Synder S, Hsu I C, Trump B F
Mutat Res. 1987 Feb;182(1):31-9. doi: 10.1016/0165-1161(87)90005-7.
The activities to activate and detoxify procarcinogens were compared in intact hepatocytes from humans, Sprague-Dawley rats and Syrian golden hamsters. Mutagenic metabolites that were released from the isolated hepatocytes were detected by mutation induction in co-cultivated Salmonella typhimurium TA98. Hepatocytes from the 3 animal species all activated aflatoxin B1 (AFB1), acetylaminofluorene (AAF) and aminofluorene (AF) and released active metabolites to induce mutation in the indicator S. typhimurium T98. Hamster hepatocytes were more effective than were human and rat hepatocytes to mediate mutation of Salmonella TA98 by AFB1, AAF and AF. Hepatocytes of human and rat failed to mediate mutation by 1-aminopyrene (1-AP). Indeed, at low concentration of 1-AP and 1-nitropyrene (1-NP), the presence of the hepatocytes decreased the number of TA98 revertants. Only at higher concentrations of 1-aminopyrene and 1-nitropyrene did hamster hepatocytes increase mutation frequencies of indicator cells over the control groups. It seems that hepatocytes, particularly human hepatocytes, are better able to absorb and detoxify 1-AP and 1-NP than to activate them.
对来自人类、斯普拉格-道利大鼠和叙利亚金黄地鼠的完整肝细胞中前致癌物的激活和解毒活性进行了比较。通过共培养的鼠伤寒沙门氏菌TA98中的突变诱导来检测从分离的肝细胞中释放的诱变代谢物。这三种动物物种的肝细胞均能激活黄曲霉毒素B1（AFB1）、乙酰氨基芴（AAF）和氨基芴（AF），并释放活性代谢物以诱导指示菌鼠伤寒沙门氏菌T98发生突变。仓鼠肝细胞介导AFB1、AAF和AF引起的鼠伤寒沙门氏菌TA98突变的能力比人类和大鼠肝细胞更强。人类和大鼠的肝细胞无法介导1-氨基芘（1-AP）引起的突变。实际上，在低浓度的1-AP和1-硝基芘（1-NP）下，肝细胞的存在会减少TA98回复突变体的数量。只有在较高浓度的1-氨基芘和1-硝基芘下，仓鼠肝细胞才会使指示细胞的突变频率高于对照组。似乎肝细胞，尤其是人类肝细胞，吸收和解毒1-AP和1-NP的能力比激活它们的能力更强。
