抄録
The seven possible mechanisms of drug resistance which Davis listed up (Davis and Maas, 1952) can be summarized into the following three: (I) Alteration of metabolic pathways, including the possibility of increased production of metabolites which antagonize the drug. (II) Increased destruction of the drug, including increased production of inactivators of the drug. (III) Changes in the permeability of the cell (or of subcellular units) to the inhibitor.
Attempts have been carried out in a series of works to elucidate the above alternative possibilities concerning CM resistance, using two CM resistant strains of E, coli derived from two different strains. In this report, at first, in relation to the possibility (I), the sensitivity of the cells to CM in the population of CM-resistant as well as sensitive strains was examined by the method of Treffers (1956) . The two resistant strains used showed cross resistance to Pn, AM, and EM, but were as sensitive to SM as the parent strains. This cross resistance was also examined by the same method. It was shown that the slopes of resitant strains was in most cases identical with those of the sensitive strains.
Secondly, the possibility (II) (inactivation of the drug) in CM resistance was also examined in this paper, using the inhibitory activity of CM to β-galactosidase formation after the contact of the drug with CM-resistant strains. The results obtained will suggest that the remaining possibility (III) may be an important factor of mechanism of resistance of the CMR strains used.
As to the possibility (I), (the alteration of metabolic pathways and other mechanisms), further studies will be presented in the following papers.
