The induction of a diabetic-like state by the drug streptozotocin (Stz) has been useful for studies on the effects of maternal glucose intolerance upon the monkey fetus. However, the question of transplacental passage of Stz and its effect upon the fetus has to be considered if the drug is to be administered post-conception. Experiments in which Stz was administered maternally and then analyzed in maternal and fetal blood by disc-plate assay indicated prompt movement to the fetal circulation. Slow maternal degradation of Stz was associated with higher fetal blood levels of the compound.

Studies with 14C-streptozotocin suggest that about one half of the radioactivity present in maternal and fetal plasma following intravenous maternal administration is intact 14C-Stz; after one hour, only one fifth of the radioactivity is still associated with the Stz molecule. By the time maximum fetal levels of the drug were achieved, maternal levels of Stz had decreased to one sixth and one tenth of initial levels. Fetal levels did not exceed one half to one third of the simultaneous maternal plasma concentration, implying placental limitation to transfer of streptozotocin from mother to fetus.

No specific localization of 14C-Stz by pancreatic beta cells was observed in either paraffin or frozen-dried autoradiographic preparations. No evidence of high levels of uptake of 14C-Stz were found in pancreatic tissue in comparison to other selected fetal tissues.

Although Stz does cross the hemochorial placenta to a limited extent, it appears to have no discernible effect upon the fetal pancreas.

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