Kalinina E V, Loknitskaia N N, Shuliakovskaia T S, Fonshteĭn L M
Vopr Onkol. 1989;35(2):220-5.
Treatment with butylated hydroxytoluene (BHT) was shown to stimulate the activity of UDP-glucuronosyltransferase and to inhibit that of sulfotransferase in liver of Wistar male rats. Addition of UDP-glucuronic acid to incubation medium in Ames' test using BHT-pretreated subfractions of rat liver resulted in decreased mutagenicity of nitrosodiethylamine, nitrosomorpholine and cyclophosphamide. Further treatment with 3'-phosphoadenosine-5'-phosphosulfate failed to affect mutagenic activity of the promutagens tested. However, an increase in mutagenicity of nitrosomorpholine and cyclophosphamide was observed in application of liver subfractions from intact animals. It was concluded that BHT-induced inhibition of active metabolite production as well as increased production of their glucuronides are responsible for inhibition of mutagenicity of the agents tested. Simultaneous decrease in the yield of sulfates potentiated this effect for nitrosomorpholine and cyclophosphamide.
研究表明，用丁基羟基甲苯（BHT）处理可刺激Wistar雄性大鼠肝脏中尿苷二磷酸葡萄糖醛酸基转移酶的活性，并抑制硫酸转移酶的活性。在使用BHT预处理的大鼠肝脏亚组分进行的艾姆斯试验中，向孵育培养基中添加尿苷二磷酸葡萄糖醛酸可降低亚硝基二乙胺、亚硝基吗啉和环磷酰胺的致突变性。用3'-磷酸腺苷-5'-磷酸硫酸进一步处理未能影响所测试前诱变剂的诱变活性。然而，在应用完整动物的肝脏亚组分时，观察到亚硝基吗啉和环磷酰胺的致突变性增加。得出的结论是，BHT诱导的活性代谢产物生成抑制以及其葡萄糖醛酸苷生成增加是所测试试剂致突变性抑制的原因。同时，亚硫酸盐产量的降低增强了对亚硝基吗啉和环磷酰胺的这种作用。
