Patent Foramen Ovale Channel Morphometric Characteristics Associated with Cryptogenic Stroke: The MorPFO Score.

BACKGROUND: It is still disputable whether the specific morphologic properties of patent foramen ovale (PFO) may contribute to the occurrence of stroke. The aim of this study was to evaluate the differences in the morphometric and functional features of the PFO channel in patients with cryptogenic stroke and those without stroke. METHODS: PFO channel morphology in 106 consecutive patients with cryptogenic stroke and 93 control patients without stroke with diagnosed PFO (by transesophageal echocardiography) was analyzed using transesophageal echocardiography. A validation cohort was established that consisted of 31 patients with cryptogenic stroke and 30 without stroke. RESULTS: Multivariable regression logistic analyses indicated PFO channel length change (odds ratio [OR], 2.50; 95% confidence interval [CI], 1.75-3.55; P < .001), PFO length/height ratio during the Valsalva maneuver (OR, 0.75; 95% CI, 0.60-0.95; P = .015), septum primum thickness (OR, 0.34; 95% CI, 0.14-0.80; P = .013), septum secundum height (OR, 0.91; 95% CI, 0.84-0.98; P = .013), the presence of an atrial septal aneurysm (OR, 3.38; 95% CI, 1.27-8.97; P = .014), and large shunt (OR, 2.49; 95% CI, 1.13-5.46; P = .022) as PFO-related stroke factors. The Morphologic Stroke Factors of PFO (MorPFO) score was developed, in which six factors were included: PFO channel length reduction (≥21%; 7 points), short septum secundum (<8.6 mm; 5 points), thin septum primum (<1.6 mm; 3 points), large right-to-left shunt (3 points), low PFO channel length/height ratio during the Valsalva maneuver (≤2.1; 2 points), and atrial septal aneurysm presence (1 point). Patients with scores of 0 to 7 points have low-risk PFO channels, those with scores of 8 to 11 points have intermediate-risk PFO channels, and those with scores of 12 to 21 points have high-risk PFO channels. External validation showed good MorPFO score performance (C index = 0.90). CONCLUSIONS: Transesophageal echocardiography can be used to differentiate pathogenic from incidental PFO channels on the basis of their morphologic characteristics. The MorPFO score may help identify high-stroke-risk PFO channels.

Tree height as the main factor causing disappearance of the terricolous lichens in the lichen Scots pine forests.

The lichen Scots pine forests habitats are undergoing rapid disappearance across Europe. Due to the semi-natural character of this habitat and an increase of the nitrification as a result of air pollution, determination of factors responsible for the decrease in lichen field layer cover requires a comprehensive approach. Our study aimed to investigate environmental factors necessary for the determination of active protection measures in order to maintain this vulnerable habitat. Specifically, we aimed to investigate: 1) the environmental factors influencing lichen cover in the lichen Scots pine forests of Bory Tucholskie National Park; 2) the differences in habitat variables between sites with lichen-rich and bryophyte-rich field layers. In our study, we used vegetation and microhabitat properties data collected over three years of surveys, as well as ALS LiDAR data. Our results indicated that lichen and bryophyte cover, tree height, tree cover, thickness of organic matter layer, soil temperature and soil water content differed between lichen-rich and bryophyte-rich sites. We found a significant negative relationship between lichen cover recorded within the field layer and tree height. The lichen-rich field layer developed better in areas with lower tree height and thinner layer of organic matter, which created a favorable habitat conditions for lichen development. Our research revealed the previously unknown impact of tree height for the development of lichen field layer. These findings can be used to plan the active conservation measures of lichen Scots pine forests.

Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores.

