Isoflavone phytoestrogens consumed in soy decrease F(2)-isoprostane concentrations and increase resistance of low-density lipoprotein to oxidation in humans.
BACKGROUND
Oxidative damage to lipids may be involved in the etiology of atherosclerosis, cardiovascular disease in general, and cancer. The soy isoflavone phytoestrogens, genistein and daidzein, and equol (a daidzein metabolite produced by intestinal microflora) are antioxidants in vitro; equol is a particularly good inhibitor of LDL oxidation and membrane lipid peroxidation.


OBJECTIVE
We sought to investigate the effects of a diet enriched with soy containing isoflavones on in vivo biomarkers of lipid peroxidation and resistance of LDL to oxidation, compared with a diet enriched with soy from which the isoflavones had been extracted.


METHODS
: A randomized, crossover design was used to compare diets enriched with soy that was low or high in isoflavones in 24 subjects. Plasma concentrations of an F(2)-isoprostane, 8-epi-prostaglandin F(2)(alpha) (8-epi-PGF(2)(alpha)), a biomarker of in vivo lipid peroxidation, and resistance of LDL to copper-ion-induced oxidation were determined.


RESULTS
Plasma concentrations of 8-epi-PGF(2)(alpha) were significantly lower after the high-isoflavone dietary treatment than after the low-isoflavone dietary treatment (326 +/- 32 and 405 +/- 50 ng/L, respectively; P = 0.028) and the lag time for copper-ion-induced LDL oxidation was longer (48 +/- 2.4 and 44 +/- 1.9 min, respectively; P = 0.017). Lag time for oxidation of unfractionated plasma and plasma concentrations of malondialdehyde, LDL alpha-tocopherol, polyunsaturated fatty acids, and isoflavonoids did not differ significantly between dietary treatments.


CONCLUSIONS
Consumption of soy containing naturally occurring amounts of isoflavone phytoestrogens reduced lipid peroxidation in vivo and increased the resistance of LDL to oxidation. This antioxidant action may be significant with regard to risk of atherosclerosis, cardiovascular disease in general, and cancer.
Department of Nutrition and Dietetics, the Nutrition, Food, and Health Research Centre, King's College London, UK. helen.wiseman@kcl.ac.uk
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Wiseman
J D
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O'Reilly
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Adlercreutz
A I
AI
Mallet
E A
EA
Bowey
I R
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Rowland
T A
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Sanders
D000328:Adult; D002318:Cardiovascular Diseases / Q000517:prevention & control; D018592:Cross-Over Studies; D004032:Diet; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000097:blood; D004968:Estrogens, Non-Steroidal / Q000008:administration & dosage*; D028441:F2-Isoprostanes; D005260:Female; D006801:Humans; D007529:Isoflavones / Q000008:administration & dosage*; D015227:Lipid Peroxidation; D008077:Lipoproteins, LDL / Q000097:blood / Q000737:chemistry*; D008297:Male; D009369:Neoplasms / Q000517:prevention & control; D048789:Phytoestrogens; D028321:Plant Preparations; D013025:Glycine max
D004968:Estrogens, Non-Steroidal; D028441:F2-Isoprostanes; D007529:Isoflavones; D008077:Lipoproteins, LDL; D048789:Phytoestrogens; D028321:Plant Preparations; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost