Dose response study of conjugated fatty acid derived from safflower oil on mammary and colon carcinogenesis pretreated with 7,12-dimethylbenz[a]anthracene (DMBA) and 1,2-dimethylhydrazine (DMH) in female Sprague-Dawley rats.

To clarify the chemopreventive effects of conjugated fatty acid derived from safflower oil (CFA-S), rich in conjugated linoleic acid (CLA), on mammary and colon carcinogenesis, 6 week old female Sprague-Dawley (SD) rats received diet containing 0.01, 0.05, 0.1, 1, or 2% CFA-S subsequent to five times subcutaneous injections of 1,2-dimethyl-hydrazine (DMH) at a dose of 40 mg/kg b.w. and a single 50 mg/kg b.w. intragastric application of 7,12-dimethylbenz[a]anthracene (DMBA) during the first 11 days. The experiment was terminated at week 36. Numbers of mammary tumors, colon aberrant crypt foci (ACF), and proliferative indices of mammary tumors, and colon epithelium were analyzed. The 1% dose was found to be optimal for suppression of carcinogenesis in both target organs, a good correlation being noted with between data for cell proliferation. These results suggest that a diet containing appropriate levels of CFA-S may be useful for prevention of mammary and colon cancer.

Effect of a mixture of conjugated linoleic acid isomers on growth performance and antibody production in broiler chicks.

The effect of dietary conjugated linoleic acid (CLA) isomers mixture on antibody titres against sheep blood erythrocytes (SRBC) and immunoglobulin (Ig) G concentration in plasma was studied in broiler chickens. In experiment 1, male and female broiler chicks (11 d of age, Cobb strain) were fed a diet supplemented with 10 g CLA or 10 g safflower-seed oil/kg diet for 2 weeks. An SRBC suspension (5:100, v/v) in a phosphate buffer was intravenously injected at 18 d of age and a blood sample was taken from the wing vein at 25 d of age. Chicks fed the CLA-supplemented diet had enhanced first antibody titres in plasma to SRBC as compared with those fed the safflower-seed oil-supplemented diet, irrespective of sex differences. In experiment 2, male broiler chicks (8 d of age, Ross strain) were fed a basal diet or a diet containing 10 g CLA/kg diet for 3 weeks. CLA in the CLA diet partially replaced the soyabean oil in the basal diet. The SRBC suspension was intravenously injected at 15 and 25 d of age and a blood sample was obtained at 21 and 29 d of age. The first antibody titres against SRBC were higher in chicks fed the CLA diet than those in chicks fed the basal diet, but the second titres were not. Plasma IgG concentrations in chicks fed the CLA diet were higher than those in chicks fed the basal diet on both sampling days. The results showed that dietary CLA enhanced antibody production in broiler chickens.

Inhibition of conjugated fatty acids derived from safflower or perilla oil of induction and development of mammary tumors in rats induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP).

Chemopreventive effects of conjugated fatty acids derived from safflower oil (CFA-S), which contains large amounts of conjugated linoleic acid, and from perilla oil (CFA-P) with abundant conjugated alpha-linolenic acid were examined in a 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced rat mammary carcinogenesis model. Groups of 20-22 6-week-old female Sprague-Dawley (SD) rats were given eight intragastric injections of PhIP at a dose of 100 mg/kg b.w. during the initial 8 week period. Powdered basal diets containing 0.1% CFA-S or CFA-P were applied during or after PhIP treatment until week 40. In the rats receiving CFA-S or CFA-P together with PhIP treatment, retardation of mammary tumor emergence was observed until week 27. The groups given CFA-S or CFA-P after PhIP treatment, in contrast, demonstrated significant decrease in the final incidences of mammary adenocarcinomas. The indices of proliferating cell nuclear antigen positive cells in mammary adenocarcinomas were significantly reduced with both CFA-S and CFA-P in the post-initiation phase. Formation of aberrant crypt foci in the colon and basophilic foci of the pancreas due to the PhIP treatment group were not affected by CFA-S or CFA-P. In a second short-term experiment, female SD rats were maintained on powdered basal diet containing 0.03% PhIP alone or together with 0.1% CFA-S or CFA-P for 4 weeks. Immunohistochemically, CFA-S and CFA-P were revealed to suppress PhIP-DNA adduct formation in the epithelial cells of mammary gland (duct and alveolar cells), colon and pancreas. These results indicated that CFA-P and CFA-S may retard development of PhIP-induced mammary tumors with inhibition of PhIP-DNA adduct formation, and decreased mammary carcinogenesis in the post-initiation period with inhibition of cell proliferation.

Combined effects of dietary conjugated linoleic acid and sesamin triacylglycerol and ketone body production in rat liver.

The effects of a combination of dietary conjugated linoleic acid (CLA) supplemented with sesamin on hepatic ketogenesis and triacylglycerol secretion were compared using the livers of rats fed diets containing 1% CLA or linoleic acid (LA) in combination with 0.2% sesamin for 14 d, respectively. The feeding of CLA, as compared to LA, caused a significant reduction in the weight of perirenal adipose tissue but not that of epididymal adipose tissue, and affected neither growth parameters nor hepatic lipid concentration. Hepatic production of ketone bodies was consistently higher in rats fed CLA than in those fed LA, while triacylglycerol secretion was reversed. No significant difference was noted in the hepatic secretion of cholesterol among the groups. Although there was no effect of the dietary combination of CLA with sesamin on adipose tissue weight, hepatic lipid parameters and ketone body production were observed: i.e., triacylglycerol secretion tended to be reduced. These results suggest that the dietary combination of CLA with sesamin may be an effective approach for lowering serum triacylglycerol levels. The decreased hepatic secretion of triacylglycerol is, in part, due to enhanced fatty acid oxidation in the liver.