In recent decades, significant progress has been made in understanding the mechanisms of platelet function and platelet hemostasis correction. Platelets are considered as the most important participants of both normal, and pathological thrombotic process characteristic of the most different diseases and states. In the present review pathophysiological mechanisms of platelet synthesis of various mediators with paracrine effects, which can influence the function of other cells, are consecrated. The physiology of platelets was considered in detail. The leading role of platelets in pathogenesis of the majority of diseases of cardiovascular system as modulators of inflammatory reactions of the immune response which are considered as the leading mechanism of development of atherosclerosis was shown. The ability of platelets to encode inflammatory proteins allowing them to influence adaptive immunity functions was discussed. The role of platelets as a key component of the innate immune system was presented, which is confirmed by the presence of Tolllike receptors (TLR) and glycoproteins, such as integrin αIIbβ3, glycoprotein Ib-IX and FcγRIIa, involved in interaction with bacterial cells. The pathogenesis of the formation of platelet-leukocyte aggregates due to the rapid reversible interaction of P-selectin (CD62P) on the platelet surface with ligand-1 glycoprotein P-selectin (PSGL-1) on the plasma of leukocytes and the mechanism of extracellular neutrophil traps (NETs), as well as the influence of platelets on the function of lymphocytes was presented. The role of platelets in cancer progression, metastasis and thrombosis is considered, and the interrelation of thrombosis and metastasis in malignant diseases was analyzed. The efficiency of the use of antithrombotic drugs in the prevention of thrombosis and, as a consequence, in the prevention of cardiovascular diseases and cancer was discussed.
To determine the biochemical disorders in the blood coagulation mechanism associated with oxidative stress parameters of the antioxidant status were examined in platelets of 57 colorectal cancer patients, (including 21 patients before and after surgery), and 40 healthy individuals. We determined the total content of nitric oxide (NOx), levels of superoxide dismutase (Cu/ZnSOD), glutathione and malondialdehyde (MDA). Before treatment, we observed the changes in the antioxidant defense system of platelets, which did not depend on the prevalence of malignancy: elevated levels of SOD by 16% (p<0.05), reduced glutathione and MDA in 5.2 and 1.7 times, respectively. NOx levels did not differ from the norm. Significant shifts were found in the postoperative period: they consisted of the increase in the generation of NOx both on the third, and on the 10-th day after surgery. These changes reflect apparently platelet response to the inflammatory process associated with the surgical trauma and confirm the role of NOx as a mediator of inflammation. The content of SOD after surgery was significantly reduced, but return to a baseline on the 10-th day. Despite the significant increase in the number of platelets, no correlations of the studied parameters and their aggregation ability were found.The findings suggest that metabolic disorders in vascular-platelet hemostasis are associated with oxidative stress, which provides a basis for further study of the relationship of cancer to thrombosis.
In order to identify the features of violations of free-radical processes in blood serum of 94 untreated cancer patients with different localization of the tumor (cancer of the stomach, colon, breast, ovarian, hemoblastoses) were determined selenium levels and indicators of oxidative stress (sum of metabolites of nitrogen - NOx, the level of superoxide dismutase - Cu/ZnSOD and malondiialdehyde-MDA, and the activity of catalase). In addition, 40 patients with malignant liver disease and clinical signs of liver failure in the early postoperative period was carried out a comparative evaluation of the efficacy of selenium-containing drug 'Selenaze' (sodium selenite pentahydrate). It was found that selenium levels in cancer patients by 25-30% below the norm of 110-120 mg/l at a rate of 73.0±2.6 mg/l. Low levels of NOx was detected in patients with all tumor localizations (22.1±1.1 mM, with normal range 28.4±0.9 mM). The exceptions were patients with extensive malignant process in the liver, in which the NOx levels were significantly higher than normal (p<0.001). The high level of NOx has a toxic effect on the hepatocyte, causing metabolic disorders and inflammatory-necrotic changes in the liver. Elevated levels of SOD and MDA in normal values of catalase activity was detected in all patients. The use of 'Selenaze' in postoperative patients with tumors of the liver increased selenium levels by 10-12%, which was accompanied by a decrease in the content of SOD and NOx, and contributed to earlier recovery of detoxic and synthetic liver function. These findings point to an intensification of oxidative stress and metabolic disorders in the malignant process, which is the basis for metabolic correction.
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