RESUMEN
The effect of benzydamine on stimulus-dependent respiratory burst activity and enzyme release was tested in human neutrophils, monocytes and monocyte-derived macrophages. Established anti-inflammatory compounds, indomethacin, phenylbutazone and bufexamac, were tested for comparison. Care was taken to avoid cytotoxic or cytolytic concentrations of the test compounds, and their effect on release of lactate dehydrogenase was also tested. Release of specific and azurophil granules contents were induced in human neutrophils by A23187, PMA and fMLP with and without cytochalasin B pretreatment. Benzydamine inhibited stimulus-dependent release of vitamin B12-binding proteins, a marker for the specific granules, in a concentration-dependent fashion. By contrast, phenylbutazone and bufexamac were practically inactive. The effect of benzydamine on exocytosis of azurophil granules was tested in cytochalasin B-pretreated neutrophils. Benzydamine, again in contrast to the two reference anti-inflammatory compounds, inhibited release concentration-dependently also under these conditions. The concentration of the compound which inhibited exocytosis by 50% was 30-100 microM in normal and 3-10 microM in cytochalasin B-treated neutrophils. The effect of benzydamine and reference compounds on the respiratory burst was tested by assaying for superoxide formation in neutrophils and H2O2 formation in mononuclear phagocytes. Benzydamine was inactive on neutrophils and inhibited slightly the burst response of monocytes and macrophages. Two reference compounds, bufexamac and phenylbutazone, were generally more active. The strongest inhibitory effect was that of phenylbutazone on fMLP-stimulated cells. Benzydamine lacked activity under these conditions, indicating that it does not bind to the receptor of formylated chemotactic peptides.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Bencidamina/farmacología , Exocitosis/efectos de los fármacos , Monocitos/fisiología , Neutrófilos/fisiología , Consumo de Oxígeno/efectos de los fármacos , Fagocitos/fisiología , Pirazoles/farmacología , Calcimicina/farmacología , Citocalasina B/farmacología , Gránulos Citoplasmáticos/enzimología , Glucuronidasa/sangre , Humanos , Peróxido de Hidrógeno/sangre , L-Lactato Deshidrogenasa/sangre , N-Formilmetionina Leucil-Fenilalanina/farmacología , Superóxidos/sangre , Acetato de Tetradecanoilforbol/farmacologíaRESUMEN
Platelet activation is linked to an increase in the cytoplasmic Ca2+ concentration and consequently can also be induced by ionophores which mobilize Ca2+ from intracellular storage sites or transport it through the plasma membrane. The ionophores mostly used in studies on platelet activation are A 23187 and lasalocid (X-537A). The effects of eight compounds with known Ca2+-ionophoric activity in synthetic or natural membrane systems were studied in order to investigate the relationship between transport Ca2+ and activation of platelets. Inomycin acts as a true Ca2+ ionophore: it elicits rapid shape change, aggregation, the release reaction (secretion) and clot retraction (contraction). Beauvericin activates platelets too, but probably not by increasing the cytoplasmic Ca2+ concentration. Lysocellin does not activate platelets but induces a passive loss of serotonin.
Asunto(s)
Antibacterianos , Plaquetas/metabolismo , Calcio/sangre , Depsipéptidos , Ionóforos/farmacología , Lasalocido/farmacología , Péptidos , Piperidinas/farmacología , Virginiamicina/farmacología , Transporte Biológico/efectos de los fármacos , Plaquetas/efectos de los fármacos , Plaquetas/ultraestructura , Membrana Celular/efectos de los fármacos , Membrana Celular/metabolismo , Éteres/farmacología , Humanos , Ionomicina , Cinética , Péptidos Cíclicos/farmacología , Agregación Plaquetaria/efectos de los fármacosAsunto(s)
Luz , Células Vegetales , Reguladores del Crecimiento de las Plantas/farmacología , División Celular/efectos de los fármacos , Medios de Cultivo , Oscuridad , Desarrollo de la Planta , Reguladores del Crecimiento de las Plantas/biosíntesis , Esporas , Sacarosa/farmacología , Factores de TiempoAsunto(s)
Plaquetas/metabolismo , Lisina/farmacología , Adhesividad Plaquetaria/efectos de los fármacos , Agregación Plaquetaria/efectos de los fármacos , Serotonina/metabolismo , Adenosina Difosfato/farmacología , Radioisótopos de Carbono , Dicroismo Circular , Densitometría , Relación Dosis-Respuesta a Droga , Fibrinógeno/farmacología , Humanos , Concentración de Iones de Hidrógeno , Peso MolecularRESUMEN
An antheridium-inducing hormone (antheridiogen) derived from the fern species Onoclea sensibilis (Polypodiaceae) is chromatographically distinct from the native antheridiogen of Pteridium aquilinum (Polypodiaceae). It also differs from the native antheridiogens of Lygodium japonicum and Anemia phyllitidis (Schizaeaceae).
RESUMEN
It has been reported that a preparation obtained from prothlalli of the fern species Anemia phyllitidis controls antheridium formation in this species. If this same preparation is applied at the spore stage it induces a physiological state antagonistic to antheridium formation. The inhibitory state is inducible only at a very early stage of development, but, once induced, it remains manifest at much later stages. Quite possibly, the inhibitory state arises in response to the factor that induces formation of anitlheridia. The inhibitory state may have an important function in fern development.