The characteristics of the acetylation of dapsone (avlosulfon) were found to parallel those of isoniazid and sulfamethazine in 19 subjects, thereby establishing the genetic polymorphism for the acetylation of dapsone. This polymorphism was revealed by the distribution of the ratios of the plasma concentration of acetylated to parent drug. The acetylation capacity for dapsone was shown to be a reproducible, individual characteristic. Acetylation of dapsone and deacetylation of monoacetyl dapsone occurred concurrently. Constant plasma ratios of acetylated to parent drug characteristic for the individual were attained immediately after administration of dapsone but only after several hours following administration of monoacetyl dapsone. The available data suggest that acetylation rather than deacetylation is the primary determinant of these ratios. Rates of disappearance of dapsone and monoacetyl dapsone from the plasma were the same regardless of which of the two was administered or of the acetylator phenotype of the subject. After dapsone, no differences between rapid and slow acetylators were found in the 24 hour urinary excretion of dapsone and its conjugates hydrolyzed by mild or strong acid treatment. Rapid acetylators excreted significantly more monoacetyl dapsone and its acidlabile conjugates than slow acetylators. Because these compounds accounted for only a very small fraction of the dose, it was not possible to phenotype individuals by these measurements. More dapsone and acid‐hydrolyzable conjugates of dapsone were found in 120 hour urine collections after monoacetyl dapsone than after dapsone in both phenotypes.
Uptake of labelled uridine into lymphocytes is restricted. Several lines of evidence, including experiments with dipyridamole, an inhibitor for membrane transport processes, and kinetic experiments indicate that transport of uridine through the cell membrane is the rate-limiting step in uridine uptake. Addition of phytohemagglutinin results in an immediate increase of uridine uptake. Saturation experiments have shown that this change is due to an increase in V , whereas the apparent K , value remains constant. The hypothesis is advanced, that phytohemagglutinin induces an increase in the number of functional carrier sites of the membrane transport system.Resting lymphocytes respond to the addition of phytohemagglutinin with a number of biochemical changes which ultimately lead to the transformation of small lymphocytes to large pyroninophilic cells.The latter actively synthesize RNA and DNA and undergo mitotic division. The mechanism of this differentiative process is still obscure although numerous alterations of the cell metabolism have been recorded.
In neonatal and adult polymorphonuclear leukocytes (PMN) we determined the content and the release of β-glucuronidase, myeloperoxidase, lysozyme and lactoferrin. We found an equal total content of these proteins in adult and neonatal PMN, except for a lower lysozyme concentration in neonatal PMN. In the presence of opsonized zymosan myeloperoxidase, lysozyme and β-glucuronidase were released in equal amounts; lactoferrin, however, was released to a lower rate from neonatal than from adult PMN (p < 0.0005).
We suggest that graft rejection-associated apoptosis, in addition to necrosis, plays an important role in the course of organ failure, and that the degree of apoptosis represents another reliable indicator for the diagnosis and prognosis of transplant rejection.
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