On the basis of an earlier model of chemical carcinogenesis, the antitumor activity of the mono-, bi-and poly-nuclear ferrocene derivatives ferricenium tri-iodide (l), ferricenium tetrachloroferrate (2), 1,l'-diethylferricenium triiodide (3), N-(ferrocenylmethy1)hexamethylenetetramine tetrafluoroborate (4), bis(ferrocenylmethy1)benzotriazolium tetrafluoroborate (3, bis(ferroceny1-a-ethy1)benzotriazolium tetrafluoroborate (6) and bis(ferrocenylmethyl)-2-methylbenzimidazolium tetrafluoroborate (7), and the oligomer (-Fc-CH,-FC+'--CH~),~-(PF& (8) was studied in uiuo (Fc = C,,H,Fe).The tumor models studied included MCH-11 (mouse sarcoma induced by methylcholantrene), P-815 (mouse mastocytoma of DBA/2 origin) and virus-induced Raucher leukemia (RLV). The cytotoxic effects of these preparations were examined against in vitro cultured normal murine cells (line L-929). The binuclear ferrocene derivatives 5, 6 and 7 inhibited the development of experimental tumors in mice. Ferricenium tri-iodide (1) was effective in Rauscher leukemia. Kinetic dependencies for most complexes had a two-phase character: the region of inhibition of tumorogenesis was followed by a region in which the complexes accelerated the development of this process. The link between the structure of compounds 1-8 and their antitumor effects is discussed.
We studied the role of eicosanoids in the regulation of macrophage phagocytic functions by products secreted in heterogeneous populations of macrophages and platelet-activating factor during endotoxic shock. Phagocytic activity depended on the metabolism of arachidonic acid in target macrophages and the ratio between its cyclooxygenase and lipoxygenase metabolites produced by heterogeneous populations of macrophages and affecting target cells. The regulatory effect of platelet-activating factor on phagocytosis was related to its interaction with products of the arachidonic acid cascade. Depending on the quantitative ratio of eicosanoids, platelet-activating factor produced various effects on phagocytic functions of heterogeneous macrophage populations.
We studied the role of eicosanoids in the regulation of macrophage phagocytic functions by products secreted in heterogeneous populations of macrophages and platelet-activating factor during endotoxic shock. Phagocytic activity depended on the metabolism of arachidonic acid in target macrophages and the ratio between its cyclooxygenase and lipoxygenase metabolites produced by heterogeneous populations of macrophages and affecting target cells. The regulatory effect of platelet-activating factor on phagocytosis was related to its interaction with products of the arachidonic acid cascade. Depending on the quantitative ratio of eicosanoids, platelet-activating factor produced various effects on phagocytic functions of heterogeneous macrophage populations.
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