Dybing E, Aune T
Acta Pharmacol Toxicol (Copenh). 1977 May;40(5):575-83.
Hexachlorobenzene (HCB)-pretreatment of rats leads to an increase in liver microsomal 2,4-diaminoanisole activation to a mutagen after a dose of 10 mg/kg intraperitoneally and to an increase in ethylmorphine N-demethylase after a dose of 50 mg/kg intraperitoneally. 2,4-Diaminoanisole mutagenicity was increased 24 hrs after HCB-pretreatment, whereas ethylmorphine N-demethylase first increased after 48 hrs. There is a sex difference in the inducing effects of HCB on ethylmorphine N-demethylase, but not on 2,4-diaminoanisole mutagenicity. HCB-pretreatment also leads to increases in 2,4-diaminoansiole mutagenicity in the kidneys, but not in the lings or in foetal liver.
用六氯苯(HCB)对大鼠进行预处理,腹腔注射10毫克/千克剂量后,肝脏微粒体对2,4 - 二氨基苯甲醚的激活作用增强,从而使其致突变性增加;腹腔注射50毫克/千克剂量后,乙基吗啡N - 脱甲基酶活性增强。HCB预处理24小时后,2,4 - 二氨基苯甲醚的致突变性增加,而乙基吗啡N - 脱甲基酶在48小时后才开始增加。HCB对乙基吗啡N - 脱甲基酶的诱导作用存在性别差异,但对2,4 - 二氨基苯甲醚的致突变性无性别差异。HCB预处理还会导致肾脏中2,4 - 二氨基苯甲醚的致突变性增加,但肺和胎儿肝脏中则不会增加。