The effects of diet and carcinogen on the natural killer cell activity of sprague dawley rats.

Abstract

This study was conducted to determine if dietary fat and/or administration of 7,12 dimethylbenz((alpha))anthracene (DMBA) to Sprague Dawley rats affected the natural killer cell activity of these animals.

There was no difference in the level of inhibitory activity of NK cells from rats on a low fat diet compared to rats on the high fat diet, when the R(, 2)T(, 2) tumor cell line was used as the target cell.

The proliferative activity of NK cells was generally higher in rats on the high fat diet compared to rats on the low fat diet. NK-induced inhibition of YAC-1 cell proliferation correlated inversely with the proliferative activity of the NK cells. Some of the rats fed high fat diets had NK cells whose proliferative activity was approximately twice that of rats fed low fat diets, and whose corresponding inhibitory activity against YAC-1 tumor cells was one-half that of rats on low fat diets.

The inhibitory activity of NK cells was dependent on the quantity of fat in the diet of the rats from which these cells were obtained. Rats which were fed a 20% corn oil diet (high fat) generally had lower levels of inhibitory activity against YAC-1 tumor cells compared to rats fed a diet containing 2% linoleic acid (low fat). While choline deficiency or treatment with DMBA did not alter NK cell activity in either dietary group, the combination of both factors caused a significant reduction in NK cell activity when rats were maintained on a high fat diet.

The incorporation of ('3)H-thymidine into YAC-1 tumor cells was inhibited when Percoll separated, rat spleen cell fractions, and unseparated spleen cells were cultured with YAC-1 tumor cells.

NK cell activity was not constant during the period of study, but tended to display cyclic responses, particularly in rats in the high fat diet.

While the ability of NK cells to inhibit proliferation of YAC-1 tumor cells in vitro was diet dependent, the inability to show diet dependency on the ability of NK cells to inhibit the proliferation of R(, 2)T(, 2) tumor cells in vitro did not necesssarily rule out an in vivo role for NK cells in the resistance of rats to DMBA-induced tumors.