The effects of respiratory deficiency on the level of NAD-dependent alcohol dehydrogenase activity were studied. Respiratory-deficient mutants produced by acriflavine, and wild-type cells grown on glucose in the presence of chloramphenicol had elevated alcohol dehydrogenase activities compared with the wild-type cells grown on glucose. The increased activity was a result of an increase in ADH-I. The respiratory-deficient mutants appeared unable to produce ADH-II or isocitrate lyase even after incubation of the cells in ethanol medium. However, this transfer to ethanol medium increased the level of ADH-I activity. The presence of chloramphenicol in the ethanol medium further increased the alcohol dehydrogenase activity of these mutants. The effect of chloramphenicol in the wild-type cultures depended on the time of its addition to the culture. If chloramphenicol was present during both the period of growth on glucose and in the ethanol medium, ADH-II activity did not appear. If the cultures were grown on glucose in the absence of chloramphenicol, allowing respiration to develop, the subsequent presence of chloramphenicol in fresh ethanol medium did not prevent the appearance of either ADH-II or isocitrate lyase activity. The respiratory-deficient mutants also contained alcohol dehydrogenase activity which resembles ADH-III in respect to electrophoretic mobility, heat stability, and relative activity with various alcohols as substrates.