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Congenital Malformations in Nonhuman Primates

1993; Springer Nature; Linguagem: Inglês

10.1007/978-3-642-84906-0_26

0177-7475

Andrew G. Hendrickx, Pamela E. Binkerd,

Hedgehog Signaling Pathway Studies

The nonhuman primate has been under close scrutiny for the characterization of spontaneous and experimentally induced malformations since the thalidomide catastrophe fueled a widespread search for a model of human teratogenicity. Early reports indicated spontaneous malformation rates of 0.44%–0.52% in a variety of nonhuman primates, mostly macaques (Macaca spp.) and baboons (Papio sp.) (Lapin and Yakovleva 1963; Hendrickx 1966; Wilson and Gavan 1967). More recent reviews have reported a somewhat higher incidence (1.02%–1.62% for Old World species; 6.0% in Saimiri sciureus) and a wide range of spontaneous defects affecting all major developmental systems in a variety of prosimians, New and Old World monkeys, and apes (Wilson 1978; Hendrickx and Prahalada 1986; Hoopes and Jerome 1987; Jerome 1987; Binkerd et al. 1988). More specifically, the cardiovascular and urinary systems represent the majority of cases studied in nine species (mostly macaques) in one survey (Hendrickx and Prahalada 1986). Jerome (1987) found that cardiovascular and central nervous system defects accounted for over half of the malformations occurring in a colony of Macaca mulatta, Macaca fascicularis, Macaca arctoides, and Cercopithecus aethiops. Saimiri sciureus appears to be susceptible to the spontaneous occurrence of cleft lip and/or palate; the fact that about one-half of these cases resulted from consanguineous matings suggests a genetic component for this particular defect (Hoopes and Jerome 1987). The reader is referred to these reviews (and references therein) for specific information on the reported defects, particularly incidence rates, discussed in the following summary. Due to the multifactorial nature of many malformations and different methods of determination, variable rates of naturally occurring defects have been reported in laboratory and domestic species and humans. While a broad spectrum of malformations is observed in most species, the frequency of individual malformations is species-specific (see Schardein 1985 and Wilson et al. 1978).