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Objective: Oral hormone therapy (HT) and menopausal age are both prothrombotic risk factors. The aim of our study was to compare the hemostatic parameters in plasma of postmenopausal women after 6 months of oral HT with parameters of control (without treatment) postmenopausal women. Methods: Twenty-seven postmenopausal women were treated with 17β-estradiol (1 mg) and dydrogesterone (5 mg) daily for 6 months. The control group (27 women) did not receive any HT. Hemostatic factors, such as fibrinogen (FG) concentration, activated partial thromboplastin time (APTT), platelet (PLT) count, maximum velocity of clot formation, and fibrin lysis half-time were estimated. Results: The hemostatic parameters in both groups differ significantly. After 6 months oral HT, APTT and the level of FG were higher than in the control group (APTT 30.08 seconds vs. 28.18 seconds, p = 0.02; FG 4.14 g/L vs. 3.03 g/L, p < 0.001). However, the higher values of maximal velocity of FG polymerization (153.53 mOD/min vs. 92.87 mOD/min, p < 0.001), maximum absorbance values (0.306 vs. 0.275, p < 0.001), and fibrin lysis half-time (32.33 minutes vs. 18.11 minutes, p < 0.001) compared with values in the control group also were observed. There was no statistically significant difference in PLT counts between control and women treated with oral HT. Conclusions: Six months of oral combined HT (17β-estradiol and dydrogesterone) caused increased initial velocity of clot formation and inhibition of fibrinolysis. The increased level of FG and its higher polymerization may help explain the increase in venous thrombosis and cardiovascular events reported after the use of oral HT. [ABSTRACT FROM AUTHOR]

OBJECTIVE: A diet rich in natural antioxidants in combination with anticancer therapy is important in reducing morbidity and mortality in addition to diminishing toxicity and side effects of chemotherapeutic agents. Cisplatin (cis-diamminedichloroplatinum II, cis-Pt) is a common chemotherapeutic agent, but it causes side effects, including hematologic toxicity with changes in the biological function of blood cells. METHODS: We compared the action of two phenolic compounds isolated from the bark of Yucca schidigera: trans-3,3',5,5'-tetrahydroxy-4'-methoxystilbene and resveratrol (trans-3,4',5 - trihydroxystilbene, present also in grapes and wine) on oxidative stress induced by cisplatin (used in chemotherapy) and selenium-cisplatin conjugate ([NH(3)](2)Pt(SeO(3) [Se-Pt], with a slight toxic effect on blood cells) in human blood platelets and peripheral blood lymphocytes. RESULTS: The trans-3,3',5,5'-tetrahydroxy-4'-methoxystilbene, like resveratrol, significantly inhibited protein carbonylation (measured by enzyme-linked immunosorbent assay and western blot analysis) in blood platelets treated with platinum compounds (10 mug/mL) and markedly reduced oxidation of thiol groups of proteins in these cells. The trans-3,3',5,5'-tetrahydroxy-4'-methoxystilbene, like resveratrol, caused a distinct reduction of platelet lipid peroxidation induced by platinum compounds. The combined action of the tested phenolic compounds with Se-Pt evoked a significant decrease in DNA damage (measured by the comet assay) in lymphocytes compared with cells treated with Se-Pt only. CONCLUSION: We conclude that one promising natural product may be trans-3,3',5,5'-tetrahydroxy-4'-methoxystilbene, because it is a stronger antioxidant in the tested models in vitro compared with resveratrol (P < 0.05). The trans-3,3',5,5'-tetrahydroxy-4'-methoxystilbene can also be useful as a protective factor against platinum compounds during chemotherapy or cancer prophylaxis. [ABSTRACT FROM AUTHOR]

The phytochemical resveratrol (3,4',5-trihydroxystilbene), which is found in grapes and wine, has been reported to have a variety of anti-inflammatory, anti-platelet and anti-carcinogenic effects. The aim of the present study was to evaluate the effects of trans-resveratrol on adhesion of blood platelets to collagen, as well as on thrombininduced platelet aggregation and malonyldialdehyde (MDA) production in vitro. Pretreatment of platelets with resveratrol (50 mu g/ml) inhibited their adhesion to collagen (by 32% in resting platelets and by 57% in thrombinactivated platelets after 1 h of preincubation) and thrombin-induced platelet aggregation (by 59% after 30 min preincubation). Resveratrol also had an inhibitory effect on the generation of malonyldialdehyde (a marker of thromboxane A2 synthesis) measured as thiobarbituric reactive substance in thrombin-activated platelets. [ABSTRACT FROM AUTHOR]