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Beta-diethylaminoethyl-diphenylpropylacetate (SKF-525-A), a surface- active agent, inhibits sickling of erythrocytes from individuals with homozygous sickle cell anemia (SS cells) in vitro. Sickling was prevented when SS cells were incubated in .0003 M SKF-525-A, washed free of excess drug, and then deoxygenated in humidified nitrogen atmosphere. Polymerization of sickle hemoglobin and submembrane vesicles could be demonstrated in these cells by electron microscopy. At .0003 M SKF-525-A approximately 10% of the cells lysed. Incubation of pretreated cells at 37C without added oxygen for 24 hours did not produce significant additional lysis. Irreversibly sickled cells were unaffected by drug treatment. Preliminary studies suggest that the oxygen affinity of sickle hemoglobin in the intact cell is not altered by SKF-525-A. It is hypothesized that inhibition of sickling is the result of drug-induced alterations of the cell membrane.

Succinic dehydrogenase (SDH), which is critical to maintaining the transparency of the cornea, is utilized in the aerobic metabolism of glucose via the tricarboxylic acid (Krebs) cycle. What happens to this enzyme when the cornea is deprived of normal concentrations of oxygen (when contact lenses, masks, etc., are worn) is not known. According to previous studies, SDH was either present in corneal epithelium in barely detectable amounts or the techniques used for measurement were not sensitive enough to detect all the SDH present. As a part of the study, the authors modified existing techniques of detecting SDH in corneal epithelium. The intensity of staining SDH was enhanced by modifying a medium containing tetrazolium to the point where it was sensitive enough for quantitative photometric measurements. The existing techniques were modified by adding a coenzyme, beta-diphosphopyridine nucleotide (DPN), and increasing the amounts of specific substrate, sodium succinate. (Author)