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Current hypotheses of the mode of bactericidal action of chlorine suppose a direct combination of some chemical 'species of the chlorine with the bacterial protoplasm producing a toxic organic complex (Porter, 1946). Although this view is a great advance over earlier concepts, it still lacks precision in terms of our present knowledge of the intermediary metabolism of cells. The marked efficiency of chlorine, exerting a bactericidal action in concentrations of 0.2 to 2.0 ppm in water, will at once classify it as a biologically active "trace substance." It may consequently be assumed to exert its effect upon the enzyme systems of the cell (Green, 1941). By investigation of the effect of chlorine on bacteria and on various enzymes, its bactericidal effect has been shown to depend upon the inhibition of certain essential enzyme systems, and the mechanism of this inhibition involves the powerful oxidative action of chlorine on the-SH groups of these enzymes. METHODS Active chlorine was estimated by the acid-iodine thiosulfate titration procedure (Calvert, 1943). Chlorine solutions, when not otherwise specified, were obtained by neutralizing and filtering a fresh solution of calcium hypochlorite. 'This investigation was conducted under contract with the Committee on Medical Research of the Office of Scientific Research and Development and at the request of the Office of the Quartermaster General.

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Plasma amino acids and the 24-h urinary excretion of copper and amino acids were measured in 18 infants receiving 0.4 g N/kg/day as free amino acids as part of a total parenteral nutrition regimen. Urinary copper excretion correlated positively with total excretion of alpha-amino nitrogen, in general, and the excretion of glycine, methionine, histidine, and lysine, in particular. Infants who received FreAmine II as compared to FreAmine III generally had increased plasma concentrations of glycine and methionine and increased urinary excretion of total alpha-amino nitrogen, glycine, methionine, and of copper. Chronic losses of copper in the urine of infants receiving free amino acid solutions may contribute to copper depletion and the development of a copper deficiency syndrome.

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Abstract— The effect of phenylalanine and phenylpyruvate on the metabolism of pyruvate by homogenates of human brain was investigated. In the presence of 5 mM pyruvate as substrate homogenates of human cerebral cortex fixed about 1 μmol of H14CO3‐‐ per g of tissue in 30 min. Phenylpyruvate at a concentration of 5 raw inhibited the fixation of H14 CO3‐‐ by homogenates of human brain by approximately 50 per cent, whereas 5 mM phenylalanine had no effect. The inhibition of pyruvate carboxylation by phenylpyruvate was dependent upon the concentration of the inhibitor. The activity of pyruvate carboxylase (EC 6.4.1.1) in human cerebral cortex was 02–0.4 units, with a Km for pyruvate of about 0.2 mM. Homogenates of human cerebral cortex decarboxylated [1‐14C]pyruvate to 14CO2 at a rate of about 5 μmol per g of tissue per 15 min, with a 20–50 per cent reduction in the presence of 5 mM phenylpyruvate; phenylalanine at the same concentration had no effect. The possible toxic effect of phenylpyruvate on the metabolism of pyruvate in the brains of untreated phenylketonuric patients is discussed.