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  • Title: T-cell mitogenesis and natural killer cell activity in colonic tumor-bearing and nontumor-bearing rats fed diets high in lipid with and without cholesterol.
    Author: Kraus LJ, Williams RM, Murphy K, Broitman SA.
    Journal: Nutr Cancer; 1987; 9(2-3):159-70. PubMed ID: 3494235.
    Abstract:
    It has been shown that rats fed diets high in lipid and cholesterol develop more 1,2-dimethylhydrazine (DMH)-induced bowel tumors than those fed diets low in lipid or without cholesterol. To further explore the effects of these dietary regimens on immune function, rats were fed diets containing 20% safflower or coconut oil, with or without cholesterol (1%) and cholic acid (0.3%), for 35 weeks during which time they were given DMH. Only rats bearing one or more colon tumors and that showed no evidence of weight loss were utilized. Two parameters of cell-mediated immune function were assessed in tumor- and nontumor-bearing control rats: a) response to the T-cell mitogen, phytohemaglutinin (PHA), and b) natural killer cell activity (NKCA). Nearly total suppression of PHA response was observed in the polyunsaturated fat diet group compared with the saturated fat diet groups. Addition of cholesterol to either the polyunsaturated or saturated fat diets diminished PHA response and, to a lesser degree, of T-lymphocytes from rats fed these diets. NKCA, however, was unaffected by either the quality of dietary fat or cholesterol. There were no detectable effects of DMH per se 15 weeks after the last injection (or in the presence or absence of tumors) on T-lymphocyte response to PHA or on NKCA. The relationships among lipid nutrition, carcinogen-induced tumorigenesis, and immunologic events is obviously complex. These studies imply that nutritional interventions may have a selective rather than a generalized effect on various immunocompetent cell populations. Furthermore, the effects of lipid nutriture, rather than long-term effects of carcinogen administration, or the presence of bowel tumors appear to play the major role on perceived alterations in in vitro immune function. Thus the effects of these lipid nutritional interventions on DMH-induced tumorigenesis seem independent of their effects on immune phenomena with the immune probes utilized.
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