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We studied the effects of exogenous glutathione (GSH) and GSH monoethyl ester (GSH-MEE) on the enhancement of endothelial GSH concentrations. The preparation of GSH-MEE used contained 91% GSH-MEE, approximately 9% GSH diethyl ester (GSH-DEE) and a trace amount of GSH. Both GSH and GSH-MEE markedly stimulated the intracellular concentrations of GSH in endothelial cells. GSH-MEE was more potent than GSH. The enhancement of endothelial GSH concentration by exogenous GSH was completely inhibited by buthionine sulfoximine (BSO), a potent inhibitor of gamma-glutamylcysteine synthase, or acivicin (AT-125), an inhibitor of gamma-glutamyl transpeptidase, suggesting that it was due to the extracellular breakdown and subsequent intracellular resynthesis of GSH. In contrast, the effect of GSH-MEE was largely resistant to BSO and acivicin, suggesting that it was primarily due to transport of GSH-MEE followed by intracellular hydrolysis. The GSH-MEE preparation, which contained 9% GSH-DEE, at concentrations of 2 mM or higher caused vacuolization of endothelial cells. The enhancement of GSH concentrations by exogenous GSH, but not by GSH-MEE, protected endothelial cells against H2O2-induced injury.

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Hurwitz, Charles (Veterans Administration Hospital, Albany, N.Y.) and Carmen L. Rosano . Accumulation of label from C 14 -streptomycin by Escherichia coli . J. Bacteriol. 83: 1193–1201. 1962.—Accumulation of label from C 14 -streptomycin by sensitive Escherichia coli occurs in the presence of chloramphenicol, provided the cells receive a prior exposure to streptomycin. The rate of accumulation increases with the concentration and length of exposure to streptomycin during the initiation phase. Accumulation of label from streptomycin in the presence of chloramphenicol is also a function of the streptomycin concentration during the killing phase. Evidence is presented for the presence of a barrier to the entry and exit of streptomycin. It is further shown that total accumulation of streptomycin can be divided into three portions: surface-adsorbed streptomycin, streptomycin present at the time of onset of loss of viability, and streptomycin accumulated by killed cells. Only about 10% of the total accumulated streptomycin is present at the onset of loss of viability and can therefore be presumed to play a role in the lethal action of the antibiotic.

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