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Biomedical subjects

Mohsen Meydani

Publications and source records attributed to Mohsen Meydani.

At least 19 recordsLinked to original sources
PubMed2007

Prostatic fatty acids and cancer recurrence after radical prostatectomy for early-stage prostate cancer.

OBJECTIVE: Results from some observational studies suggest that diet and energy balance influence the clinical course of early-stage prostate cancer. To evaluate possible mechanisms, we prospectively examined the relation between prostatic concentrations of fatty acids at diagnosis and cancer recurrence following primary therapy. METHODS: Fatty acids were measured by capillary gas chromatography in fresh, non-cancerous prostate tissue collected from 184 men undergoing radical prostatectomy for clinically localized prostate cancer. Their association with risk of biochemical disease recurrence (a rising serum prostate-specific antigen following a disease-free [<0.1 ng/ml] interval > or =6 months) was analyzed using Cox proportional hazards models incorporating patient age, body mass index, tumor characteristics at diagnosis, and ethnicity. RESULTS: During an average follow-up of 48.7 months (median = 47), 14 patients experienced biochemical recurrence. Percent total polyunsaturated fatty acid and the ratio of oleic-to-stearic acid associated with risk (multivariable hazards ratio [HR] = 0.51, 95% confidence interval [CI] = 0.29 to 0.90, p = 0.021 and HR = 1.68, 95% CI = 1.21 to 2.33, p = 0.002, respectively, per 1 standard deviation increase). CONCLUSIONS: The results of this study are preliminary, but they suggest that pre-diagnostic prostatic concentrations of fatty acids associate with risk of biochemical recurrence following radical prostatectomy for clinically localized prostate cancer.

Black or African American↗
PubMed2006

Mechanism by which avenanthramide-c, a polyphenol of oats, blocks cell cycle progression in vascular smooth muscle cells.

Previously, we reported that avenanthramide-c (Avn-c), one of the major avenanthramides, polyphenols of oats, inhibited the serum-induced proliferation of vascular smooth muscle cells (SMC), which is an important process in the initiation and development of atherosclerosis. In the present study, we further investigated its cell cycle inhibitory mechanism. Rat embryonic aortic smooth muscle cell line A10 was used in this study. Flow cytometry analysis revealed that treatment of A10 cells with 80 muM Avn-c arrested the cell cycle in G1 phase as indicated by an increase in the number of cells in G1 phase and a decrease in the number of cells in S phase. This cell cycle arrest was associated with a decrease in the phosphorylation of retinoblastoma protein (pRb), whose hyperphosphorylation is a hallmark of the G1 to S transition in the cell cycle. The inhibition of pRb phosphorylation with Avn-c was accompanied by a decrease in cyclin D1 expression and an increase in cyclin-dependent kinase inhibitor p21cip1 expression, without significant changes in p27kip1 expression. Furthermore, Avn-c treatment increased the expression level and stability of p53 protein, which could account for the increase of p21cip1 expression. Our results demonstrate for the first time that Avn-c, which is a unique polyphenol found in oats, arrests SMC proliferation at G1 phase by upregulating the p53-p21cip1 pathway and inhibiting pRB phosphorylation. This inhibitory effect of Avn-c on SMC proliferation is an additional indication for the potential health benefit of oat consumption in the prevention of coronary heart disease beyond its known effect through lowering blood cholesterol.

Animals↗
PubMed2006

Green tea catechin, epigallocatechin-3-gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex.

A potential mechanism by which green tea may prevent cancer development is through the inhibition of angiogenesis. We have shown previously that the green tea catechin, epigallocatechin gallate (EGCG), inhibits endothelial cell tube formation through the inhibition of vascular endothelial growth factor (VEGF)-induced Akt activation and vascular endothelial (VE)-cadherin phosphorylation. Furthermore, EGCG can suppress oxidant-induced production of the proangiogenic cytokine interleukin (IL)-8. To further elucidate the antiangiogenic mechanisms of EGCG, we investigated its regulation of other molecular processes in VEGF-induced signaling in human umbilical vein endothelial cells (HUVECs). We show that EGCG at physiological doses (0.5-10 microM) markedly inhibits the formation of a vascular endothelial growth factor receptor 2 complex formed upon the binding of its ligand VEGF. This disruption results in a significant and dose-dependent decrease in PI3-kinase activity. Electrophoretic mobility shift assay revealed that EGCG decreased the PI3 kinase-dependent activation and DNA-binding ability of NF-kappaB, likely acting through decreasing phosphorylation and degradation of IkappaB. VEGF-induced IL-8 production at the mRNA (real time RT-PCR) and protein levels (ELISA) are also suppressed with EGCG. These results suggest a novel mechanism for green tea's anticancer effects where EGCG can abrogate VEGF signaling by interfering with the formation of a receptor complex, resulting in attenuated mitogenic and angiogenic signaling.

