摘要
目的探讨ＨＢＶ与ＡＴＢ１协同致肝癌的机理．方法用ＲＩＡ法测定ＨＢＶ转基因小鼠与正常小鼠暴露ＡＴＢ１后０，０５，１，２，４，８，２４ｈ７个不同时相肝脏ＡＴＢ１ＤＮＡ加成物的含量变化．结果暴露ＡＴＢ１后，ＨＢＶ转基因小鼠肝脏ＡＴＢ１ＤＮＡ加成物含量在各时相均高于正常小鼠，尤以１ｈ高峰时相值（５５９２ｐｍｏｌ／ｍｇ±４１５ｐｍｏｌ／ｍｇ比４１３６ｐｍｏｌ／ｍｇ±２８２ｐｍｏｌ／ｍｇＤＮＡ，Ｐ＜００１）及２４ｈ时相值（２４８７±２０３比９８９±８５，Ｐ＜００１）最显著．２４ｈ后，转基因小鼠肝脏ＡＴＢ１ＤＮＡ加成物仍维持高水平，但正常小鼠已基本恢复至暴露前水平．结论ＨＢＶ转基因小鼠暴露ＡＴＢ１后肝脏ＡＴＢ１ＤＮＡ加成物含量增加可能为ＨＢＶ与ＡＴＢ１协同致肝癌的直接原因．
AIM To elucidate the mechanism of synergistic interaction between HBV and aflatoxin B 1 (ATB 1) on hepatocarcinogenesis. METHODS With a competitive radioimmunoassay, seven different time phases of hepatic ATB 1 DNA adducts were detected in HBV transgenic mice and normal mice at 0, 0 5, 1, 2, 4, 8, 24 hours after exposure to ATB 1. RESULTS The levels of hepatic ATB 1 DNA adducts in HBV transgenic mice were higher than those in normal mice, especially remarkable at 1 hour (559 2±41 5 vs 413 6±28 2pmol/mg DNA, P <0 001) and at 24 hours (248 7±20 3 vs 98 9±8 5pmol/mg DNA, P <0 01) after exposure to ATB 1. At 24 hours after treated intraperitoneally with ATB 1, the level of hepatic ATB 1 DNA adducts in HBV transgenic mice was still high, but in normal mice it almost returned to the level before exposure to ATB 1. CONCLUSION The increased hepatic ATB 1 DNA adducts in HBV transgenic mice after exposure to ATB 1 might contribute to the synergistic interaction between HBV and ATB 1 on hepatocarcinogenesis.
关键词
乙型肝炎病毒
转基因动物
黄曲霉素B1
肝肿瘤
Liver/chemistry\ \ aflatoxin B 1/analysis\ \ DNA adducts\ \ Hepatitis B virus\ \ Animals, transgenic\ \ Liver neoplasms/etiology