Iron deficiency (ID) commonly occurs in chronic heart failure (HF) and is associated with poor prognosis. Neither its causes nor pathophysiological significance are clearly understood. We aimed to assess iron status and the effect of iron supplementation in the rat model of post-myocardial infarction (MI) HF. Four weeks after induction of MI to induce HF or sham surgery, rats received intravenous iron (ferric carboxymaltose) or saline, 4 doses in 1-week intervals. HF alone did not cause anemia, systemic or myocardial ID, but reduced myocardial ferritin, suggesting depleted cardiomyocyte iron stores. Iron therapy increased serum Fe, ferritin and transferrin saturation as well as cardiac and hepatic iron content in HF rats, but did not increase myocardial ferritin. This was accompanied by: (1) better preservation of left ventricular (LV) ejection fraction and smaller LV dilation, (2) preservation of function of Ca2+ handling proteins in LV cardiomyocytes and (3) reduced level of inflammatory marker, CRP. Furthermore, iron supplementation did not potentiate oxidative stress or have toxic effects on cardiomyocyte function, but increased activity of antioxidant defenses (cardiac superoxide dismutase). Despite lack of systemic or myocardial ID we found evidence of depleted cardiomyocyte iron stores in the rat model of HF. Furthermore we observed positive effect of iron supplementation and confirmed safety of iron supplementation in this setting.

Acute Heart Rate-Dependent Hemodynamic Function of the Heart in the Post-Myocardial Infarction Rat Model: Change Over Time.

BACKGROUND: Optimal heart rate (HR) for acute hemodynamic efficiency in heart failure (HF) is unknown. METHODS: Wistar-Kyoto rats were followed-up for 3 and 7 days, 1 or 2 months after myocardial infarction (MI) or sham operation (ShO) and left ventricle (LV) pressure-volume (PV) loops were obtained at various HRs: baseline 400 beats per minute (bpm), reduced by ivabradine to 320 bpm, increased by atrial pacing to 480 bpm, under normal conditions and after preload increase (PI). RESULTS: In the ShO group, PI augmented cardiac output (CO) by 55%, 67%, 84% at reduced, baseline, and increased HR, respectively. In post-MI rats, PI augmented CO 3 and 7 days, but not 1 and 2 months after MI. At increased HR, in response to PI, CO increased 3 and 7 days, tended to fall 1 and 2 months after MI; this hemodynamic response was salvaged by HR reduction. Further beneficial effects of HR reduction included reduction of LV end-diastolic pressure, increase of ejection fraction, contractility and relaxation velocity 1 and 2 months after MI. CONCLUSIONS: In a rat HF model, optimal HR with regard to acute hemodynamic performance is shifted. Whereas in ShO rats increased HR facilitates CO increase induced by PI, in HF rats, such increase reduces CO, and HR reduction has beneficial effects. Thus, besides reducing progression of HF, HR-reducing interventions also offer immediate hemodynamic benefits.

Omega-3 Fatty Acids Do Not Protect Against Arrhythmias in Acute Nonreperfused Myocardial Infarction Despite Some Antiarrhythmic Effects.

Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). To elucidate the effect of the omega-3 polyunsaturated fatty acids (PUFAs) on ventricular arrhythmias in acute nonreperfused MI, rats were fed with normal or eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA)-enriched diet for 3 weeks. Subsequently the rats were subjected to either MI induction or sham operation. ECG was recorded for 6 h after the operation and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. Six hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca(2+) handling was assessed and expression of proteins involved in Ca(2+) turnover was studied separately in non-infarcted left ventricle wall and infarct borderzone. EPA and DHA had no effect on occurrence of post-MI ventricular arrhythmias or mortality. Nevertheless, DHA but not EPA prevented Ca(2+) overload in LV cardiomiocytes and improved rate of Ca(2+) transient decay, protecting PMCA and SERCA function. Moreover, both EPA and DHA prevented MI-induced hyperphosphorylation of ryanodine receptors (RyRs) as well as dispersion of action potential duration (APD) in the left ventricular wall. In conclusion, EPA and DHA have no antiarrhythmic effect in the non-reperfused myocardial infarction in the rat, although these omega-3 PUFAs and DHA in particular exhibit several potential antiarrhythmic effects at the subcellular and tissue level, that is, prevent MI-induced abnormalities in Ca(2+) handling and APD dispersion. In this context further studies are needed to see if these potential antiarrhythmic effects could be utilized in the clinical setting. J. Cell. Biochem. 117: 2570-2582, 2016. © 2016 Wiley Periodicals, Inc.

