Alterations in the activities of ornithine and histidine decarboxylases provoked by testosterone in mice.

1. The urinary excretion of putrescine has been determined in female mice before and during repeated injections of testosterone.2. Testosterone administration effected a striking increase in the excretion of free putrescine.3. Ornithine decarboxylase (L-ornithine carboxy-lyase; E.C. 4.1.1.17) and histidine decarboxylase (L-histidine carboxy-lyase; E.C. 4.1.1.22) activities of mouse kidney and liver were examined. In the kidney, following testosterone administration, ornithine decarboxylase activity was found to be substantially elevated, whereas that of histidine decarboxylase was depressed. In the liver, by contrast, the activity levels of these enzymes were not significantly altered by testosterone treatment.4. The possibility of a functional interrelation between putrescine and histamine, via the two enzyme activities investigated, is discussed.

Retardation of protein synthesis in rat foetal liver on inhibiting rate of histamine formation.

1. The rate of protein synthesis, as gauged by the incorporation of [(14)C]leucine, has been determined in vitro in foetal and 5-day-old rat liver, tissues with respectively high and low histidine decarboxylase activity.2. Incorporation of [(14)C]leucine was considerably faster in foetal liver than in liver of the young.3. Following inhibition of histamine formation by alpha-methyl histidine, a specific inhibitor of histidine decarboxylase, the rate of incorporation of [(14)C]leucine was substantially diminished in foetal but not in liver of the young.4. The retarded incorporation of [(14)C]leucine consequent on inhibition of endogenous histamine formation could not be restored by extracellular histamine, i.e. by adding histamine to foetal liver tissue.5. On complete inhibition of protein synthesis by puromycin in foetal and 5-day-old rat liver the rate of histamine formation was not affected.6. The present observations support the view of endogenous histamine formation, ;nascent histamine', as an essential part of the metabolic machinery in some rapidly growing tissues.

Accelerated mobilization and formation of histamine in the gastric mucosa evoked by vagal excitation.

1. The changes in the rate of histamine formation and in the histamine content of the parietal cell containing region of the gastric mucosa have been studied in rats under the influence of agents which evoke or abolish vagal excitation.2. The hypoglycaemia producing agents, insulin and 2-deoxyglucose (2-DG), raised the mucosal histamine-forming capacity (HFC) in a way similar to that previously observed on re-feeding, gastrin injection, and distension of the stomach wall.3. In cats, insulin injection elicited an elevation of mucosal HFC similar to the corresponding effect of insulin in rats.4. Hoechst 9980, which inhibits post-ganglionic cholinergic transmission, counteracted the elevation of mucosal HFC following vagal excitation, but did not inhibit changes produced by gastrin, thus indicating the absence of a cholinergic intermediary link between gastrin and changes in mucosal histamine.5. It is emphasized that although re-feeding, vagus excitation, gastrin and distension all produce similar changes in mucosal histamine, the clarification of the precise role of histamine as a natural stimulant for the parietal cells may require a fresh kind of approach.