Mutagenic interactions of model chemical mixtures
Mutagenic interactions of model chemical mixtures
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DOI：
10.1016/s0045-6535(98)00123-4
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发表时间：
1998-09-01
期刊：
影响因子：
8.8
通讯作者：
Capizzi, JL
中科院分区：
文献类型：
--
作者：
Donnelly, KC;Claxton, LD;Capizzi, JL
虽然目前的人类健康风险评估方法假定复杂混合物的污染物之间存在相加作用，但可能会发生产生协同或拮抗效应的化学作用。本研究采用沙门氏菌/微粒体法对三种模型化合物--苯并(A)芘(B(A)P)、五氯苯酚(PCP)和2，4，6-三硝基甲苯(TNT)分别在二元和三级溶液中的致突变效应进行了检测。对所有菌株来说，B(A)P是具有代谢活性的致突变物质(阿罗氯1254诱导的SD大鼠肝脏S9组分)，TNT是无代谢活性的致突变物质，五氯苯酚在有或没有代谢活性的情况下都是失活的。在二元和三元溶液中，五氯酚对B(A)P或TNT的致突变性没有影响，与代谢活化无关。对于TA97a菌株，在TNT存在下，具有代谢激活作用的B(A)P的致突变性略有下降，在存在B(A)P和PCP的情况下，没有代谢激活作用的TNT的致突变性略有降低，具有代谢激活作用的三级溶液(496个回复菌株/10ug)的致突变性低于单独使用B(A)P时的致突变性(729个回复菌株/10ug)。TNT对激活的TA98菌株的致突变性有抑制作用。用不同浓度的TNT或B(A)P进行的研究表明，随着TNT浓度的增加，对B(A)P致突变性的抑制作用增强。用四种浓度的S9进行的检测表明，S9的水平对B(A)P的致突变性的抑制作用相对较小。这些数据表明，在TNT存在的情况下，相互作用限制了能够达到或结合细菌DNA的B(A)P的浓度。(C)1998爱思唯尔科学有限公司。保留所有权利。
Although current methodology for human health risk assessment assumes additive interactions among the contaminants of a complex mixture, chemical interactions may occur which produce synergistic or antagonistic effects. In this study, the mutagenic response of three model compounds, benzo(a)pyrene (B(a)P), pentachlorophenol (PCP) and 2,4,6-trinitrotoluene (TNT), were tested individually and in binary and tertiary solutions, using the Salmonella/microsome assay with each of three bacterial tester strains (TA97a, TA98, and TA100). For all strains, B(a)P was mutagenic with metabolic activation (Arochlor 1254-induced Sprague-Dawley rat liver S9 fraction), TNT was mutagenic without metabolic activation, and pentachlorophenol was inactive both with and without metabolic activation. In binary and tertiary solutions, pentachlorophenol had no effect on the mutagenicity of B(a)P or TNT, independent of metabolic activation. For strain TA97a, the mutagenicity of B(a)P with metabolic activation was slightly decreased in the presence of TNT; the mutagenicity of TNT without metabolic activation was slightly decreased in the presence of B(a)P and PCP; and the mutagenicity of the tertiary solution (496 revertants/10 ug) with metabolic activation was lower than the mutagenicity of B(a)P alone (729 revertants/10 ug). The mutagenicity of B(a)P in strain TA98 with activation was inhibited by the addition of TNT. Studies conducted using several concentrations of TNT or B(a)P indicate that the inhibition of B(a)P mutagenicity was increased as the concentration of TNT increased. Assays performed using four concentrations of S9 indicated the inhibition of B(a)P mutagenicity was relatively unaffected by the level of S9. The data suggest that an interaction in the presence of TNT limits the concentration of B(a)P that is capable of reaching or binding with bacterial DNA. (C) 1998 Elsevier Science Ltd. All rights reserved.