[DNase II activation in rat liver in the course of acute diethylnitrosamine-induced damage (author's transl)].

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.