[Food hypersensitivity in patients with pollen allergy].

Clinical observations indicate the frequently reported food hypersensitivity among patients, sensitive to airborne allergens. Symptoms of food hypersensitivity in this group of patients are often exacerbated during the pollen season. These reactions may be the results of cross-reactions between pollen and food allergens or food and pollen allergy coexisting. The aim of the study was to determine the incidence of food hypersensitivity in patients allergic to airborne allergens, the type of clinical manifestations and a kind of food frequently causing the symptoms. Retrospective analyses of case records of 55 randomly selected patients with airborne allergy aged from 18 to 72 yrs (mean 55 yrs), including 28 women ranging in age from 18 years to 62 yrs (mean 36 yrs) and 27 men aged from 18 to 72 yrs (mean 34 yrs) were carried out. All patients underwent skin prick tests with the following allergens: grass, rye, birch, alder, hazel, mugwort, plantain, Dermatophagoides farinae, Dermatophagoides pteronyssinus, skin dog, cat dander, Alternaria alternata, Cladosporium herbarum. We assessed the type of clinical manifestations of pollen allergy and evaluated the type of clinical manifestations of food hypersensitivity and the type of foods that caused it. In the examined 55 patients, 15 individuals reported food hypersensitivity (27.2%), the most frequently after consumption of apples, carrots, cherry, peach, hazelnut, walnut, celery and nectarines. Clinical manifestation of food hypersensitivity was mainly oral allergy syndrome (OAS). Hypersensitivity to food above all was reported by patients with allergic rhinitis, sensitive to grass and tree pollen. Due to the high prevalence of food hypersensitivity in patients allergic to airborne allergens, it seems advisable to consider avoiding eating some foods, such as apple, carrots, cherries, peach, particularly frequently cross-reacting with grass and trees allergens. This dietary restriction can prevent about 30% of patients with inhalant allergy against onset of oral allergy.

The role of fibrinogen, fibrin and fibrin(ogen) degradation products (FDPs) in tumor progression.

Participation of fibrin, fibrinogen, and their degradation products in pathogenesis and progression of cancer may lead to complications of thromboembolic events. The tumor may be a source of fibrinogen. Fibrinogen inside the tumor is one of the factors of its growth and metastasis. Fibrinogen, fibrin and their degradation products possess proinflammatory activity. They indirectly stimulate endothelium to secrete von Willebrand factor, leading to activation of platelets accompanying neoplastic disorders. Fragments E and D are the end products of fibrin(ogen) degradation and E and DD are the end products of stabilized fibrin. E stimulates proliferation, migration and differentiation of endothelial cells, contributing to tumor vasculature. Increased levels of DD are observed in malignant neoplasms, such as breast, lung, colon and ovary cancers. In breast cancers DD correlates with progression of disease and metastasis. The role of fibrinogen and the products of its degradation in the progression of various tumors is not sufficiently understood.

The disturbance of hemostasis induced by hyperhomocysteinemia; the role of antioxidants.

Elevated concentration of homocysteine (Hcy) in human tissues, definied as hyperhomocysteinemia has been correlated with some diseases, such as cardiovascular, neurodegenerative, and kidney disorders. Homocysteine occurs in human blood plasma in several forms, including the most reactive one, the homocysteine thiolactone (HTL) - a cyclic thioester, which represents up to 0.29% of total plasma Hcy. In the article, the effects of hyperhomocysteinemia on the complex process of hemostasis, which regulates the flowing properties of blood, are described. Possible interactions of homocysteine and its different derivatives, including homocysteine thiolactone, with the major components of hemostasis such as endothelial cells, blood platelets, plasmatic fibrinogen and plasminogen, are also discussed. Modifications of hemostatic proteins (N-homocysteinylation or S-homocysteinylation) induced by Hcy or its thiolactone seem to be the main cause of homocysteine biotoxicity in hemostatic abnormalities. It is suggested that Hcy and HTL may also act as oxidants, but various polyphenolic antioxidants are able to inhibit the oxidative damage induced by Hcy or HTL. We also discuss the role of phenolic antioxidants in hyperhomocysteinemia -induced changes in hemostasis.

