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Platelets are the smallest, depleted of nucleus blood cells which contain a typical cellular organelles including the mitochondria, so that have active metabolism. Platelets possess the highly organized cytoskeleton, specific secretory granules and unique membrane receptors system responsible for their high reactivity. The key role of blood platelets is to maintain normal hemostasis, but they also play important roles in inflammation, immune processes and the cancer progression. The anucleated, small platelets occur in representatives of all clusters of mammals, so it seems to be an adaptation feature. In other vertebrates similar hemostatic functions are played by large nucleated platelets, which are much more weakly reactive. Small, reactive platelets, appearing in the evolution of mammals, allowed the formation of clots faster and slower blood loss in case of injury, but also increased the risk of thromboembolic and cardiovascular diseases. Daily the human body forms about 1x10¹¹ platelets, which are produced by a process of differentiation, maturation and fragmentation of the cytoplasm of mature megakaryocytes. The emergence of platelets is the final stage of megakaryocyte differentiation and is followed by formation of the direct precursors called proplatelets. The anucleated platelets are regarded as terminally differentiated cells, which are not capable of further cell division. However, despite the absence of a nucleus, in blood platelets the synthesis and transcription of mitochondrial DNA and protein synthesis occurring on the basis of mRNA from megakaryocytes has been confirmed. However, recent studies published in 2012 show that the platelets are capable not only of the process of protein synthesis, but also of generation of new cells, which are functionally and structurally similar to the parent platelets.

Platelets are the smallest, unnucleated blood cells that play a key role in maintaining normal hemostasis. In the human body about 1x1011 platelets are formed every day, as a the result of complex processes of differentiation, maturation and fragmentation of megakaryocytes. Studies done over 4 decades ago demonstrated that circulating in blood mature platelets can synthesize proteins. Recent discoveries confirm protein synthesis by unnucleated platelets in response to activation. Moreover, protein synthesis alters the phenotype and function of platelets. Platelets synthesize several proteins involved in hemostasis (COX, αIIbβ3, TF PAI-1, Factor XI, protein C inhibitor) and in inflammatory process (IL-1β, CCL5/RANTES). In spite of lack of transcription platelets have a stable mRNA transcripts with a long life correlated with platelet life span. Platelets also show expression of two important key regulators of translation eIF4E and EIF-2α and have a variety of miRNA molecules responsible for translational regulation. This article describes the historical overview of research on protein synthesis by platelets and presents the molecular mechanisms of protein synthesis in activated platelets (and synthesis of the most important platelet proteins).

The diseases of blood circulation system--cardiovascular diseases are the main causes of mortality in developing, low and middle-income countries all over the world. The specialists recommend the prophylaxis to avoid the dangerous complications connected with these diseases, what can reduce the final treatment costs. All over the world there is continuous research of novel, therapeutically better, more effective anticoagulant or anti-platelet agents, with multiple targets, without so many side effects. Plant material is a good source to do this kind of research. The authors show the results of their few years research on polyphenolic-polysaccharide plant conjugates, isolated from medicinal plants, popular in Poland, which is continuing in the framework of the project WROVASC--Integrated Center of Cardiovascular Medicine. This research group has been working on isolation, structure characterization and biological activity of these macromolecular compounds. Because of anticoagulant, antioxidant as well as anti-platelet properties of these plant structures they are promising to be a new source of the innovative therapeutic agent.

The normal hemostatic mechanisms consist of a balance between hemorrhage and thrombosis that is achieved through the interaction of the blood vessels, blood platelets, the coagulation and fibrinolytic factors. The vascular endothelium sustains the balance between prevention and stimulation of platelet activation, thrombogenesis and fibrinolysis and between vasoconstriction and vasodilatation. Endothelial dysfunction associated with different cardiovascular diseases is related to the local formation of reactive oxygen/nitrogen species, mainly peroxynitrite that is produced in a rapid reaction between nitric oxide and superoxide anion. Reactive oxygen/nitrogen species induce changes in the structure and function in hemostatic elements. Proteins and lipids are major initial targets in endothelial cells, blood platelets and plasma. Reaction of reactive oxygen species and nitrogen species, including peroxynitrite, with cellular proteins can lead to nitration of aromatic amino acid residues, oxidation of thiol groups and conversion of some amino acid residues into carbonyl derivative. Oxidative/nitrative modifications of platelet proteins may induce changes of their signaling and haemostatic function (activation). Peroxynitrite also causes oxidation and nitration of fibrinogen--a key protein in coagulation cascade and plasminogen (the main protein of fibrinolysisprocess) changing their hemostatic functions. Oxidative/nitrative modifications of different components of haemostasis system have been observed in several cardiovascular diseases.

