A series of experiments studying meiosis in Xenopus laevis oocytes, inhibiting or by-passing progesterone, seem to indicate a mode of action of the steroid at a membrane level with concomitant release of calcium normally bound to membrane phospholipids.

Gammexane (γ-chlorocyclohexane) is an inositol analogue, which inhibits progesterone-induced maturation in a dose-dependent manner; this widely used insecticide may act by affecting phosphatidylinositol metabolism of the oocyte membrane. Maturation can also be induced by a variety of amphiphilic cationic drugs known to interact with acidic phospholipids. Those include propranolol and some other β-adrenergic-blocking agents, some local anesthetics and some drugs acting on the central nervous system (e.g., neuroleptics). Moreover, an element known to act specifically at the superficial membrane Ca²⁺-sites, i.e., lanthanum, as well as quinidine, verapamil (D 200) and methoxy-verapamil (D 600), whose cellular action involves Ca²⁺ permeability or/and displacement, are also potent inducers of maturational events.

In the course of progesterone action, the preferential synthesis of various soluble proteins has been observed by double-labelling electrophoretic analysis, the induced proteins being also produced in enucleated oocytes. This increased labelling starts very early after progesterone exposure, within the first hour and before any appearance of MPF activity. The evolution pattern includes relatively late development of small molecular weight proteins.

A parallelism seems to exist between he effects of drugs on meiosis and protein synthesis. However, the inhibiting effect of gammexane is not found to be effective at the level of protein synthesis, since gammexane-treated oocytes injected with MPF are still able to induce protein peaks and to undergo GVBD.

The efficacy of the amphiphilic cationic compounds and lanthanum to induce maturation and concomitant protein-synthesis changes seems to correlate known effects of the same agents on membrane Ca²⁺ displacing activity. These results favour the idea that membrane-bound calcium is released from the membrane as an initial step following hormone exposure.