Inhibition of beta-aminopropionitrile (beta APN)-induced skeletal teratogenesis by the flavonoid beta-hydroxyethylrutosides (HR) in hamster fetuses.
Since biochemical studies have shown that flavonoids such as beta-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 beta-aminopropionitrile (beta APN). A dose of 2,500 mg/kg of beta APN 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 beta APN to pregnant animals resulted in a significantly decreased teratogenic response (P less than 0.05). These data provide evidence to support the view that the primary mechanism for the beta APN-induced skeletal dysmorphogenesis is the inhibition of cross linking during the maturation of collagen fibers.
D000014:Abnormalities, Drug-Induced / Q000517:prevention & control*; D000629:Aminopropionitrile / Q000633:toxicity*; D000818:Animals; D001842:Bone and Bones / Q000002:abnormalities* / Q000196:embryology; D003094:Collagen / Q000378:metabolism; D006224:Cricetinae; D005260:Female; D005333:Fetus / Q000187:drug effects; D006896:Hydroxyethylrutoside / Q000494:pharmacology*; D008647:Mesocricetus; D011247:Pregnancy; D012431:Rutin / Q000031:analogs & derivatives*
D006896:Hydroxyethylrutoside; D000629:Aminopropionitrile; D012431:Rutin; D003094:Collagen