Summary: Triethyllead and tripropyllead cations affected growth, energy metabolism and ion transport in K12. The tripropyllead compound was more liposoluble than the triethyl analogue and was also more effective in inhibiting cell growth and the oxygen uptake of both intact cells and membrane particles. Triethyllead acetate (5 μ) inhibited growth on non-fermentable carbon sources, such as glycerol and succinate, more markedly than on glucose. At higher concentrations, triethyllead caused significant inhibition of respiration rates of intact cells; the concentration giving 50% inhibition was 60 μ for glycerol-grown cells and 158 μ for glucose-grown cells. Oxidation of succinate by membrane particles was less sensitive to inhibition by the tripropyl- or triethyllead compounds than were the oxidations of -lactate or NADH. Triethyllead acetate [1.9 μmol (mg membrane protein)] inhibited the reduction by NADH of cytochromes; evidence for more than one site of inhibition in the respiratory chain was obtained. Membrane-bound ATPase activity was strongly inhibited by triethyllead acetate in the absence or presence of Cl. The concentration of inhibitor giving 50% inhibition [0.02 μmol (mg membrane protein)] was about two orders of magnitude lower than that required for 50% inhibition of substrate oxidation rates in membranes. Triethyllead acetate (1 μ) induced swelling of spheroplasts in iso-osmotic solutions of either NHCl or NHBr, presumably as a result of the mediation by the organolead compound of Cl-/OH and Br/OH- antiports across the cytoplasmic membrane. Similar exchanges of OH for F, NO or SO or the uniport of H could not be demonstrated. Comparisons are drawn between the effects of trialkyllead compounds and those of the more widely studied trialkyltin compounds.


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