Fibrinolytic system constitutes a part of the haemostasis responsible for the degradation of fibrin deposits. Plasminogen proenzyme, the main component of the fibrinolytic system is activated into its active enzyme form--plasmin by activators, mainly by tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA). t-PA is the main plasminogen activator in the intravascular fibrinolysis, whereas u-PA is rather involved in the extracellular proteolysis. Fibrinolytic activity can be regulated as well by plasminogen activation inhibition (inhibitors: PAl-1 and PAl-2) as by plasmin activity inhibition (alpha2-antiplasmin). Under physiological conditions a balance between coagulation and fibrinolysis exists, that may be altered under pathophysiological conditions. It has been reported that in the pathogenesis of many diseases, the inflammatory processes, expression of proinflammatory mediators, enhanced tissue factor level and/or impaired fibrinolysis are involved. Inflammation disturbs haemostasis and shifts the haemostatic mechanisms in favor of thrombosis. Moreover, the endothelial dysfunction may contribute to the decrease of antithrombotic properties of vessel wall endothelium. Under pathophysiological conditions where a hypofibrinolytic state occurs, impaired fibrinolysis is considered to be an additional risk factor of thrombosis.

Lipopolysaccharide (LPS) is the major component of the outer membranes of the walls of gramnegative bacteria that protects bacterial cells against antibacterial agents. LPS is the heteropolimer consisting of two parts: the hydrophobic lipid A and hydrophilic polisaccharide. After lysis of bacterial cells LPS is released into the circulation and it is able to activate the immunological system by stimulation of monocytes, macrophages, neutrophils, blood platelets and endothelial cells. LPS can bind to plasma proteins and form complexes that increase toxic activity of LPS and affinity of LPS to cell receptors. The activation of immune cells by LPS leads to release of inflammatory mediators: cytokines, chemokines, enzymes, eicosanoids, adhesion agents and free radicals that are responsible for progression of inflammatory reactions and may induce pathophysiological processes including septic shock.

Free radicals and reactive oxygen or nitrogen species generated during oxidative stress and as by-products of normal cellular metabolism may damage all types of biological molecules. Proteins are major initial targets in cell. Reactions of a variety of free radicals and reactive oxygen and nitrogen species with proteins can lead to oxidative modifications of proteins such as protein hydroperoxides formation, hydroxylation of aromatic groups and aliphatic amino acid side chains, nitration of aromatic amino acid residues, oxidation of sulfhydryl groups, oxidation of methionine residues, conversion of some amino acid residues into carbonyl groups, cleavage of the polypeptide chain and formation of cross-linking bonds. Such modifications of proteins leading to loss of their function (enzymatic activity), accumulation and inhibition of their degradation have been observed in several human diseases, aging, cell differentiation and apoptosis. Formation of specific protein oxidation products may be used as biomarkers of oxidative stress.

Resveratrol is a phytoalexin found in many plants, mainly in grapes. It has been shown to prevent coronary heart diseases and to exert a variety of anti-cancer and anti-inflammatory effects.

Thrombin is a serine protease that plays a central role in hemostatic and thrombotic events. The structure, different forms of thrombin, its role in platelet activation and in other cellular effects are reviewed. Two distinct receptors involved in platelet activation induced by alpha-thrombin are presented: a high affinity (GPIb) coupled to phospholipase A2 and a moderate affinity, G protein associated with seven transmembrane domain receptor (STDR) coupled to phospholipase C.

Cisplatin is a widely used chemotherapeutic agent, highly effective in the treatment of various types of human malignancies. The antitumor activity of cisplatin is attributed mainly to its ability to form adducts with DNA. Cisplatin may react with proteins and also with glutathione forming complex GS-Pt. This agent causes haematological, neurological toxicity and changes function of different cells. Recently, is has been reported that administration of sodium selenite reduces cisplatin toxicity without inhibiting the antitumour activity of cisplatin. This review focuses on the mechanism of cisplatin-induced cytotoxicity and the protective role of selenium.

The study aimed at comparing an effect of suloctidil and acetylsalicylic acid on malonyldialdehyde levels resulting from the arachidonic acid metabolism in blood platelets. It was shown that inhibitory effect of suloctidil is more potent than that of acetylsalicylic acid. Therefore the first is more inhibitor of an enzymatic metabolism of arachidonate in blood platelets than the latter.

Centrifugation technique of thrombocytes through silicone oil permits rapid separation of cells from plasma with simultaneous measurement of plasma trapped between the cells in the pellet. This technique was used for determination of 5-HT uptake by turkey thrombocytes. The volume of trapped plasma proportional to the number of thrombocytes was measured using 125I-human serum albumin as a marker. The uptake of 14C-serotonin by thrombocytes was measured as the difference between total radioactivity and that of the trapped plasma. It was shown that turkey thrombocytes like mammalian platelets are able to take up great amounts of serotonin.