Catechin↗
PubMed2006

Effect of concomitant consumption of fish oil and vitamin E on T cell mediated function in the elderly: a randomized double-blind trial.

OBJECTIVES: To determine if concomitant consumption of fish oil and vitamin E would modify the vitamin E level needed for improving T cell mediated function in elderly. METHODS: A randomized and double-blind study was conducted using 40 healthy male and female elderly subjects (>65 y) who were randomly assigned to one of 4 groups (n = 10/group). All the subjects received 5 g of fish oil daily containing 1.5 g eicosapentaenoic acid (EPA) and 1 g docosahexaenoic acid (DHA), and a capsule containing different doses of dl-alpha-tocopherol (0, 100, 200 or 400 mg/day) for 3 mo. Plasma vitamin E and fatty acid levels, and in vivo [delayed-type hypersensitivity skin response (DTH) and T cell sub-population analysis] and ex vivo [mitogen-stimulated peripheral blood mononuclear cells (PBMC) proliferation and interleukin (IL)-2 production] immune functions were determined at baseline and after supplementation. RESULTS: The control group (fish oil only) did not show a statistically significant change in either DTH or PBMC proliferation. DTH response, however, was significantly increased from baseline in all groups supplemented with fish oil plus vitamin E and a significant positive correlation between DTH response and plasma concentrations of alpha-tocopherol was observed. PBMC proliferation was only significantly increased in the group supplemented with fish oil plus 200 mg vitamin E. However, the changes caused by fish oil plus vitamin E in either DTH or PBMC proliferation were not significantly different from those observed in control group. Plasma levels of alpha-tocopherol were significantly increased in all three fish oil plus vitamin E groups and the increase in plasma alpha-tocopherol level was less profound than that previously reported when vitamin E was given alone. CONCLUSIONS: The immuno-enhancing effect of vitamin E in the elderly is dampened when it is concomitantly consumed with fish oil. This may be due to the smaller increase in plasma concentrations of vitamin E in the presence of fish oil.

Aged↗
PubMed2005

Avenanthramide, a polyphenol from oats, inhibits vascular smooth muscle cell proliferation and enhances nitric oxide production.

The proliferation of vascular smooth muscle cells (SMC) and impaired nitric oxide (NO) production are both crucial pathophysiological processes in the initiation and development of atherosclerosis. Epidemiological data have indicated that diets rich in whole grain foods are associated with a reduced risk of developing atherosclerosis. Avenanthramides are polyphenols found exclusively in oats (Avena sativa L.). The present study was conducted to examine the effect of synthetically prepared avenanthramide-2c on the proliferation of SMC and NO production by SMC and human aortic endothelial cells (HAEC). Avenanthramide-2c significantly inhibited serum-induced SMC proliferation. At a concentration of 120 microM, avenanthramide-2c inhibited more than 50% of SMC proliferation, as measured by [3H] thymidine incorporation, and increased the doubling time of rat SMC line (A10) from 28 to 48 h. Treatment of human SMC with 40, 80, and 120 microM avenanthramide-2c inhibited cell number increase by 41, 62, and 73%, respectively. In addition, avenanthramide-2c treatment significantly and dose-dependently increased NO production in both SMC and HAEC. At a concentration of 120 microM, avenanthramide-2c increased NO production by three-fold in SMC, and by nine-fold in HAEC. These increases were in parallel with the up-regulation of mRNA expression for endothelial NO synthase (eNOS) in both vascular SMC and HAEC. These results suggest that the avenanthramides of oats may contribute to the prevention of atherosclerosis through inhibition of SMC proliferation and increasing NO production.

Animals↗
PubMed2005

Chemical structure of flavonols in relation to modulation of angiogenesis and immune-endothelial cell adhesion.

