Effect of combined treatment with perindoprilat and low-power red light laser irradiation on human erythrocyte membrane fluidity, membrane potential and acetylcholinesterase activity.

Erythrocyte membrane fluidity, membrane potential and acetylcholinesterase activity were estimated after in vitro combined treatment of human erythrocytes with perindoprilat and low-power red light irradiation. Membrane fluidity was determined using fluorescent labels spectroscopy; membrane potential was evaluated by means of potential-sensitive fluorescent dyes; and acetylcholinesterase activity was estimated using the Ellman method. Both perindoprilat and laser irradiation, when used separately, increase microviscosity in the polar region and hyperpolarize the membranes in comparison with control erythrocytes.

Interaction of perindoprilat with human red blood cells.

The effects of perindoprilat on the morphology and dynamic properties of human erythrocytes were studied by light microscopy, electron spin resonance spectroscopy and spectrophotometric methods. Erythrocytes were exposed to perindoprilat at 37 degrees C for 30 and 120 min. It was shown that the drug at a concentration of 0.

Effect of low-power red light laser irradiation on the viability of human skin fibroblast.

Human skin fibroblast monolayers (S-126 cell line) were exposed to laser radiation (wavelength 670 nm, power density 40 mW/cm2). The energy densities were 2 J/cm2 and 12 J/cm2, respectively, and the irradiation was carried out at a temperature of 22 degrees C. For fibroblast viability evaluation, the colorimetric assay (conversion of thiazolyl blue to formazan) was used.

Effect of perindopril therapy on fluidity and potential of erythrocyte membrane from individuals with coronary heart disease.

Erythrocyte membrane fluidity and membrane potential were measured in patients suffering from coronary heart disease (CHD) and treated with perindopril. Membrane fluidity was determined using electron paramagnetic resonance (EPR) spectroscopy, and membrane potential was evaluated using potential-sensitive fluorescent dyes. CHD does not change membrane fluidity at the depth of the 5 carbon in the fatty acid chain of membrane phospholipids.

Role of membrane components in thermal injury of cells and development of thermotolerance.

Exposure of cells to hyperthermia induces a transient resistance to subsequent heat treatment. The specific mechanisms responsible for hyperthermic cell killing and thermotolerance development are not well understood. It seems that heat may induce at least two different states of thermotolerance, of which one is dependent on protein synthesis.