Perinatal hepatocarcinogenesis.
The mouse species is biologically characterized by a short gestation period that precludes completion of the intrauterine development before birth. Thus, in the mouse the late phase of intrauterine development is carried over into the postnatal age period. For this reason, we studied chemically induced hepatocarcinogenesis in B6C3F1 mice that were exposed transplacentally, postnatally, or during adulthood to benzidine x 2HCl, safrole, amitrol, ethylnitrosourea (ENU), and diethylnitrosamine (DEN). Data showed that perinatal exposure to those agents were significantly more hepatocarcinogenic than similar adult exposure. As regards the perinatally treated animals, the infants were shown to be more responsive than fetuses. The discussion shows that the higher "susceptibility" of infants was causally related to the presence of enzymatic complement required for the activation of procarcinogens and the concurrent high rate of macromolecular replication. It has been concluded that carcinogenesis in infants may be viewed as a part of the late "intrauterine" development. Thus, observed carcinogenicity has been construed as being relevant to the potential risk that might occur in other species exposed to these carcinogens during the late phase of intrauterine life.
D000367:Age Factors; D000640:Amitrole; D000818:Animals; D000831:Animals, Newborn; D002273:Carcinogens; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced*; D005260:Female; D005865:Gestational Age; D008113:Liver Neoplasms / Q000139:chemically induced*; D008297:Male; D051379:Mice; D009374:Neoplasms, Experimental / Q000139:chemically induced*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D002273:Carcinogens; D000640:Amitrole