FORMATION OF REACTIVE OXYGEN AND NITROGEN SPECIES IN RAT LIVER TISSUES UNDER CONDITIONS OF SURGICAL TRAUMA REPRODUCED ON THE BACKGROUND OF EXPERIMENTAL MODEL OF POST-TRAUMATIC STRESS DISORDER

Abstract

In an experiment on 42 white rats, the mechanisms of oxidative-nitrosative stress in liver tissues under conditions of surgical trauma reproduced on the background of post-traumatic stress disorder were studied. It has been shown that the reproduction of an experimental model of posttraumatic stress disorder (single prolonged stress) causes the development of oxidative-nitrosative stress in rat liver tissues: it increases the rate of superoxide anion radical generation by microsomes, mitochondria and leukocyte NADPH oxidase, increases NO-synthase activity by activating the inducible isoform, reduces the activity and conjugation of constitutive NO-synthases, which is accompanied by an increase in the concentration of peroxynitrites of alkaline and alkaline-earth metals. On the 7th day after laparotomy against the background of reproduction of the experimental model of post-traumatic stress disorder, the indicators of oxidative-nitrosative stress in rat liver tissues, such as the production of superoxide anion radical by microsomes, microsomes and leukocyte NADPH oxidase total and inducible NO-synthase activity and concentration of peroxynitrites of alkaline and alkaline-earth metals, significantly exceed their values after a single laparotomy and after a sham operation against the background of simulated single prolonged stress.