Pathogenesis of bromodeoxyuridine‐induced polydactyly

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Abstract
Intraperitoneal injection of BUdR on day 11 or 12 of rat gestation produced preaxial polydactyly of the hindlimb. The pathogenesis of this deformity differed from that of other polydactyly regimes in that drug‐induced mesenchymal necrosis was not an essential feature. Likewise an altered pattern of physiological necrosis in the apical ectodermal ridge (AER) was not evident in hindlimbs of BUdR‐treated embryos. In keeping with earlier studies, a zone of physiological necrosis within the preaxial mesoderm thought to be instrumental in controlling preaxial digitation was abolished. Speculation has focused on the incorporation of BUdR into these prospectively necrotic cells as the means by which they survive. Support for this idea is gained from the protective effect of concomitant thymidine administration, which presumably prevents BUdR incorporation.