Previous work by Ip and co-workers showed that
mammary cancer prevention by
conjugated linoleic acid (CLA) is independent of the level of fat in the diet. Because CLA is an isomer of
linoleic acid, there is the question regarding whether the effect of CLA is due to a displacement of
linoleic acid in cells. To further evaluate whether there might be an interaction between
linoleic acid and CLA, the present study was designed to examine the dose response to CLA (at 0.5%, 1%, 1.5%, and 2%) in rats fed a 2% or a 12%
linoleate diet (both basal diets contained 20% total fat by weight). The end points of investigation included the bioassay of mammary
tumorigenesis in the rat dimethylbenz[a]
anthracene model as well as the incorporation of CLA,
linoleic acid, and
arachidonic acid in mammary glands. The mammary
carcinogenesis results showed that the efficacy of
tumor suppression by CLA was not affected by
linoleate intake. With either
linoleate diet, no further protection was evident with levels of CLA > 1%. Analysis of neutral
lipids and
phospholipids of the mammary tissue indicated that 1) the accumulation of CLA in mammary tissue was dose dependent from 0.5% to 2%, 2) CLA concentration was 10 times higher in neutral
lipids than in
phospholipids, 3) the incorporation of CLA in either fraction was not affected by the availability of
linoleic acid, and 4) CLA did not appear to displace
linoleic acid or
arachidonic acid in the mammary tissue. The above findings suggest that there may be distinctive mechanisms in the modulation of
tumor development by
linoleic acid and CLA.