Inhibition of β-aminopropionitrile (βAPN)-induced skeletal teratogenesis by the flavonoid β-hydroxyethylrutosides (HR) in hamster fetuses



Since biochemical studies have shown that flavonoids such as β-hydroxyethylrutosides (HR) protect against the damage to collagen induced by lathyrogens in adult rats, this compound was given to pregnant hamsters in order to determine its effects on the teratogenicity induced by β-aminopropionitrile (βAPN). A dose of 2,500 mg/kg of βAPN alone given by gavage on day 11 produced a high frequency (69.5%) of skeletal anomalies in the offspring of hamsters. Administration of HR immediately following βAPN to pregnant animals resulted in a significantly decreased teratogenic response (P < 0.05). These data provide evidence to support the view that the primary mechanism for the βAPN-induced skeletal dysmorphogenesis is the inhibition of cross linking during the maturation of collagen fibers.