Clovamide-rich extract from Trifolium pallidum reduces oxidative stress-induced damage to blood platelets and plasma

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Numerous plants (including clovers) have been widely used in folk medicine for the treatment of different disorders. This in vitro study was designed to examine the antioxidative effects of the clovamide-rich fraction, obtained from aerial parts of Trifolium pallidum, in the protection of blood platelets and plasma against the nitrative and oxidative damage, caused by peroxynitrite (ONOO−). Carbonyl groups and 3-nitrotyrosine in blood platelet and plasma proteins were determined by ELISA tests. Thiol groups level was estimated by using 5,5¡ä-dithio-bis(2-nitro-benzoic acid, DTNB). Plasma lipid peroxidation was measured spectrophotometrically as the production of thiobarbituric acid reactive substances. The results from our work indicate that clovamide-rich T. pallidum extract may reveal the protective properties in the prevention against oxidative stress. The presence of clovamide-rich T. pallidum extract (12.5¨C100 ¦Ìg/ml) partly inhibited ONOO−-mediated protein carbonylation and nitration. All the used concentrations of T. pallidum extract reduced lipid peroxidation in plasma. The antioxidative action of the tested extract in the protection of blood platelet lipids was less effective; the extract at the lowest final concentration (12.5 ¦Ìg/ml) had no protective effect against lipid peroxidation. The present results indicate that the extract from T. pallidum is likely to be a source of compounds with the antioxidative properties, useful in the prevention against the oxidative stress-related diseases (AU)

In vitro study of the antioxidative properties of the glucose derivatives against oxidation of plasma components

No disponible

Oxidative stress has been implicated in the pathogenesis of variety of diseases. Since the endogenous antioxidant defense may be not adequate to counteract the enhanced generation of oxidants, a growing interest in research for exogenous nutrients has been observed. The present study was designed to assess in vitro the antioxidative properties of the glucose derivatives: calciumD-glucarate, D-gluconic acid lactone, and sodium D-gluconate (0.5–3 mM) in the protection of plasma proteins and lipids, against the damage caused by 0.1 mM peroxynitrite (ONOO−). Exposure of plasma to ONOO− resulted in carbonyl groups increase, 3-nitrotyrosine (3-NT) formation, reduction in thiol groups, and enhanced lipid peroxidation. D-Gluconic acid lactone and sodium D-gluconate effectively decreased 3-NT formation; the antinitrative action of calcium D-glucarate was less effective. In plasma samples incubated with ONOO− and tested compounds, the level of carbonyl groups was decreased in comparison to plasma samples treated only with ONOO−. The level of protein −SH groups and glutathione was significantly higher in the presence of glucose derivatives than in plasma samples treated with ONOO− only. All the tested compounds had the inhibitory effect on the peroxynitrite-induced plasma lipids peroxidation. The results obtained from our work indicate that calcium D-glucarate, D-gluconic acid lactone, and sodium D-gluconate may partly protect plasma proteins and lipids against peroxynitrite-induced damages (AU)

[Balance of proteinases and antiproteinases and smoking tobacco]. / Równowaga proteazowo-antyproteazowa a palenie tytoniu.

