M. Ya. Akhalaya

Molecular action mechanisms of solar infrared radiation and heat on human skin

The generation of ROS underlies all solar infrared-affected therapeutic and pathological cutaneous effects. The signaling pathway NF-kB is responsible for the induced therapeutic effects, while the AP-1 for the pathological effects. The different signaling pathways of infrared-induced ROS and infrared-induced heat shock ROS were shown to act independently multiplying the influence on each other by increasing the doses of irradiation and/or increasing the temperature. The molecular action mechanisms of solar infrared radiation and heat on human skin are summarized and discussed in detail in the present paper. The critical doses are determined. Protection strategies against infrared-induced skin damage are proposed.

Short-term cold exposure improves antioxidant status and general resistance of animals.

We studied the effect of short-term swimming in cold water (13°C) on parameters of the blood antioxidant system (activities of superoxide dismutase and catalase, concentrations of ceruloplasmin and nonprotein thiols), heme oxygenase activity, and nonprotein thiol level in mouse liver. The test parameters of antioxidant protection increased 1 h after cold exposure and remained high 1 day after treatment. These changes were accompanied by an increase in the adaptive capacity. After swimming in cold water the resistance of animals to another stress factor (administration of epinephrine) was higher compared to controls.

Studies of the blood antioxidant system and oxygen-transporting properties of human erythrocytes during 105-day isolation

Effects of strict 105-day isolation on the blood antioxidant status, processes in erythrocyte membranes, and oxygen-binding properties of hemoglobin were studied in six male volunteers (25 to 40 years old) in ground-based simulation of a mission to Mars (Mars-105 experiment). The study was performed with venous blood samples and red blood cells isolated from them, which were collected during the baseline data collection period, on days 35, 70, and 105 of the experiment, and on days 7 and 14–15 after its completion. Biochemical (determination of enzyme activity and thin-layer chromatography) and biophysical (laser interference microscopy and Raman spectroscopy) methods showed changes in the relative content of lipid and phospholipid fractions, suggesting an increase in the membrane microviscosity and the content of TBA-RP (active lipid peroxidation products interacting with thiobarbituric acid). A significant increase in the activity of glucose-6-phosphate dehydrogenase and superoxide dismutase and a reduction in the catalase activity was found, which indicates both reparative processes in red blood cells and imbalance between the amount of generated reactive oxygen species and antioxidant protection mechanisms in cells. The hemoglobin affinity for oxygen and the blood level of oxyhemoglobin also increased. It is assumed that the adaptation of the body to stresses experienced during and after the experiment can disturb the balance between the antioxidant defense systems. The latter, in turn, leads to peroxidation of membrane phospholipids, alteration in their content, increase in membrane microviscosity, and eventual disturbance of the gas-exchange function of red blood cells.

Changes in plasma membrane viscosity and hemoporphyrin conformation in erythrocyte hemoglobin under the conditions of ischemia and reperfusion of rat brain.

Hypoxia of various origin and localization is accompanied by changes in some physical and chemical properties of erythrocytes: deformability, plasma membrane viscosity, and the oxygen-binding capacity of hemoglobin [1, 4‐6]. Under the conditions of brain ischemia, these properties are studied insufficiently. After postischemic reperfusion (PIR) that restores blood circulation, the oxygen partial pressure in plasma increases, which may stimulate the generation of reactive oxygen species (ROS) and affect the erythrocyte functions. In blood plasma, Cu,Zn-superoxide dismutase (SOD) and ceruloplasmin (CP) are involved in utilization of superoxide anion radical ( ) that triggers ROS formation. In this study, changes in the viscosity of erythrocyte plasma membrane and the e 2 -binding ability of hemoporphyrin of deoxyhemoglobin were studied. SOD activity and CP level were also measured in blood plasma of rats with brain ischemia before and after brain PIR. White outbred male rats weighing 272 ± 11 g were used in experiments. The animals were divided into three groups: the sham-operated rats (the control) ( n = 10), the rats with brain ischemia ( n = 10), and the rats with postischemic brain reperfusion ( n = 7). One day before the experiment, both carotids of the anesthetized animals were underpinned with a fishing line (0.3 mm) that was later withdrawn under skin through the polyethylene tubes into the interscapular region. After one day, a one-stage complete occlusion of both carotids was induced by carotid retraction into the tubes by means of the fishing line; subsequent release of carotids led to PIR. Blood samples (3 ml of blood mixed with heparin, 10 U/ml) were taken from the jugular veins of

Effect of middle-wave ultraviolet irradiation and red light on degranulation of peritoneal mast cell in rats.

Middle-wave UV-irradiation inhibits liberator-induced histamine release from mast cells. Red light stimulated liberator-induced degranulation of mast cell. The existence of a membrane-dependent system activated by long-wave (red) light in mammalian cells is discussed.

Protective effect of carnosine in hyperthermia

Under the conditions of hyperthermia, carnosine (β-alanine-l-histidine) normalizes tissue contents of lipid peroxidation products, cytochrome P-450, serotonin, and histamine in rats and increases their survival after extreme hyperthermia.

Effects of Cold Stress and Epinephrine on Degranulation of Peritoneal Mast Cells in Rats

We studied the effects of histamine liberators calcium ionophore A23187 and substance 48/80 on mast cells during cold stress and epinephrine load. Under the effect of both stress factors, ionophore A23187-induced histamine release from mast cells underwent more pronounced changes than that stimulated by substance 48/80. Cold stress and epinephrine load produce different changes in functional activity of Ca2+ channels in mast cell membranes.

Effect of ultraviolet B irradiation on immobilization stress-induced changes in the protective systems of C57Bl/6 mice.

We studied the effect of ultraviolet B irradiation on superoxide dismutase activity, ceruloplasmin level in the plasma, and steroid hormone concentration in the adrenal glands of C57Bl/6 mice subjected to immobilization stress. Ultraviolet B irradiation did not abolish the increase in superoxide dismutase activity, but decreased ceruloplasmin level in the plasma and corticosteroid concentration in the adrenal glands of mice exposed to immobilization stress.

Tissue-Specific Changes in Heme Oxygenase Activity and Level of Nonprotein Thiols in C57Bl/6 Mice after Whole-Body γ-Irradiation

Heme oxygenase catalyzes heme degradation and is an important component of the antioxidant defense. Nonprotein thiols participate in redox regulation of heme oxygenase gene expression. Changes in heme oxygenase activity and levels of nonprotein thiols in the liver, lungs, and brain of C57Bl/6 mice were studied on days 1–7 after whole-body γ-irradiation in a dose of 10 Gy. The maximum increase in heme oxygenase activity was observed in the liver (to 196% in females and to 250% in males) and was associated with an 8-fold increase in the level of heme oxygenase-1 (inducible form of the enzyme) mRNA. The increase in heme oxygenase activity was less pronounced in the lungs, while in the brain this parameter slightly decreased. Changes in the levels of nonprotein thiols were sex-dependent: in the liver and lungs this parameter increased in females and decreased in males.

Effect of X-ray irradiation on activity of key enzymes of heme synthesis and degradation in rat liver

: A modified method has been elaborated for induction of delayed type hypersensitivity (DH) in CBA mice with the use of Evans blue (EB) as adjuvant. This model permitted studying the mechanism of DH development, establishing the dependence of DH on the dose of EB, the dose and type of protein antigen, and realizing passive transfer of DH with the aid of splenocytes from active-synthesized mice. EB is a convenient and effective adjuvant for induction and study of the mechanism of DH development.