The antioxidant activity of flavonoids has been suggested to contribute to several health benefits associated with the consumption of fruits and vegetables. Four flavonols - myricetin (M), quercetin (Q), kaempferol (K) and galangin (G), all with different numbers of hydroxyl moieties (-OH) - were examined for their antioxidant activity and cytotoxicity on human umbilical vein endothelial cells (HUVECs) and for their potential antiangiogenic and cell adhesion effects. The relative antioxidant capacity of these flavonols in cell culture medium (cell-free system) and their intracellular antioxidant activity were M = Q > K = G, which correlated respectively with the presence of 3, 2, 1 and 0 moieties of -OH on their B-ring. The higher the numbers of -OH moieties on the B-ring the less toxic the flavonol was to HUVEC, and the LD50 was determined as: M (100 microM) > Q (50 microM) > K (20 microM) > G (10 microM). These flavonols at approximately 0.5 LD50 doses suppressed the vascular endothelial growth factor (VEGF)-stimulated HUVEC tubular structure formation by: M (47%) > Q (37%) > K (15%) > G (14%), which was not linearly associated with their numbers of -OH moieties. However, the magnitude of flavonols' suppression of activated U937 monocytic cells adhesion to HUVEC was associated with the number of -OH moieties on the B-ring. This was prominent when U937 cells were pretreated with these flavonols. In contrast, the numbers of -OH moiety had no apparent influence on the adhesion or expression of adhesion molecules when activated HUVECs were pretreated with these flavonols. The presence of different numbers of -OH moieties on the B-ring of the flavonols may contribute to their antioxidant activity as well as their toxicity and may play an important role in their potency for biological action such as angiogenesis and immune-endothelial cell adhesion, which, respectively, are important processes in the development of cancer and atherosclerosis.

Antioxidants↗
PubMed2005

Vitamin E increases production of vasodilator prostanoids in human aortic endothelial cells through opposing effects on cyclooxygenase-2 and phospholipase A2.

Impairment of endothelium-dependent vasodilation is associated with the initiation and development of atherosclerosis. Vasodilator prostanoids constitute a protective mechanism in maintaining normal vasomotor function. In the current study, we determined the effect of in vitro vitamin E supplementation at physiologically relevant concentrations (10-60 micromol/L) on the production of the vasodilator prostanoids prostaglandin I(2) (PGI(2); prostacyclin) and prostaglandin E(2)(PGE(2)) by human aortic endothelial cells (HAECs) as well as its underlying mechanism. Results showed that vitamin E dose dependently (10-40 micromol/L) increased the production of both prostanoids by HAECs. This was associated with a dose-dependent (10-40 micromol/L) upregulation of cytosolic phospholipase A(2) (cPLA(2)) expression and arachidonic acid release. In contrast, vitamin E dose dependently (10-60 micromol/L) inhibited cyclooxygenase (COX) activity but did not affect the expression of either COX-1 or COX-2, indicating that the effect of vitamin E on COX activity was post-translational. Thus, vitamin E had opposing effects on the 2 key enzymes in prostanoid biosynthesis; at the concentrations used in this study, this resulted in a net increase in the production of vasodilator prostanoids. The vitamin E-induced increase in PGI(2) and PGE(2) production may contribute to its suggested beneficial effect in preserving endothelial function.

Aorta↗
PubMed2005

A Mediterranean-style diet and metabolic syndrome.

A moderate increase in physical activity and a detailed and tailored Mediterranean-style diet reduce the prevalence of metabolic syndrome and associated cardiovascular risks through reducing systemic vascular inflammation and endothelium dysfunction, particularly in those patients who do not lose weight.

Cardiovascular Diseases↗
PubMed2005

Myocardial concentrations of fatty acids in dogs with dilated cardiomyopathy.