Smoking tobacco can induce formation of inflammable state in respiratory tract and cause lungs damage. Experimental investigations affirm, that the exposure to tobacco smoke causes growth of penetrability of blood-vessels, which favors the enlarged migration of inflammable cells. The growth of exposure to reactive forms of oxygen and concentration changes of cellular antioxidants enzymes, leads to disorders in balance of proteinases and antiproteinases and oxidative stress. As the years go, the disorders mentioned above can lead to deterioration of ventilating efficiency of lungs, and consequently to pronouncement chronic obstructive pulmonary disease (COPD), which becomes serious problem on a world scale.

Clovamide-rich extract from Trifolium pallidum reduces oxidative stress-induced damage to blood platelets and plasma.

Numerous plants (including clovers) have been widely used in folk medicine for the treatment of different disorders. This in vitro study was designed to examine the antioxidative effects of the clovamide-rich fraction, obtained from aerial parts of Trifolium pallidum, in the protection of blood platelets and plasma against the nitrative and oxidative damage, caused by peroxynitrite (ONOO(-)). Carbonyl groups and 3-nitrotyrosine in blood platelet and plasma proteins were determined by ELISA tests. Thiol groups level was estimated by using 5,5'-dithio-bis(2-nitro-benzoic acid, DTNB). Plasma lipid peroxidation was measured spectrophotometrically as the production of thiobarbituric acid reactive substances. The results from our work indicate that clovamide-rich T. pallidum extract may reveal the protective properties in the prevention against oxidative stress. The presence of clovamide-rich T. pallidum extract (12.5-100 µg/ml) partly inhibited ONOO(-)-mediated protein carbonylation and nitration. All the used concentrations of T. pallidum extract reduced lipid peroxidation in plasma. The antioxidative action of the tested extract in the protection of blood platelet lipids was less effective; the extract at the lowest final concentration (12.5 µg/ml) had no protective effect against lipid peroxidation. The present results indicate that the extract from T. pallidum is likely to be a source of compounds with the antioxidative properties, useful in the prevention against the oxidative stress-related diseases.

The extract from hop cones (Humulus lupulus) as a modulator of oxidative stress in blood platelets.

The plant Humulus lupulus is known as the raw material of the brewing industry. Hop cones, rich in polyphenolic compounds and acyl phloroglucides, are widely used to preserve beer and to give it a characteristic aroma and flavor. Hop cones have long been used for medicinal purposes. In particular, hop preparations were mainly recommended for the treatment of sleeping disorders. The antioxidative action of hop cones, however, is poorly understood. The aim of our present study was to investigate in vitro changes in human blood platelets induced by peroxynitrite (ONOO(-), the compound of particular importance for vascular thrombosis and inflammatory process) in the presence of hop cone extract (Humulus lupulus). The antioxidative action of the extract was also compared with the properties of a well-characterized antioxidative commercial monomeric polyphenol, resveratrol (3,4',5-trihydroxystilbene) in a model system in vitro. Various biomarkers of oxidative/nitrative stress, such as carbonyl groups, 3-nitrotyrosine and thiobarbituric acid reactive substances (TBARS) were estimated. The 3-nitrotyrosine formation and carbonyl group generation was assessed by the use of a competition ELISA test and ELISA test, respectively. Tested plant extract (12.5-50 µg/ml), like resveratrol, significantly inhibited protein carbonylation and nitration in the blood platelets treated with ONOO(-) (0.1 mM). The extract from hop cones, like resveratrol, also caused a distinct reduction of platelet lipid peroxidation induced by ONOO(-). The present results indicate that the hope cone extract has in vitro protective effects against ONOO(-), such as induced oxidative/nitrative damage to the human platelet proteins and lipids. However, in comparative studies the extract was not found to be a more effective antioxidant than the solution of pure resveratrol.

Antioxidative properties of curcumin in the protection of blood platelets against oxidative stress in vitro.

