This paper is focused on the present state-of-the art of modifi cations and effects of dietary oxidized lipids during their transit along the gastrointestinal tract. A survey of the literature reporting changes and effects of oxidized lipids before absorption, fi rst in the stomach and then during enzymatic lipolysis in the small intestine, are addressed. Also, the fate of non-absorbed compounds and their potential implications at the colorectal level are discussed. Among the results found, it is shown that acidic gastric conditions and the infl uence of other dietary components may lead to either further oxidation or antioxidative effects in the stomach. Also, changes in oxidized functions, especially of hydroperoxy and epoxy groups, seem likely to occur. Enzymatic hydrolysis by pancreatic lipase is not effective for triacylglycerol polymers, and hence they can be found as non-absorbed oxidized lipids in the large intestine. Interactions of oxidized lipids with cholesterol absorption in the small intestine and with microfl ora metabolism have been also observed.

Our results support the hypothesis that progesterone and MPA increased HUVEC prostacyclin production in a progesterone receptor-dependent manner, by enhancing COX-1 and COX-2 expression and activities.

Free radical-generated F2α-isoprostanes are a group of compounds with vasoconstrictor properties. To investigate whether estradiol exerts antioxidant actions modifying F2α-isoprostane production, cultured human umbilical vein endothelial cells were exposed to estradiol and other compounds and F2α-isoprostanes were measured in culture medium. Exposure to 1 and 10 nM estradiol for 24 h reduced F2α-isoprostane production by 36 and 49%, respectively ( P < 0.001 vs. control). Exposure to antiestrogens alone (ICI-182780 or EM-652) slightly reduced F2α-isoprostanes ( P < 0.05 vs. control), but much less than exposure to estradiol ( P < 0.05). ICI-182780 reversed the estradiol-induced reduction of F2α-isoprostane concentration ( P < 0.05). Along with time-course analysis, these results suggest that estradiol effects were mediated through estrogen receptor-dependent and -independent mechanisms. Progestogens alone (progesterone or medroxyprogesterone acetate) did not modify F2α-isoprostane production at any of the tested concentrations (1, 10, and 100 nM). Progesterone completely reversed estradiol-induced reduction of F2α-isoprostane production ( P < 0.05 vs. control and estradiol), but medroxyprogesterone acetate did not ( P < 0.05 vs. control).

A series of events, such as increase of cytoplasmic free calcium (Ca2+) and expression of P-selectin (CD62P), an adhesion molecule, on the platelet surface, are significant indicators of platelet activation. We have used flow cytometry to examine Ca2+ mobilization and CD62P expression in platelets in whole blood obtained in women prior to, and after, different forms of hormone replacement therapy. Thirty-two women completed a protocol consisting of two consecutive 1-month periods under oestradiol (E2), administered orally (2 mg/day) or transdermally (50 microg/day) in random order, followed by a 4-week transdermal sequential regime, in which, during the last 14 days, either progesterone (300 mg/day) or medroxyprogesterone acetate (5 mg/day) was added to the 50 microg/day E2, administered orally in random order. None of the hormonal combinations determined significant changes in Ca2+ mobilization or CD62P expression in non-stimulated platelets. However, stimulation of platelets with adenosine diphosphate, but not with thrombin, caused a significant increase in cytoplasmic Ca2+ concentration during treatment with transdermal E2 plus progesterone. Also when stimulating with thrombin, transdermal E2 was more active than oral E2 in increasing CD62P expression, a difference that was not reduced by the addition of progestogens. In conclusion, hormone replacement therapy only increased Ca2+ mobilization or CD62P expression in stimulated platelets, and then followed a varied pattern that was dependent on the stimulant and on the specific hormonal formulation.

Both ICI 182780 and EM-652 exhibited potent antioxidant activity, which could have important biological implications.