OBJECTIVE: To compare myocardial concentrations of fatty acids in dogs with dilated cardiomyopathy (DCM) with concentrations in control dogs. SAMPLE POPULATION: Myocardial tissues from 7 dogs with DCM and 16 control dogs. PROCEDURE: Myocardial tissues were homogenized, and total fatty acids were extracted and converted to methyl esters. Myocardial concentrations of fatty acids were analyzed by use of gas chromatography and reported as corrected percentages. RESULTS: The amount of docosatetraenoic acid (C22:4 n-6) was significantly higher in myocardial samples from dogs with DCM (range, 0.223% to 0.774%; median, 0.451%), compared with the amount in samples obtained from control dogs (range, 0.166% to 0.621%; median, 0.280%). There were no significant differences between DCM and control dogs for concentrations of any other myocardial fatty acids. CONCLUSIONS AND CLINICAL RELEVANCE: Although concentrations of most myocardial fatty acids did not differ significantly between dogs with DCM and control dogs, the concentration of docosatetraenoic acid was significantly higher in dogs with DCM. Additional investigation in a larger population is warranted to determine whether this is a primary or secondary effect of the underlying disease and whether alterations in fatty acids may be a target for intervention in dogs with DCM.

Animals↗
PubMed2004

Inverse association between prostatic polyunsaturated fatty acid and risk of locally advanced prostate carcinoma.

BACKGROUND: An effect of fatty acids has been implicated in men with advanced-stage prostate carcinoma and in men who have died of the disease. To evaluate the influence of fatty acids in men with prostate carcinoma at earlier stages, the authors examined the relation between prostatic concentrations of fatty acids and locally advanced prostate carcinoma in men with clinically organ-confined disease. METHODS: Fatty acids were measured by capillary gas chromatography in fresh, nonmalignant prostate tissue specimens collected during surgery from 196 men undergoing radical prostatectomy for localized prostate carcinoma. Two-sided, two-sample Student t tests compared mean concentrations in men with extraprostatic disease (pT3-4N0-1M0) with control men with organ-confined disease. Logistic regression accounted for clinical stage, prostate-specific antigen level, Gleason sum, and other factors. RESULTS: Percent total prostatic polyunsaturated fatty acid (PUFA) was found to be inversely associated with risk of locally advanced prostate carcinoma (n=52) (odds ratio [OR]=0.93, 95% confidence interval [95% CI], 0.87-0.99; P=0.035). Risk of seminal vesicle involvement accounted for this association (OR=0.86, 95% CI, 0.78-0.95; P=0.003). Percent omega-3 fatty acid (eicosapentanoic + docosahexanoic acids) and percent arachidonic acid also were found to be inversely related to the risk of seminal vesicle involvement (OR=0.52, 95% CI, 0.30-0.90; P=0.02; and OR=0.84, 95% CI,; 0.75-0.95; P=0.005, respectively). CONCLUSIONS: Prostatic PUFA levels appear to influence the risk of locally advanced prostate carcinoma in men with clinically organ-confined disease. This association may be mediated through the immune system.

Aged↗
PubMed2004

The antiatherogenic potential of oat phenolic compounds.

Avenanthramides are phenolic antioxidants, which are present in oats. Avenanthramides A, B, and C are the major constituents of the total soluble antioxidant phenolic compounds in oats. We tested the potential antiatherogenic activity of partially purified avenanthramides from oats by examining their effects on adhesion of monocytes to human aortic endothelial cell (HAEC) monolayers, expression of adhesion molecules, and production of proinflammatory cytokines and chemokines by HAEC. The oat avenanthramides mixture was prepared and partially purified by column chromatography. This avenanthramide-enriched mixture (AEM) had no toxicity to HAEC as tested up to 40 ng/ml. The pre-incubation of HAEC with 4, 20, and 40ng/ml AEM for 24h significantly decreased adhesion of U937 monocytic cells to interleukin (IL)-1beta-stimulated HAEC in a concentration-dependent manner. Pre-incubation of HAEC with AEM at 20 and 40 microg/ml, but not at 4 microg/ml, for 24h significantly suppressed IL-1beta-stimulated expressions of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin and the secretion of proinflammatory cytokines IL-6, chemokines IL-8 and monocyte chemoattractant protein (MCP)-1. These data provide evidence for the potential anti-inflammatory and antiatherogenic effects of antioxidant avenanthramides present in oats.

Antioxidants↗
PubMed2004

Vitamin E supplementation suppresses macrophage accumulation and endothelial cell expression of adhesion molecules in the aorta of hypercholesterolemic rabbits.