The present in vitro study was designed to estimate the antioxidative activity of curcumin in the protection of human blood platelets and plasma against peroxynitrite (ONOO(-))-induced oxidative stress. The effects of curcumin (12.5-50 µg/ml) on ONOO(-)-induced damage of proteins and lipids were determined by the estimation of protein carbonyl groups, 3-nitrotyrosine formation, and thiobarbituric acid reactive substance (TBARS) generation. Exposure of blood platelets and plasma to 100 µM ONOO(-) resulted in an increased level of carbonyl groups, nitration of protein tyrosine residues, and enhanced lipid peroxidation. Curcumin inhibited carbonyl group formation in plasma and in platelet proteins. The highest dose of curcumin (50 µg/ml) reduced blood platelet protein carbonylation by approximately 40%. In the protection of blood plasma protein, the lower doses of curcumin (12.5 and 25 µg/ml) were more effective. Curcumin partially prevented 3-nitrotyrosine formation in plasma proteins; the effect of curcumin was only statistically significant in blood platelets at the highest dose (50 µg/ml). The antioxidative action of curcumin in the protection against lipid peroxidation caused by ONOO(-) was also observed. Curcumin suppressed the formation of TBARS both in blood platelets and in plasma samples. The highest concentration of curcumin (50 µg/ml) decreased the TBARS level by approximately 35% in both blood platelets and plasma samples. In conclusion, the present study demonstrates the antioxidative properties of curcumin and its protective effects against oxidative/nitrative changes of blood platelets and plasma components, especially proteins and lipids.

In vitro study of the antioxidative properties of the glucose derivatives against oxidation of plasma components.

Oxidative stress has been implicated in the pathogenesis of variety of diseases. Since the endogenous antioxidant defense may be not adequate to counteract the enhanced generation of oxidants, a growing interest in research for exogenous nutrients has been observed. The present study was designed to assess in vitro the antioxidative properties of the glucose derivatives: calcium D-glucarate, D-gluconic acid lactone, and sodium D-gluconate (0.5-3 mM) in the protection of plasma proteins and lipids, against the damage caused by 0.1 mM peroxynitrite (ONOO⁻). Exposure of plasma to ONOO⁻ resulted in carbonyl groups increase, 3-nitrotyrosine (3-NT) formation, reduction in thiol groups, and enhanced lipid peroxidation. D-gluconic acid lactone and sodium D-gluconate effectively decreased 3-NT formation; the antinitrative action of calcium D-glucarate was less effective. In plasma samples incubated with ONOO⁻ and tested compounds, the level of carbonyl groups was decreased in comparison to plasma samples treated only with ONOO⁻. The level of protein -SH groups and glutathione was significantly higher in the presence of glucose derivatives than in plasma samples treated with ONOO⁻ only. All the tested compounds had the inhibitory effect on the peroxynitrite-induced plasma lipids peroxidation. The results obtained from our work indicate that calcium D-glucarate, D-gluconic acid lactone, and sodium D-gluconate may partly protect plasma proteins and lipids against peroxynitrite-induced damages.

L-Carnitine protects plasma components against oxidative alterations.

OBJECTIVE: L-Carnitine as a dietary supplement has been reported to have a beneficial effect on several cardiovascular risk parameters and exercise capacity, but the biological relevance of its activity is poorly understood. Dietary supplements (including L-carnitine) are often used to foster exercise performance; however, these may affect some pathways of human body metabolism. The aim of this study in vitro was to determine antioxidative properties of L-carnitine (0.1-100 µM) added to plasma and to assess if L-carnitine might protect plasma proteins and lipids against oxidative/nitrative damage (determined by levels of protein carbonyl groups, thiols, 3-nitrotyrosine formation and thiobarbituric-acid reactive substances generation) caused by 100 µM peroxynitrite (ONOO(-)), a strong physiologic oxidative/nitrative agent. METHODS: The level of carbonyl group generation was measured by a colorimetric method. For the estimation of 3-nitrotyrosine formation, a competition enzyme-linked immunosorbent assay was performed. Plasma lipid peroxidation was measured spectrophotometrically as the production of thiobarbituric-acid reactive substances. High-performance liquid chromatography was used to analyze total free thiol groups of plasma proteins and low-molecular-weight thiols (glutathione, cysteine, and homocysteine) in plasma. RESULTS: The L-carnitine added to plasma inhibited in vitro ONOO(-)-induced oxidation and nitration of blood plasma proteins. Incubation of plasma with peroxynitrite resulted in the decrease of protein thiols. L-Carnitine had a protective effect on peroxynitrite-induced decreased -SH level in plasma proteins. The presence of L-carnitine also prevented the decrease of low-molecular-weight thiols (glutathione, cysteine, and homocysteine) in plasma caused by peroxynitrite and protected plasma lipids against peroxidation induced by peroxynitrite. CONCLUSIONS: These results demonstrated that L-carnitine possesses antioxidative activity.

