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Biomedical subjects

M R Cooper

Publications and source records attributed to M R Cooper.

At least 217 records · Page 12Linked to original sources
PubMed1972

Stimulation of the hexose monophosphate shunt in human neutrophils by ascorbic acid: mechanism of action.

The addition of either ascorbic acid or dehydroascorbic acid to a suspension of polymorphonuclear leukocytes caused a dramatic increase in the resting hexose monophosphate shunt activity. A sequence of reactions involving dehydroascorbate, reduced glutathione, and reduced nicotinamide adenine dinucleotide phosphate is described to explain this stimulation. This sequence could provide an alternate method of producing H(2)O(2) and a bactericidal mechanism which is independent of myeloperoxidase.

Ascorbic Acid↗
PubMed1972

Effect of catecholamines on the bactericidal activity of polymorphonuclear leukocytes.

Epinephrine, norepinephrine, and dihydroxyphenylalanine at 8 mm concentrations prevented iodination of zymosan by intact neutrophils and decarboxylation of l-alanine by leukocyte sonic extracts. The same concentration of epinephrine also reduced bactericidal activity of the leukocyte against Staphylococcus aureus, Enterobacter cloacae, and Proteus rettgeri without decreasing phagocytosis of bacteria. Spectral studies indicated that epinephrine interferes with the myeloperoxidase-mediated reactions by competing for available H(2)O(2) via its enzymatic oxidation to adrenochrome. These findings support a mechanism in which H(2)O(2) plays an important role in the bactericidal activity of the leukocyte.

Aldehydes↗
PubMed1972

Complete deficiency of leukocyte glucose-6-phosphate dehydrogenase with defective bactericidal activity.

A 52 yr old Caucasian female (F. E.) had hemolytic anemia, a leukemoid reaction, and fatal sepsis due to Escherichia coli. Her leukocytes ingested bacteria normally but did not kill catalase positive Staphylococcus aureus, Escherichia coli, and Serratia marcescens. An H(2)O(2)-producing bacterium, Streptococcus faecalis, was killed normally. Granule myeloperoxidase, acid and alkaline phosphatase, and beta glucuronidase activities were normal, and these enzymes shifted normally to the phagocyte vacuole (light and electron microscopy). Intravacuolar reduction of nitroblue tetrazolium did not occur. Moreover, only minimal quantities of H(2)O(2) were generated, and the hexose monophosphate shunt (HMPS) was not stimulated during phagocytosis. These observations suggested the diagnosis of chronic granulomatous disease. However, in contrast to control and chronic granulomatous disease leukocytes, glucose-6-phosphate dehydrogenase activity was completely absent in F. E. leukocytes whereas NADH oxidase and NADPH oxidase activities were both normal. Unlike chronic granulomatous disease, methylene blue did not stimulate the hexose monophosphate shunt in F. E. cells. Thus, F. E. and chronic granulomatous disease leukocytes appear to share certain metabolic and bactericidal defects, but the metabolic basis of the abnormality differs. Chronic granulomatous disease cells lack oxidase activity which produces H(2)O(2); F. E. cells had normal levels of oxidase activity but failed to produce NADPH due to complete glucose-6-phosphate dehydrogenase deficiency. These data indicate that a complete absence of leukocyte glucose-6-phosphate dehydrogenase with defective hexose monophosphate shunt activity is associated with low H(2)O(2) production and inadequate bactericidal activity, and further suggest an important role for NADPH in the production of H(2)O(2) in human granulocytes.

Autoradiography↗