Abstract
Environmental agents, such as drugs and pollutants, can cause congenital malformations when the fetus is exposed to them at a critical period during development at an optimal fetal concentration. Although much research has been carried out to elucidate the teratogenic mechanisms, little knowledge exists on the precise mechanisms involved. Thus, although a teratogen may be shown to inhibit or affect a biochemical pathway in a fetal tissue, usually it is not known how this biochemical lesion expresses itself in the observed malformation. In some instances the teratogen affects morphogenesis. Glucocorticoids have been observed to delay palate shelf rotation1 and causes myopathy in adult animals and humans2. Therefore, it would seem possible that glucocorticoids exert their teratogenic effects on a contractile system. However, although an intrinsic shelf force’ within the palate has been postulated to move the shelf3, the actual mechanism of palate shelf rotation has not been elucidated. Therefore, for the last few years we have been studying the mechanisms by which palate shelves undergo their morphogenetic movement in order to be able to study mechanisms of teratogenic action. This research has explored the possibility that the intrinsic shelf force’ is derived from the function of contractile proteins organized into muscle or non-muscle systems.
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Zimmerman, E.F. (1979). Palate morphogenesis: role of contractile proteins and neurotransmitters. In: Persaud, T.V.N. (eds) Abnormal Embryogenesis. Advances in the Study of Birth Defects, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-6654-6_9
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DOI: https://doi.org/10.1007/978-94-011-6654-6_9
Publisher Name: Springer, Dordrecht
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