Introduction

It is well established that PUFAs have a protective effect in BC. The aim of this research was to investigate the effect the EPA on the OE2DH system. OE2DH is responsible for the interconversion of E, and E2. Of the three endogenous estrogens, E2 is the most potent because it has the highest affinity for estrogen receptors (ER). E,, on the other hand has very little and, at times, no significant biological activity. Several studies have indicated increased levels of E2 in malignant breast tissue when compared to normal breast tissue (1-4).

Whilst it has been shown that progestins and estrogens directly stimulate reductive OE2DH activity (5), there are relatively few other studies examining the control of this complex. To the best of our knowledge, only one publication has considered the effects of fatty acids upon the activity of this enzyme. Blomquist, el al. (6) showed that isolated human placental OE2DH activity was inactivated by several unsaturated fatty acids (oleic, arachidonic, linoleic, linolenic), and postulated that the soluble enzyme may contain a binding site at or near pyridine nucleotide binding sites. The work presented herein is novel since it is the first to consider the effects of fatty acids upon the OE2DH system within afunctioning cell, and to consider the significance of this process in cancer.

Blomquist, et al. suggested that fatty acid manipulation of the OE2DH system was possible. Adams, et al. (5) showed that altering the OE2DH activity had a profound influence upon the growth of MCF7 cells in culture. Taken together these observations (6, 5) suggest a potential mechanism through which dietary PUFA's might influence cell growth in malignant breast tissue. The aim of this report is to investigate whether EPA might in part exert its anti-tumour effects through manipulation of E2DH activity.

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