ABSTRACT
It is shown that in the presence of reduced glutathione at low concentrations (1-5 microM) the extent of platelet aggregation with neutrophils increases and the lag period of platelet aggregation induced by tumor cells decreases. At the same time in the presence of reduced glutathione at high concentration (3 mM) the extent of platelet aggregation with neutrophils decreases, and the lag period of platelet aggregation induced by tumor cells increases. It is established that glutathione-dependent regulation of the intercellular contact formation between platelets and neutrophils depends on the ratio of glutathione oxidized and reduced forms: at fixed total glutathione concentration of 5 microM, increase of glutathione redox potential from -175 mV to 0 mV led to reduction in platelet aggregation with neutrophils. Thus, it is shown for the first time, that GSH has priming effect on the platelet aggregation with neutrophils and tumor cells, which may contribute to the regulation of inflammatory diseases and cancer.
Subject(s)
Blood Platelets/drug effects , Cell Communication/drug effects , Glutathione Disulfide/pharmacology , Glutathione/pharmacology , Neutrophils/drug effects , Blood Platelets/cytology , Blood Platelets/metabolism , Dose-Response Relationship, Drug , HeLa Cells , Humans , Neutrophils/cytology , Neutrophils/metabolism , Oxidation-Reduction , Platelet Aggregation/drug effects , Respiratory Burst/drug effects , SpectrophotometryABSTRACT
We studied the effect of dinitrosyl iron complexes with glutathione ligands on platelet aggregation with HeLa tumor cells. It was shown that dinitrosyl iron complexes not only inhibited cell aggregation, but being added at early stages can also block this process. These findings dictate further studies of dinitrosyl iron complexes as a compound reducing metastasizing and thrombus-formation in tumor patients.
