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用雄性Wistar大鼠,体重130～150 g,实验组31只,对照组10只,连续喂黄曲霉毒素B_1结晶品45周,每只大鼠受毒总剂量3.88 mg,分别在第8、9、11、12、13、14、15、16个月处死,每次处死给药组3只,对照组1只,第17个月后自然死亡7只。肝组织切片用HE染色;对28只大鼠肝组织进行了AFP免疫酶染色的形态学观察,15只鼠作了电镜观察,其结果:(1)光镜观察的主要表现为肝细胞的水样变性、嗜酸性变、嗜碱性改变、脂肪变性以及肝细胞的灶性坏死。其应答反应显示卵圆细胞和小胆管增殖、肝细胞的再生及炎细胞浸润。上述改变为慢性非特异性中毒性肝炎;(2)电镜观察主要改变有肝细胞核仁均质化,核样体形成,线粒体肿胀和基质均质化,继而形成空泡和灶性坏死;(3)85.71％(24/28)宿主肝细胞AFP免疫酶染阳性,多呈全胞浆型分布,阳性程度多为弱至中等度。AFP阳性肝细胞呈散在或灶性分布。这一改变表明,是由于AFB_1对肝细胞毒性损害所产生的返祖现象。
Using male Wistar rats weighing 130-150 g, 31 in the experimental group and 10 in the control group. 45 weeks of continuous feeding of the aflatoxin B 1 crystal product. The total dose of toxicant to each rat was 3.88 mg, respectively, at the 8th and 9th. They were sacrificed at 11, 12, 13, 14, 15, and 16 months. Three rats in each group were sacrificed and one in the control group. Seven patients died after the 17th month. Liver tissue sections were stained with HE; 28 liver tissues were observed by morphological observation of AFP immunostaining, and 15 rats were observed by electron microscopy. The results were as follows: (1) The main manifestation of light microscopy was the appearance of hepatocyte water. Degeneration, eosinophilia, basophilic changes, steatosis, and focal necrosis of hepatocytes. The response showed proliferation of oval cells and small bile ducts, regeneration of hepatocytes, and infiltration of inflammatory cells. The above changes were chronic non-specific toxic hepatitis; (2) Electron microscopic examination mainly changed the nucleolus homogenization, nucleosome formation, mitochondrial swelling and matrix homogenization, followed by the formation of vacuoles and focal necrosis; (3) 85.71% (24/28) of the host liver cells stained positive for AFP immunoreactive enzymes, most of them were in cytoplasmic distribution, and the positive degree was mostly weak to moderate. AFP-positive hepatocytes were scattered or focally distributed. This change indicates that this is due to a return to ancestral phenomenon caused by AFB 1 toxic damage to hepatocytes.