Two strains of Escherichia coli—ML 30, which is both permease and β-galactosidase inducible, and ML 35, permease-less (cryptic) and β-galactosidase constitutive— were used to study the effects of phenolic disinfectants on protein (β-galactosidase) synthesis and membrane damage (β-galactosidase activity in the absence of permease). 2,4-Dichlorophenol in a concentration (67 mcg./ml.) adequate to ... [Show full abstract] inhibit growth of E. coli ML 30 in synthetic medium inhibited permease production but not β-galactosidase production. A higher concentration (133 mcg./ml.) of this phenolic inhibiting β-galactosidase synthesis also inhibited incorporation of leucine-C-14 into cells. p-tert-Amylphenol in a concentration (63 mcg./ml.) inhibiting growth did not inhibit β-galactosidase synthesis, although a higher concentration (100 mcg./ml.) inhibited both growth and β-galactosidase synthesis, A number of phenol derivatives damaged the cell membrane of E. coli ML 35 (cryptic), evidenced by β-galactosidase activity. Further evidence for membrane damage was the release of C-14 from uracil-C-14 or adenine-C-14 labeled cells in the presence of p-tert-amylphenol and the parallel increase in β-galactosidase activity of E. coli ML 35 (permease-less). Higher concentrations of the phenolic germicide caused additional release of C-14 but did not increase β-galactosidase activity.