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explained by a readier access of choline to the enzyme in vitro. It has always been difficult to accept that the toxicity of HC 3 is due to effects on the central nervous system (Schueler, 1955; Kase & Borison, 1958) because it is unlikely that a bisquaternary ammonium compound of this type would penetrate sufficiently. Recently, evidence has appeared suggesting that HC 3 interrupts neuromuscular transmission in the respiratory musculature (Longo, 1959; Holmes & Wilson, 1960). This effect appears only when the rate of stimulation is high and sustained; this would deplete the acetylcholine in the nerve endings and would aggravate any limitation on its resynthesis. Moreover, the effect was rapidly and readily reversed by choline, which is in keeping with the nature of the inhibition found in the present work.

Incorporation of [2-14C]mevalonic acid and [2-14C]acetic acid into lipids of mycobacteria