Mammalian ingestion of jervane, solanidane, and spirosolane steroidal alkaloids produces craniofacial congenital malformations in offspring upon administration during the primitive s t r d n e u r a l plate developmental phase. Structure-terata studies have shown that hamster teratogenicity induced by steroidal alkaloids is primarily related to the presence of C-5, C-6 unsaturation and secondarily to the molecular configuration at C-22 (spirosolanes and solanidanes). Teratogenic potencies of jervanes and solanidanes are appreciably higher than those of spirosolanes whereas the potency of jervanes is generally greater than that of solanidanes. The enhanced teratogenicity of functionalized steroidal alkaloids implies that their amphiphilic nature may be important in facilitating their passage of the embryonic membrane.
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