Abstract
Experimental riboflavin deficiency has served as a useful tool of teratologic research in mammals. It had been possible for over 100 years to produce congenital malformations in chicks by various environmental disturbances, and for many years a variety of monstrosities had been produced experimentally in amphibia and fishes. Eggs and embryos of animals of lower classes are easily accessible to modification, but mammalian ova that develop in the mother’s body are well protected against adverse influences of the outside world. It was generally assumed until 35 years ago that environmental insults to pregnant mammals terminate in death of the embryos—or leave them morphologically intact, resulting in the birth of normal young. It was believed, and often dogmatically stated, that in mammals and in man systemic and internal congenital malformations must be genetically determined and hereditary, since, with the exception of rare amputations by mechanical intrauterine disturbances, no exogenous factors were known that could bring about prenatal deformities in embryos and fetuses. It was thought in particular that in mammals symmetrical and serial malformations (that is, defects involving upper and lower extremities) must be hereditary. This belief was expressed not only in the medical literature but also incorporated in the German Law of 1933 for Prevention of Offspring with Heritable Diseases.(59,65)
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Warkany, J. (1975). Riboflavin Deficiency and Congenital Malformations. In: Rivlin, R.S. (eds) Riboflavin. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-4419-3_9
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DOI: https://doi.org/10.1007/978-1-4613-4419-3_9
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