Suppression of cell adhesion molecule expression and macrophage accumulation by the endothelium is believed to play an important role in preventing the development of atherosclerosis. Earlier, we have shown that in vitro supplementation of human aortic endothelial cells with Vitamin E dose-dependently reduced expression of adhesion molecules and monocyte adhesion. Here, we report the in vivo down-regulation of endothelial cell adhesion molecules expression and macrophage accumulation in the aortas of hypercholesterolemic rabbits supplemented with Vitamin E. To this end, New Zealand White rabbits were fed a semi-purified diet containing 30 (control) or 1000 IU/kg Vitamin E. After 4 weeks, both groups' diets were switched to an atherogenic diet (0.3% cholesterol, 9% hydrogenated coconut oil, and 1% corn oil) containing the respective levels of Vitamin E and fed for 2, 4, and 6 weeks. Vitamin E supplemented rabbits had significantly higher levels of Vitamin E in their plasma and aortas. Frozen aorta sections were fixed and stained by an avidin-biotin complex method using Rb2/3 and Rb1/9 monoclonal antibodies against rabbit ICAM-1 and VCAM-1, respectively, and with RAM-11 for macrophage and von Willebrand factor for endothelial cells, followed by staining with secondary antibodies and counterstaining and evaluation under the microscope. At 6 weeks on atherogenic diet treatment, a trend (P = 0.08) toward a lower score of ICAM-1 expression by endothelial cells was observed in the aorta of Vitamin E treated rabbits compared to the control. However, a decrease in the score of VCAM-1 expression by endothelial cells in Vitamin E treated rabbits did not reach to a statistical significance. At 4 and 6 weeks on atherogenic diet, Vitamin E supplementation also significantly (P = 0.003) inhibited the accumulation of macrophages in the aorta. These results support the concept that down-regulation of adhesion molecule expression and suppression of monocyte/macrophage activation by Vitamin E in vivo is one of the potential mechanisms by which Vitamin E may suppress the development of aortic lesions in a rabbit model of atherosclerosis.

Administration, Oral↗
PubMed2004

Vitamin E modulation of cardiovascular disease.

Endothelium in the vascular system is an important modulator of vasomotor tone and coagulation, and it plays a crucial role in the inhibition of adhesion and activation of platelets and leukocytes. Evidence indicates that dietary antioxidants may modulate these endothelium-dependent vascular functions through several mechanisms and may contribute to the prevention of vascular diseases such as atherosclerosis. Several cell cultures as well as animal and human clinical and observational studies have tested the efficacy of vitamin E on vascular function and the prevention of atherosclerosis. Our cell culture studies have indicated that vitamin E (alpha-tocopherol) inhibits the activation of endothelial cells stimulated by high levels of low-density lipoprotein cholesterol and pro-inflammatory cytokines. This inhibition is associated with the suppression of chemokines, the expression of cell surface adhesion molecules, and the adhesion of leukocytes to endothelial cells, all of which contribute to the development of lesions in the arterial wall. The molecular mechanisms by which alpha-tocopherol and other tocopherols modulate endothelial cells and smooth muscle functions have been delineated. We, and others, have also demonstrated a positive effect of dietary vitamin E on endothelium and vascular function in animal models of atherosclerosis. Several human clinical trials have also shown an improvement in the surrogate markers of atherosclerosis and vascular function by vitamin E supplementation. However, these findings have been contradicted by several vitamin E supplementation trials for the prevention of secondary cardiovascular events showing null effect. Intervention at a relatively late stage of disease and the single use of vitamin E rather than in combination with other antioxidants might have contributed to these contradictory findings. Evidence from cell cultures, as well as animal and human clinical and observational studies, strongly supports the contribution of dietary vitamin E to the maintenance of vascular function and health, in particular when it is used in combination with other dietary antioxidants, which are found in fruits, vegetables, and nuts.

Animals↗
PubMed2004

Effect of concomitant consumption of fish oil and vitamin E on production of inflammatory cytokines in healthy elderly humans.

A beneficial effect of fish oil in reducing inflammatory and cardiovascular diseases has been suggested. This effect occurs in part through fish oil's inhibition of synthesis of pro-inflammatory cytokines. Epidemiologic studies have shown a link between increased intake of vitamin E in diet and reduced risk of cardiovascular disease. Since pro-inflammatory cytokines have been indicated in pathogenesis of cardiovascular diseases, the current study was designed to determine the effect of concomitant consumption of fish oil and vitamin E on interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha production by peripheral blood mononuclear cells (PBMCs). Healthy elderly subjects consumed fish oil plus different doses of vitamin E for 3 months. The results indicated that, in general, fish oil inhibited production of pro-inflammatory cytokines and vitamin E did not interfere with this effect of fish oil; rather its supplementation might further contribute to the fish oil-induced inhibition of these cytokines, in particular at the 200 mg/d dose.