The effect of polyphenolic-polysaccharide conjugates from selected medicinal plants of Asteraceae family on the peroxynitrite-induced changes in blood platelet proteins.

Lots of plants belonging to Asteraceae family are very popular in folk medicine in Poland. These plants are also known as being rich in acidic polysaccharides, due to the presence of hexuronic acids or its derivatives. Our preliminary experiments have shown that the extract from Conyza canadensis L. possesses various biological activity, including antiplatelet, antiocoagulant and antioxidant properties. The aim of our study was to assess if macromolecular glycoconjugates from selected herbal plants of Asteraceae family: Achillea millefolium L., Arnica montana L., Echinacea purpurea L., Solidago virgaurea L., Chamomilla recutita (L.) Rauschert., and Conyza canadensis L. protect platelet proteins against nitrative and oxidative damage induced by peroxynitrite, which is responsible for oxidative/nitrative modifications of platelet proteins: the formation of 3-nitrotyrosine and carbonyl groups. These modifications may lead to changes of blood platelet functions and can have pathological consequences. The role of these different medicinal plants in the defence against oxidative/nitrative stress in human platelets is still unknown, therefore the oxidative damage to platelet proteins induced by peroxynitrite and protectory effects of tested conjugates by the estimation of carbonyl group level and nitrotyrosine formation (a marker of protein nitration) were studied in vitro. The antioxidative properties of the polyphenolic-polysaccharide conjugates from selected tested medicinal plants were also compared with the action of a well characterized antioxidative commercial polyphenol - resveratrol (3,4',5-trihydroxystilbene). The obtained results demonstrate that the compounds from herbal plants: A. millefolium, A. montana, E. purpurea, C. recutita, S. virgaurea, possess antioxidative properties and protect platelet proteins against peroxynitrite toxicity in vitro, similar to the glycoconjugates from C. canadensis. However, in the comparative studies, the polyphenolic-polysaccharide conjugates from selected tested medicinal plants were not found to be more effective antioxidant, than the solution of pure resveratrol.

May modifications of human plasma proteins stimulated by homocysteine and its thiolactone induce changes of hemostatic function of plasma in vitro?

Homocysteine (Hcys) may be implicated in different diseases, especially in cardiovascular illnesses. The most reactive form of Hcys is its cyclic thioester-homocysteine thiolactone (HTL), which is formed in plasma and represents up to 0.29% of plasma total Hcys. Recently, it has been observed that Hcys and HTL may modify plasma proteins, including albumin, hemoglobin or fibrinogen, but the role of this process is not yet well known. The aim of our study in vitro was to investigate the modifications of human plasma total proteins after incubation with the reduced form of Hcys in concentrations 10-100 micromol/l, and HTL in concentrations 1-0.1 micromol/l, which correspond to levels found in human plasma during hyperhomocysteinemia in vivo. The aim of our study was also to explain the effects of Hcys and HTL on coagulation activity of human plasma. We showed that in model system in vitro Hcys and HTL change the level of thiol, amino and carbonyl groups in plasma total proteins. Moreover, our studies reported that not only Hcys (10-100 micromol/l), but also HTL (at lower concentrations than Hcys) modulates the coagulation properties of human plasma.