Virginia Minnich

Immunologic mechanisms in idiopathic and neonatal thrombocytopenic purpura.

Excerpt The mechanisms responsible for the low platelet count in idiopathic thrombocytopenic purpura are not well understood despite the careful studies by many competent investigators. The thrombo...

Glutathione synthetase deficiency as a cause of hereditary hemolytic disease.

Abstract Two enzymes are required for de novo glutathione synthesis: glutamyl-cysteine synthetase and glutathione synthetase. In a 32-year-old man with a well compensated hemolytic disorder, the er...

Glutathione Synthesis in Human Erythrocytes: II. PURIFICATION AND PROPERTIES OF THE ENZYMES OF GLUTATHIONE BIOSYNTHESIS

The two enzymes required to synthesize glutathione de novo have been purified from human erythrocytes. Glutamylcysteine synthetase was purified 4300-fold and was approximately 80% pure based on polyacrylamide gel electrophoresis. The purified enzyme catalyzes the formation of 30.5 mumoles of gamma-glutamyl-cysteine per mg of protein per hr and is inhibited by sulfhydryl inhibitors. Glutathione synthetase was purified 6000-fold from erythrocytes to homogeneity as determined by polyacrylamide gel electrophoresis. The erythrocyte enzyme has a molecular weight of 150,000 and catalyzes the formation of 35.9 mumoles of glutathione per mg of protein per hr. Comparison of the amino acid composition and some kinetic parameters of yeast glutathione synthetase and the erythrocyte enzyme demonstrate similarities between these enzymes.

Detection of mutagenic activity in human urine using mutant strains of Salmonella typhimurium.

Histidine‐requiring mutants of Salmonella typhimurium that can be reverted to prototrophy by a variety of mutagens were used to detect mutagenic activity in the urine of patients receiving chemotherapeutic agents. Patients given cyclophosphamide and BCNU had detectable urinary mutagenic activity over a 24‐hour period, with maximal levels occurring 12 to 21 hours after drug injection. Whereas native cyclophosphamide required the presence of a rat liver extract to be mutagenic in the test system, the cyclophosphamide metabolites in the urine were fully active in the absence of added liver extract. Mutagenic activity was detected in only the first voided urine specimen of patients receiving fluorouracil. Patients receiving Adriamycin, methotrexate, Mitomycin C, and low doses of oral melphalan did not have detectable mutagenic activity in their urines. One thousand and ten random urine specimens were screened for mutagenic activity. Only eight had greater than 26 revertant colonies per plate. Four of the eight had received metronidazole (Flagyl) for vaginitis while two others had received chemotherapeutic drugs. We were unable to detect increased mutagenic metabolites in the urine of 43 patients with known malignancies, using the standard assay conditions.

The Incidence of Elevated Hemoglobin A2 Levels in the American Negro.

Excerpt Hemoglobin A2is present in a concentration of less than 3.3 per cent of the total hemoglobin in all normal adults (1). Elevation above this level is known to accompany the erythrocyte abnor...

Erythrocyte glutathione synthesis in the neonate.

Red blood cell glutathione and the enzymes responsible for its synthesis in erythrocytes were measured in mothers and their offspring at time of delivery. γ-Glutamyl cysteine (GC) synthetase was the s

Pyrogens and the Viability of Stored Erythrocytes

Addition prior to storage of a bacterial pyrogen failed to influence the viability of erythrocytes placed in a blood bank for 26 days. Parameters studied were gross appearance of the samples, osmotic and mechanical fragility of the red cells and patterns of destruction following infusion into normal recipients.

Whole Blood and Plasma Ascorbic Acid Concentrations in Patients with Pellagra and Associated Deficiency Diseases.

Summary and Conclusions Whole blood and plasma ascorbic acid determinations made on 70 patients in the nutrition clinic of the Hillman Hospital indicate that 55 of these persons had a whole blood concentration of ascorbic acid lower than in normal controls. In 8 of the 70 cases, the concentration was so low as to suggest that depletion may have been advanced. Most of these patients had clinical evidence of other deficiencies, such as pellagra, beriberi and riboflavin deficiency, but no significant correlation could be made between the blood ascorbic acid values and the symptoms of these deficiency states, nor indeed of scurvy itself. These observations seem pertinent in view of the fact that they were made in late June, at a period when leafy vegetables and berries had been available to the patients for some time, and probably indicate that ascorbic acid deficiency is still greater at other periods. These studies give strong support to the concept that natural-occurring deficiency diseases exist as complexities rather than as single entities.

Effects of Clinical Doses of Phenobarbital on Blood and Urine Ascorbic Acid in Human Subjects

Summary There was no significant change in whole blood, plasma, or urinary excretion of ascorbic acid following administration of 180 mg of phenobarbital daily to human subjects. Twenty-five mg of crystalline ascorbic acid daily is insufficient to maintain whole blood or plasma values when the subjects take an ascorbic acid-free diet.