Prasanna P, Jacobs M M, Yang S K
Mutat Res. 1987 Feb;190(2):101-5. doi: 10.1016/0165-7992(87)90039-x.
Selenium (Se) decreased the mutagenicity of benzo[a]pyrene (BP), 3-methylcholanthrene (3MC), and 3-methylcholanthrylene (3MCE) in Salmonella typhimurium strains TA98 and TA100. Metabolism of BP, 3MC and 3MCE to mutagens was accomplished with the liver S9 fraction from Aroclor 1254-treated male Sprague-Dawley rats. Exposure of the bacteria to 4 nmoles BP, 10 nmoles 3MC, or 10 nmoles 3MCE in the presence of S9, and up to 200 nmoles Se as Na2SeO3 resulted in decreased mutagenicities up to 39, 66 and 60% of their respective control activities without Se in TA98 and up to 46, 52 and 64% of their respective control activities without Se in TA100. Se (200 nmoles) alone was not mutagenic in strains TA98 or TA100 with or without S9. BP, 3MC and 3MCE were not mutagenic in either strain without S9. None of the tested concentrations of BP, 3MC, 3MCE and Se were cytotoxic. Assays of the aryl hydrocarbon hydroxylase (AHH) activity in the S9 preparation revealed decreased AHH activity with increase in Se concentration. The decreased mutagenicity and AHH activity were Se (as Na2SeO3) dependent and could not be duplicated by sulfur (S as Na2SO3). Inhibition of AHH activity by Se provides an explanation of the mechanism of Se inhibition of BP, 3MC and 3MCE mutagenicities in S. typhimurium TA98 and TA100.
硒（Se）降低了苯并[a]芘（BP）、3-甲基胆蒽（3MC）和3-甲基胆蒽烯（3MCE）在鼠伤寒沙门氏菌TA98和TA100菌株中的致突变性。BP、3MC和3MCE向诱变剂的代谢是通过用Aroclor 1254处理的雄性Sprague-Dawley大鼠的肝脏S9组分来完成的。在S9存在的情况下，将细菌暴露于4纳摩尔BP、10纳摩尔3MC或10纳摩尔3MCE，以及高达200纳摩尔作为亚硒酸钠的Se，导致在TA98中致突变性分别降低至其各自无Se对照活性的39%、66%和60%，在TA100中降低至其各自无Se对照活性的46%、52%和64%。单独的Se（200纳摩尔）在有或无S9的TA98或TA100菌株中均无致突变性。在无S9的情况下，BP、3MC和3MCE在两种菌株中均无致突变性。所测试的BP、3MC、3MCE和Se的浓度均无细胞毒性。对S9制剂中芳烃羟化酶（AHH）活性的测定显示，随着Se浓度的增加，AHH活性降低。致突变性和AHH活性的降低依赖于Se（作为亚硒酸钠），并且不能被硫（作为亚硫酸钠的S）复制。Se对AHH活性的抑制为Se抑制鼠伤寒沙门氏菌TA98和TA100中BP、3MC和3MCE致突变性的机制提供了解释。
