Butler W H, Gabriel K L, Preiss F J, Osimitz T G
BIBRA International, Carshalton, Surrey, UK.
Mutat Res. 1996 Dec 20;371(3-4):249-58. doi: 10.1016/s0165-1218(96)90113-5.
The genotoxicity of piperonyl butoxide has been investigated in bacterial mutation assays using tester strains TA98, TA100, TA1535, TA1537 and TA1538. The assays were conducted both with and without metabolic activation. Piperonyl butoxide was tested for mutation with and without metabolic activation in the CHO/HGPRT assay. Chromosomal aberrations were investigated also using Chinese hamster ovary (CHO) cells and effects on DNA were evaluated by in vitro unscheduled DNA synthesis (UDS) test using rat liver primary cell cultures. Piperonyl butoxide was not shown to be genotoxic in any assay system. The data presented supports the view that the liver tumors observed in rodents at dose levels above the maximally tolerated dose (MTD) result from a secondary non-genotoxic mechanism.
已使用测试菌株TA98、TA100、TA1535、TA1537和TA1538在细菌突变试验中研究了胡椒基丁醚的遗传毒性。试验在有和没有代谢活化的情况下进行。在CHO/HGPRT试验中,对有和没有代谢活化的胡椒基丁醚进行了突变测试。还使用中国仓鼠卵巢(CHO)细胞研究了染色体畸变,并通过使用大鼠肝原代细胞培养物的体外非程序性DNA合成(UDS)试验评估了对DNA的影响。在任何试验系统中,均未显示胡椒基丁醚具有遗传毒性。所提供的数据支持这样一种观点,即在高于最大耐受剂量(MTD)的剂量水平下在啮齿动物中观察到的肝肿瘤是由继发性非遗传毒性机制引起的。