The antibiotic streptozotocin under a variety of growth conditions rapidly and irreversibly inactivates the capacity to divide or to form colonies of a series of sensitive bacteria, containing the phosphoenolpyruvate-dependent sugar-phosphotransferase system. Cells can be sensitized towards the drug by pregrowth in N-acetyl-glucosamine and can be protected by adding this amino-glucoside to the medium. Starvation for energy, especially for phosphoenolpyruvate, or prevention of the induction of a transport system involved in streptozotocin uptake will protect the cells, while a block in protein synthesis does not. The killed cells neither lyse, nor are they transformed into spheroplasts. At first, the capacity of such "dead" cells to respire, to swim actively or to keep the cytoplasmic membrane impermeable for small molecules remains intact. Their capacity for over-all RNA and protein synthesis, and for carbohydrate and amino acid uptake by facilitated diffusion or active transport is not affected. However, they loose rapidly their ability to take up carbohydrates by the phosphoenolpyruvate dependent process of group translocation or to synthesize inducible enzymes, e.g. the enzyme beta-galactosidase. These inhibitory effects apparently are caused by the accumulation of phosphorylated, toxic derivatives of the antibiotic and eventually lead to a pronounced bacteriostasis. Killing of the cells seems to be caused by a direct effect of the strongly mutagenic drug on replicating DNA.