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Biomedical subjects

A M Woodin

Publications and source records attributed to A M Woodin.

At least 19 recordsLinked to original sources
PubMed1970

Leukocidin, tetraethylammonium ions, and the membrane acyl phosphatases in relation to the leukocyte potassium pump.

The response of the leukocyte to leukocidin and its relevance to excitable and secreting tissues are described. New data are presented on the leukocyte membrane phosphatases and the action of tetraethylammonium ion (TEA) on the leukocyte. The leukocyte surface membrane lacks a cation-sensitive ATPase but possesses a potassium- and ouabain-sensitive p-nitrophenyl phosphatase. The p-nitrophenyl phosphatase shows peak activity at three pH values and the pH dependence and potassium sensitivity depend on the state of the membranes. In the presence of magnesium, potassium can stimulate over the range pH 6 to 8. The relation of the leukocyte p-nitrophenyl phosphatase to electrolyte control in the leukocyte and to the properties of cation-sensitive phosphatases in other cells suggests that the leukocyte enzyme is a component of an electrogenic potassium pump. Leukocidin stimulates the leukocyte p-nitrophenyl phosphatase under all the conditions studied. The effect is specific and occurs under conditions that induce cytotoxic effects in the cell. It is concluded that the potassium pump is the site of action of leukocidin. TEA prevents the effects of leukocidin by inhibiting the action of leukocidin and not the responses of the cell to injury. TEA does not inhibit the p-nitrophenyl phosphatase nor prevent its stimulation by leukocidin. The enhancement of leukocidin by diisopropylphosphofluoridate (DFP) is briefly described. It is concluded that TEA acts in the opposite way to DFP and blocks the ion pathway activated by leukocidin in the leukocyte potassium pump.

Adenosine Monophosphate↗
PubMed1967

The participation of phospholipids in the interaction of leucocidin and the cell membrane of the polymorphonuclear leucocyte.

1. The interaction of the two components of leucocidin with various lipids has been studied by sedimentation, flotation, light-scattering and changes in the biological activity of leucocidin. 2. Phosphatidylserine, phosphatidylcholine, diphosphoinositide, triphosphoinositide and phosphatidic acid, but not phosphatidylethanolamine, lysophosphatidylcholine, cerebrosides, gangliosides or tristearin, induce aggregation of the F component of leucocidin. 3. The S component of leucocidin does not interact directly with these phospholipids, but interacts with the F component of leucocidin after its modification by lipids. 4. The increased sedimentation or light-scattering induced by low phospholipid concentrations is reversed at higher phospholipid concentrations. 6. The aggregates formed by phospholipids and leucocidin are due, not to adsorption of leucocidin alone, but also to the formation of leucocidin polymers. 7. It is concluded that the aggregation is due to the interaction of the F component with the fatty acid side chains in the lipid micelle. 8. The S component of leucocidin is inactivated by triphosphoinositide at physiological ionic strength; the F component of leucocidin is inactivated at low ionic strength by triphosphoinositide and remains inactive when the ionic strength is increased. 9. It is suggested that in the leucocyte cell membrane the S component of leucocidin interacts with the polar hydrophilic groups of triphosphoinositide and that the F component of leucocidin interacts with the hydrophobic parts of triphosphoinositide.

Journal Article↗
PubMed1967

The polyphosphoinositide content of the leucocyte, erythrocyte and macrophage.

1. The polyphosphoinositide content of macrophages and the cell membranes of leucocytes and erythrocytes was determined by an extension of the ;acid-hydrolysis' procedure of Dawson & Eichberg (1965). The estimation was controlled by adding a little highly radioactive polyphosphoinositide to the tissue extracts before fractionation. Several standard methods for determining polyphosphoinositides gave low recoveries when applied to leucocytes, and it is suggested that these cells contain materials that form complexes with the polyphosphoinositides and interfere with the assay. 2. The method for the preparation of leucocyte cell surface membranes has been modified.

Journal Article↗
PubMed1966

The modification of the cytotoxic effect of leucocidin by N-ethylmaleimide, flavine mononucleotide and mendione.

1. The movement of the cytoplasmic granules in the leucocidin-treated leucocyte is prevented in the presence of N-ethylmaleimide or menadione. This effect follows a change of state in the cytoplasm. It may not be due to reaction with SH groups. When granule movement is prevented in this way the subsequent addition of Ca(2+) and ATP does not induce the secretion of the proteins of the granules. 2. Menadione or iodoacetate stimulates some effects of suboptimum amounts of leucocidin. This effect probably follows a reaction with SH groups. 3. Flavine mononucleotide inhibits some effects of suboptimum amounts of leucocidin. 4. Leucocidin decreases the stimulation of glucose oxidation due to menadione but increases that due to flavine mononucleotide. Leucocidin decreases the adsorption of menadione by leucocytes but increases that of flavine mononucleotide. 5. The redox state of the nicotinamide-adenine nucleotide coenzymes is not altered during leucocidin action and flavine mononucleotide and menadione do not undergo significant continuous oxidation and reduction when added to the leucocyte.

Cytoplasmic Granules↗