Horiuchi T, Ohtsubo K, Saito M
Jpn J Exp Med. 1976 Apr;46(2):111-21.
Oral administration of furylfuramide (2-(2-furyl)-3-(5-nitro-2-furyl) acrylamide), used as an antimicrobial food preservative until recently, caused centrolobular coagulation necrosis of the liver of the mouse (ddYS, male) in the degree corresponding to the doses. The recovery process after a single oral administration was characteristic: the necrotic cells were laden with calcium and replaced by foreign body granuloma accompanied by multinucleate giant cells. Complete healing ensued in about a month. Phenobarbital pretreatment reduced injurious effect of furylfuramide on the liver with preservation of the centrolobular region. In this case necrosis occurred in the intermediate zone in a ring-like shape. This indicates enhanced detoxication of furylfuramide by microsomal drug metabolizing enzyme(s) of the liver cells induced by phenobarbital.
直到最近还用作抗菌食品防腐剂的糠基糠酰胺(2-(2-呋喃基)-3-(5-硝基-2-呋喃基)丙烯酰胺)经口给予小鼠(ddYS,雄性)后,会导致肝脏中央小叶发生与剂量相应程度的凝固性坏死。单次经口给药后的恢复过程具有以下特点:坏死细胞充满钙,并被伴有多核巨细胞的异物肉芽肿所取代。约一个月后完全愈合。苯巴比妥预处理减轻了糠基糠酰胺对肝脏的损伤作用,中央小叶区域得以保留。在这种情况下,坏死呈环状发生在中间带。这表明苯巴比妥诱导的肝细胞微粒体药物代谢酶增强了糠基糠酰胺的解毒作用。