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Agonists of glutamate ionotropic (NMDA) and metabotropic receptors (mGluRI and mGluRIII) had the regulatory effect on ADP-ribosyl cyclase/CD38 activity in cerebellar granular cells of newborn rats. Perinatal hypoxic-ischemic brain injury was followed by dysregulation of this mechanism.

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The aim of this work was to evaluate contribution of released membrane particles (RMP) to the development of systemic inflammatory response (SIR) after aortocoronary bypass grafting (ACBG). The number of RMP carrying surface adhesion molecules, CD62L, CD62P, CD62E, was shown to increase in the early postoperative period in parallel with the enhancement of lymphocyte plasma membrane blebbing and elevation of cytokine levels in peripheral blood. It is concluded that (1) activation of plasma membrane blebbing in peripheral blood cells underlies the appearance of RMP in circulation; (2) increased number of RMP expressing CD62L, CD62P, CD62E is a marker of intercellular communication associated with the development of SIR and suggests new mechanisms of RMP involvement in the reaction of organism to massive surgical injury.

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Oxytocin is important for regulating a number of physiological processes. Disruption of the secretion, metabolism or action of oxytocin results in an impairment of reproductive function, social and sexual behaviours, and stress responses. This review discusses current views on the regulation and autoregulation of oxytocin release in the hypothalamic-neurohypophysial system, with special focus on the activity of the CD38/cADP-ribose system as a new component in this regulation. Data from our laboratories indicate that an impairment of this system results in alterations of oxytocin secretion and abnormal social behaviour, thus suggesting new clues that help in our understanding of the pathogenesis of neurodevelopmental disorders.

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The pathogenesis of neuronal dysfunction was evaluated from the viewpoint of cellular disturbances in NAD(+) metabolism and changes in activity of NAD(+)-utilizing enzymes (e.g., ADP-ribosyl cyclase/CD38). S-100B concentration and CD38 expression on peripheral blood lymphocytes were altered in patients after surgery for coronary heart disease with extracorporeal circulation. These changes in patients during the early postoperative period correlated with variations in CD38 expression on neuronal cells from postischemic rats with cognitive dysfunction.

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We studied apoptosis and expression of peripheral benzodiazepine receptors in granulosa cells of dominant follicles from women with endocrine sterility. The expression of peripheral benzodiazepine receptors in granulosa cells depends on the degree of granulosa cell apoptosis and type of disorders in follicular steroidogenesis, which suggests the involvement of peripheral benzodiazepine receptors into the regulation of folliculogenesis in health and disease.

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The expression of connexin 43 and CD38 and ADP ribosyl cyclase activity in brain cells were studied in rats with experimental hypoxic and ischemic damage to the CNS. Changes in the expression and activity of the enzyme were detected over the course of ischemic injury indicating a possible contribution of NAD(+)-converting activity and NAD(+)-transporting processes to the pathogenesis of acute cerebral ischemic injury.

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Obesity is one of the urgent problems of modern health care. In the 21st century, obesity, one of the most common chronic diseases, takes on the character of a global epidemic, covering almost all countries and peoples of the world. WHO experts suggest that the number of people with obesity by 2005 compared with 2000 will increase by almost 2 times and amount to more than 300 million people. Every year, the situation is getting worse, obesity is getting younger, it becomes a problem not only for adults, but for children and adolescents. Currently, in developed countries, up to 20% of adolescents are overweight, and 15% are obese. In the Russian Federation, 5.5% of children living in rural areas and 8.5% of children in urban areas are obese. Obesity is a social problem, as it leads to early disability and reduces the average life expectancy. Finally, obesity accompanies diseases such as type 2 diabetes, hypertension, dyslipidemia, coronary heart disease, as well as insulin resistance and hyperinsulinemia.

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Mechanisms of myelotoxic action of Doxorubicin associated with changes in NAD(+)-glycohydrolase/CD38 expression and activity have been assessed. During the acute and subacute exposure of bone marrow cells to Doxorubicin in vivo, expression of CD38 is decreased corresponding to elevation of intracellular and extracellular NAD+ concentrations. These changes are associated with increased susceptibility of hemopoietic cells to the apoptogenic action of Doxorubicin. Possible role of NAD(+)-glycohydrolase/CD38 in the regulation of sensitivity of the cells to the cytotoxic effects of the xenobiotic is discussed.

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We studied the role of disturbances in cell Ca(2+) homeostasis in plasma membrane blebbing and death of thymocytes. Capacitance Ca(2+) channels of the plasma membrane and intracellular Ca(2+) stores are involved in the induction and progression of changes in the membrane and cytoskeleton and apoptosis induced by acrylonitrile.

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ATP activity in mouse bone marrow cells was in vitro estimated by expression of phosphatidylserine on the outer membrane surface using FITC-labeled annexin. ATP induced apoptosis in bone marrow cells. Purinergic receptor antagonists PPADS and suramin modulated the apoptotic effect of ATP on hemopoietic cells. Acute and subacute administration of doxorubicin, an inductor of oxidative burst, decreased cell sensitivity to ATP and abolished its apoptotic effect.

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