Abstract
Chronic administration of α-monofluoromethyl histidine, a specific inhibitor of histidine decarboxylase, to pregnant mice blocked histidine decarboxylase activity and markedly depleted histamine levels in 18-day-old foetuses and in newborn mice. Such treatment had no effect on implantation or embryonic development or parturition suggesting that de novo synthesis of histamine is not a significant factor in these processes in the mouse.
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