Aged↗
PubMed2004

Effect of vitamin E on prostacyclin (PGI2) and prostaglandin (PG) E2 production by human aorta endothelial cells: mechanism of action.

Vitamin E has been suggested to reduce the risk of cardiovascular diseases. Prostanoids are vasoactive molecules, the change in whose production contributes to homeostasis and pathophysiology of the cardiovascular system. In the current study, we determined the effect of vitamin E on production of vasodilative PGI(2) and PGE(2) by human aorta endothelial cells (HAECs) and its underlying mechanism. Results showed that vitamin E increased production of both prostanoids by HAECs. This effect of vitamin E is due to increased release of substrate arachidonic acid, which in turn results from increased expression of phospholipase A(2) (PLA(2)).

Aorta↗
PubMed2003

Green tea catechins inhibit VEGF-induced angiogenesis in vitro through suppression of VE-cadherin phosphorylation and inactivation of Akt molecule.

Studies have indicated that the consumption of green tea is associated with a reduced risk of developing certain forms of cancer and angiogenesis. The mechanism of inhibition of angiogenesis by green tea or its catechins, however, has not been well-established. Vascular endothelial (VE)-cadherin, an adhesive molecule located at the site of intercellular contact, is involved in cell-cell recognition during vascular morphogenesis. The extracellular domain of VE-cadherin mediates initial cell adhesion, whereas the cytosolic tail binding with beta-catenin is required for interaction with the cytoskeleton and junctional strength. Therefore, the cadherin-catenin adhesion system is implicated in cell recognition, differentiation, growth and migration of capillary endothelium. Using tube formation of human microvascular endothelial cells (HMVEC) in culture as an in vitro model of angiogenesis, we reported that vascular endothelial growth factor (VEGF)-induced tube formation is inhibited by anti-VE-cadherin antibody and dose-dependently by green tea catechins. We also demonstrated here that inhibition of tube formation by epigallocatechin gallate (EGCG), one of the green tea catechins, is in part mediated through suppression of VE-cadherin tyrosine phosphorylation and inhibition of Akt activation during VEGF-induced tube formation. These findings indicate that VE-cadherin and Akt, known downstream proteins in VEGFR-2-mediated cascade, are the new-targeted proteins by which green tea catechins inhibit angiogenesis.

Angiogenesis Inhibitors↗
PubMed2003

Bioavailability of soybean isoflavones from aglycone and glucoside forms in American women.

BACKGROUND: Test results on the bioavailability of isoflavones in the aglycone or glucoside form in Eastern and Western human subjects are contradictory. OBJECTIVE: The objective was to investigate the bioavailability of the soy isoflavones daidzein and genistein in American women with typical American dietary habits after ingestion of the aglycone or glucoside form of isoflavones. DESIGN: Fifteen American women aged 46 +/- 6 y participated in a randomized, double-blind study. Blood samples were collected 0, 1, 2, 4, 8, 12, 24, and 48 h after consumption of aglycone or glucoside tablets with breakfast. The plasma curves for daidzein, genistein, and equol were constructed and the postprandial maximum concentration (C(max)), time to the maximum concentration (t(max)), and area under the curve (AUC) were determined. RESULTS: Isoflavone concentrations peaked early (1-2 h) in plasma and peaked again at 4-8 h. Mean C(max), t(max), and AUC values for genistein were not significantly different after ingestion of aglycone or glucoside. However, C(max) and AUC values, but not t(max), were significantly higher for daidzein after aglycone ingestion, which was partly due to its higher content in the aglycone tablets. Equol appeared after 4 h and remained elevated after 48 h. Despite a higher content of daidzein in the aglycone tablets, the AUC for equol was significantly higher after ingestion of the glucoside tablets, probably because of the metabolic action of intestinal bacteria during the long intestinal transit time of glucoside. CONCLUSION: The apparent bioavailability of genistein and daidzein is not different when consumed as either aglycone or glucoside by American women.

Adult↗