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At least 19 recordsLinked to original sources
PubMed1955

The effect of iodoacetate and other inhibitors on phage production and lysis in three phage systems.

The minimal bacteriostatic concentration of iodoacetate, azide, or proflavine was added at intervals during the latent periods of virus in three different bacterium-bacteriophage systems (M. aureus, B. mycoides, E. coli). For each interval at which inhibitor was added, the occurrence of lysis and the final yield of phage were determined. In the B. mycoides and E. coli systems, when added during the first part of the latent period, inhibitor prevented lysis and no phage was released. Introduction of inhibitor during the last part of the latent period resulted in normal lysis and in a linear increase in phage that progressively approached the yield obtained in the absence of inhibitor (the later the introduction, the higher the yield). In the M. aureus system, phage production and lysis in the presence of inhibitor followed the same general pattern, except that release of phage and normal lysis occurred in infected cells to which inhibitor had been added quite early in the latent period. Our results, when compared with those of Foster (1948) with proflavine and Bozeman et al. (1954) with chloramphenicol, suggest that (1) the final phage yields represent the amount of mature intracellular virus present at the time of addition of inhibitor and (2) the reactions leading to lysis proceed independently of those leading to the formation of mature virus once phage infection has reached a critical point in time.

Azides↗
PubMed1958

Effects of azide and choretone on the sodium and potassium contents and the respiration of frog sciatic nerves.

Azide (0.2 to 5.0 mM) and chloretone (2.0 to 15.0 mM) reversibly inhibited 20 to 90 per cent of the resting respiration of frog sciatic nerves, and caused a loss of potassium and a gain of sodium in this tissue. The changes in ionic contents that developed after 5 or 10 hours were roughly correlated with the degree of respiratory depression, but the time courses of these changes were different with the two reagents. In azide these changes appeared to begin immediately, while in chloretone, at concentrations between 3.0 and 5.0 mM, the ionic shifts developed after a delay of several hours. Fifteen millimolar chloretone produced immediate changes in ionic contents several times greater than those produced by anoxia. The changes in ionic distribution produced in 5 hours by anoxia, 5.0 mM azide, or 5.0 mM chloretone were at least partially reversible; those produced by 15.0 mM chloretone were irreversible. With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway. Concentrations of azide or chloretone that depressed the resting rate of oxygen consumption more than 50 per cent produced a slow conduction block, while 15.0 mM chloretone blocked conduction within 15 minutes.

Animals↗