title: Influence of dietary-fat on growth of mda-mb231 human breast carcinomas maintained in female athymic nude-mice.
abstract: The purpose of this study was to assess the effects of the type of dietary fat [corn oil (controls), olive oil, linseed oil, primrose oil, canola oil and fish (Menhaden) oil] and the amount of dietary fat on the growth of MDA-MB231 human breast carcinomas in female athymic nude mice. The different types of fats examined in these studies differ widely in their omega-3, -6 and -9 fatty acid contents, fatty acid chain length and their degree of unsaturation. These fats were fed to the carcinoma bearing mice at 20% of the diet by weight and for 5 to 8 weeks. No significant effect of these diets on mouse body weight gains throughout the study was observed. Compared to the corn oil controls, none of the dietary fats significantly affected the growth of the human breast carcinomas in these animals, with the exception of fish oil which consistently and significantly (P<0.05 to P<0.001) suppressed carcinoma growth. DNA synthesis of the human breast carcinomas derived from the fish oil fed mice was assessed by BrdU and PCNA labeling indices and by H-3-thymidine autoradiographic analysis. Despite the fact that the carcinomas derived from the fish oil fed mice were significantly smaller than the carcinomas from the corn oil fed mice, there were no significant differences in any of these parameters of DNA synthesis between the two groups (corn oil and fish oil) of carcinomas. In contrast, in the human breast carcinomas derived from the fish oil fed mice, a significant increase (P<0.01 to P<0.001) in the rate of (125)IUrd loss (K-L/day) and a significant increase (P<0.05 to P<0.001) in the cell loss factor (phi) (phi=1-T-P/T-D) was observed, compared to carcinomas derived from corn oil fed mice. Analysis of the human breast carcinomas for TBARS, a measure of secondary products of lipid peroxidation, revealed that the carcinomas derived from the fish oil fed mice had significantly increased (P<0.001) concentrations of these products compared to carcinomas derived from corn oil fed mice. These results provide evidence that the suppression of growth of human breast carcinoma MDA-MB231 in athymic nude mice by dietary fish oil appears to be due primarily to an increase in the loss of cells from the carcinomas in lieu of a suppression of DNA synthesis, a phenomenon that may be due to the increased concentration of lipid peroxidation products in the tumor tissue. In the studies designed to examine the effect of the amount of fat on growth of MDA-MB231 human breast carcinomas in athymic nude mice, one group of mice was fed a high fat diet (corn oil, 29%) and a second group of mice was fed a low fat diet (corn oil, 1.8%). Both diets were fed at a restricted level, i.e., 65% of ad libitum. A third group of mice was fed a high fat diet (corn oil, 18.1%) ad libitum. The diets were formulated to assure that mice of each group consumed equal amounts of protein, vitamins, minerals and fiber; mice fed the high fat diets (ad libitum and restricted) consumed equal amounts of fat. Growth of the human breast carcinomas in mice fed the high fat and low fat restricted diets was not significantly different despite the large difference in fat consumption. Growth of the carcinomas in mice fed the high fat diet ad libitum was substantially greater than carcinoma growth in mice fed the restricted high fat diet (P<0.001) despite equal amounts of fat consumption. These results demonstrate that in an environment of energy (caloric) restriction, high levels of dietary fat will not enhance growth of MDA-MB231 human breast carcinomas in athymic nude mice, thus emphasizing the important role for energy (calories) in the enhancement of mammary (breast) tumorigenic processes by high fat diets.
authors.forename: C
authors.initials: C
authors.lastname: Welsch
authors.forename: M
authors.initials: M
authors.lastname: Welsch
authors.forename: L
authors.initials: L
authors.lastname: Huelskamp
authors.forename: M
authors.initials: M
authors.lastname: Gonzalez
authors.forename: L
authors.initials: L
authors.lastname: Vanderploeg