The effect of the following acridines on the electrophoretic mobility of Streptococcus faecalis was studied at constant values of pH and ionic strength: acridine hydrochloride, 9-hydrazinoacridine acetate, 9-aminoacridine hydrochloride, acriflavine hydrochloride, and proflavine dihydrochloride. Increasing times of contact of the bacteria with acridines rendered the electrophoretic mobility less negative or more positive due to the interaction with nucleic acids released from the bacteria through the action of the acridines. Stirring of the bacterial suspensions minimized this effect. Hence, electrophoretic mobilities were measured on samples withdrawn from stirred bacterial suspensions at successive time intervals after the addition of the acridines, and the mobilities were extrapolated to zero time. The mobility-concentration curves had similar shapes for all acridines. With increasing concentration of the acridinium salts, the negative mobilities or ζ-potentials of the bacteria decreased slowly at first but at a much faster rate as they approached zero. When the neutralization of the carboxylate groups in the bacterial cell wall by chemisorption of acridinium ions was complete, the ζ-potential was reduced to zero because the resultant acridinium carboxylates were only slightly dissociated. Further concentration increases inverted the electric charge of the bacteria to positive by physical adsorption of the entire acridinium salts. The positive mobilities increased with the acridine concentrations. rapidly at first but at slower rates for still higher concentrations. The acridine concentrations required to reduce the mobility or ζ-potential of the bacteria to zero were lower in more acid media. For four of the five acridines, there was an inverse relationship between these concentrations and the base strength of the acridines. The acridines of highest pKa were most strongly chemisorbed by the carboxylate groups in the cell wall, saturating them at the lowest concentrations. Relatively high concentrations of acridines caused the bacteria to agglomerate. This agglutination was not due to a reduction in the absolute value of the ζ-potential; it was probably caused by nucleic acids leaked from the bacteria or by their complex coacervates with the acridines, possibly through bridging. Aminoacridine hydrochloride and proflavine dihydrochloride did not inhibit the growth of S. faecalis even at concentrations 10 times greater than those at which they reduced the ζ-potential to zero. This suggests that the primary site of attack of these acridines is not the cell wall.