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On the other hand, the teratogenic potential of transplacental exposure to MB has not been determined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MB was administered subcutaneously to ICR (CD\u20101) mice at 0, 35, 50, 60, or 70 mg\/kg on gestation day 8 (plug day = day 0). Teratological assessments were carried out at term gestation, on gestation day 18. Since MB inhibits soluble guanylate cyclase enzyme activity, zaprinast (ZPN), a selective cGMP\u2010phosphodiesterase type V inhibitor, was administered to prevent developmental disorders initiated by MB at 50 mg\/kg.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>There was a dose\u2010dependent increment of embryolethality. MB treatment also produced axial skeleton and neural tube defects. Coadministration of ZPN (20 mg\/kg per three times) abolished completely MB\u2010induced neural tube defects and reduced by one\u2010half the incidence of fetuses exhibiting axial skeletal defects. ZPN did not provide protection against the embryocidal effects of MB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This study showed that transplacental exposure to MB is teratogenic in the mouse. Coadministration of ZPN prevented partly MB\u2010induced teratogenesis, which supports the hypothesis that imbalance of cGMP pathway accounts, in part, for the teratogenicity of MB. 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