Summary and conclusionsHuman retroplacental blood serum significantly (p <0 01) suppresses the in-vitro uptake of 3H-thymidine-that is, synthesis of deoxyribonucleic acid-by spontaneously growing human lymphocytes in the presence of exogenous spermine, but only in concentrations with a higher polyamine oxidase activity than that found in maternal peripheral blood serum during pregnancy.These findings together with observations that the placenta is rich in spermine and that interaction of polyamine oxidase and substrate arrests cell proliferation suggest that such interaction might represent a localised immunoregulatory mechanism in the placental bed, which might contribute to the protection of the fetoplacental unit from possible maternal immune rejection.

Summary The existence of a spermine oxidizing enzyme was established in human pregnancy serum by a radiochemical method, and a cross‐sectional study of its quantitative profile between 10 and 40 weeks gestation was undertaken. Though there was a wide scatter of values, the rise in the average activity was continuous and highly significant. The flavoprotein inhibitor, quinacrin, inhibited the enzyme activity, while the pyridoxal phosphate inhibitor, isoniazid, had no significant inhibitory effect suggesting that the enzyme is of tissue origin. The possible role of polyamines and their oxidation in physiological immunoregulation is discussed.

Summary Polyamine oxidase activity was measured in different compartments of the feto‐maternal unit by a radiochemical method. The activity in the retroplacental serum (mainly of intervillous origin) was 20 to 30 times higher than in maternal uterine or peripheral venous blood sera. No activity was found in the fetal cord blood sera. The enzyme level in the maternal peripheral sera fell to undetectable levels within 72 hours post partum. Preliminary data indicate that the enzyme might be produced by the decidua rather than by the placenta. It is suggested that the enzyme may constitute an important part of a supposed local immunological barrier formed at the placental bed to help to protect the fetal allograft from maternal immune rejection through a local suppressive effect on maternal cellular immunity.