Schmerold I, Tempel K
Arch Toxicol. 1981 Sep;48(2-3):183-97. doi: 10.1007/BF00310487.
Single oral treatment of rats with acutely toxic doses of diethylnitrosamine (DENA) caused a temporary increase of liver-deoxyribonuclease II (DNase II) in homogenate, parenchymal cell, and diverse cell compartments. Highest stimulation resulted in nuclear fraction and cytosol. Due to largely congruent in vitro features, it was suggested that the normal as well as the DENA-activated DNase II were identical. Non-ionic detergents enhanced the enzyme activity only in control samples to a relatively small extent. Suitable conditions of reaction provided, the activation was suppressed by cycloheximide. The results indicated different mechanisms of DNase II activation in the course of an acute DENA-intoxication: 1. release of structurally bound DNase II fractions into cytosol; 2. induction of the enzyme and/or of an effector; 3. enhancement of the nucleus bound enzyme activity by translocation of activated DNase II from cytosolic to nuclear area.
用急性毒性剂量的二乙基亚硝胺（DENA）对大鼠进行单次口服治疗，导致匀浆、实质细胞和不同细胞区室中的肝脏脱氧核糖核酸酶II（DNase II）暂时增加。最高刺激作用出现在细胞核部分和胞质溶胶中。由于体外特征在很大程度上一致，因此有人提出正常的DNase II和被DENA激活的DNase II是相同的。非离子去污剂仅在对照样品中使酶活性有相对较小程度的增强。在提供合适反应条件的情况下，环己酰亚胺可抑制这种激活作用。结果表明在急性DENA中毒过程中DNase II激活的不同机制：1. 结构结合的DNase II组分释放到胞质溶胶中；2. 酶和/或效应物的诱导；3. 通过激活的DNase II从胞质溶胶向核区域的转位增强细胞核结合酶的活性。
