[A new approach to the rating of psychological disadaptation in extreme conditions].

Infraconscious psychic adaptation and role of the sympathoadrenal system (SAS), the front defense echelon of organism, were investigated in 48 men under the chronic stress in the zone of hostilities on the days out. The purpose was to define and to verify individual quantitative predictors of psychic deadaptation. The investigation was fulfilled with the method of neurosemantic diagnostics ("ousting"--"accentuation" of traumatic information by way of catatonic psychological protection on the level of perception) and computerized determination of the EEG alpha-intensity (Kvasovets et al., 2002), and SAS evaluation by beta-ARM values (ARM-AGAT assay kits, AGAT-MED company, Moscow). The subjects divided into two groups. In group-1 (n = 33) beta-ARM values were under 45 conv. units (27.2 +/- 1.8 conv. units) suggesting a moderate SAS activity and a moderate stress reaction. In group-2 (n = 15), beta-ARM values exceeded 45 conv. units. (60.4 +/- 2.7 conv. units) suggesting SAS hyperactivity associated with the intensive and extended exposure to stress-factors. Analysis of group average values and distribution and correlations of individual data made it possible to identify the following three objective quantitative indices as the individual criteria of developing deadaptation: 1) SAS hyperactivation with beta-ARM exceeding 45 conv. units, "ousting" or "accentuation" above 8.7 conv. units (neurosemantic diagnostis on the perception level), and 3) EEG alpha-activity reduced to 0.4-0.7 rated units in both hemispheres.

The effect of hexadecylphosphocholine on the degradation of mitochondrial phospholipids.

Hexadecylphosphocholine (HePC) is known as antitumor agent but the mechanism has not yet been understood. In rat liver mitochondria its effect on phospholipid transformation has been studied by quantitative HPTLC and phosphorus determination. From the results it can be concluded that HePC influences the activities of phospholipase A2, phospholipase C, phospholipase D, and lysophospholipase A. The phospholipid transformation as well as the influence of HePC are affected by exogenous calcium ions. In the presence of calcium HePC has been found to inhibit enzyme activities, whereas in the absence of exogenous calcium ions enzymatic phospholipid transformations are activated or inhibited depending on HePC concentrations.

The role of membrane structure in the activation of mitochondrial phospholipases. 1. Activation of mitochondrial phospholipases by lipid peroxidation products.

Induction of lipid peroxidation is shown to alter the structure of mitochondrial membrane and to activate endogenous phospholipases A2, C, D, and lysophospholipase A. Fe(2+)-, cumene hydroperoxide- and ultraviolet-induced lipid peroxidation results in the activation of mitochondrial phospholipases.

The role of membrane structure in activation of mitochondrial phospholipases. 2. Mechanism of crambin action on the activities of mitochondrial membrane phospholipases and microviscosity.

Effects of crambin on the phospholipase activity, lipid peroxidation and structure of mitochondrial membranes have been investigated. Crambin has been shown to inhibit lipid peroxidation and phospholipase activity induced by Ca2+ and freezing-thawing of mitochondria. As shown by ESR studies, these effects are based on the ability of crambin to cause changes in mitochondrial membrane structure.