, and Public Health Service Environmental Toxicology Training Grant HEW PHS 07-001.
2 Animals were maintained under guidelines set forth by the Institute of Laboratory Animal Resources, National Research Council.
3 Present address: The University of Chicago, The Pritzker School of Medicine, Department of Medicine, 5841 South Maryland Ave., Chicago, IL 60637.
4 Present address: Dallas/Ft. Worth Medical Center in Grand Prairie, 2709 Hospital Boulevard, Grand Prairie, TX 75051.
5 To whom reprint requests should be made.
Manuscript received 14 February 1984.