The effect of experimental hyperoxia on erythrocytes’ oxygen-transport function

The aim of this study was to investigate the effect of hyperoxia, calcium ions and pH value on the composition of major phospholipids in human erythrocyte membranes and erythrocytes’ oxygen-transport function. To create a model of hyperoxia, we saturated the incubated mixture with oxygen by constant passing of oxygen–air mixture through the incubation medium. To assess the effect of elevated calcium ion concentrations, CaCl2 was added to the incubation medium. An incubation medium with different pH was used to study the effect of various pH values. Lipids were extracted from erythrocytes and chromatographic separation was carried out in a thin layer of silica gel deposited on a glass plate. The thiobarbituric acid (TBA)-active products and the content of diene conjugates (DC) in erythrocytes were determined. The oxygen-binding capacity of haemoglobin was evaluated using Raman spectroscopy. The obtained results indicated that hyperoxia causes deep changes both in the composition and character of bilayer lipids of erythrocyte membranes, which affects the functional characteristics of erythrocytes, primarily the oxygen-transport properties of erythrocyte haemoglobin. It should be noted that a combination of Ca2+ ions and change in the pH value intensify the processes associated with disruption of phospholipids’ composition. The findings indicate that the lipid phase is one of the key elements in the functioning of erythrocytes in norm as well as during development of various pathological processes

Do Statins Influence the Activity of c-fos Gene Following Transient Forebrain Ischaemia in the Adult Rat Hippocampus?

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been associated with stroke prevention. This stroke prevention appears to occur apart from cholesterol lowering effects. A number of mechanisms have been postulated for this prevention. The aim of our study was to investigate the effect of simvastatin on the c-fos gene activity and its relation to delayed neuronal death in CA1 region of hippocampus following transient forebrain ischemia in the adult rat hippocampus. A total of 17 male Wistar albino rats were used in this study. The animals were divided into three groups: 5 sham-operated animals; 6 ischemised rats without statin pre-treatment and 6 ischemised rats with statin pre-treatment. We used simvastatin at the dose of 20 mg/kg during 14 days prior to the ischemic attack. Fifteen min long transient forebrain ischemia was induced by the four-vessel occlusion. Two and a half h reperfusion was used for the c-Fos activity detection using immunostaining and 72 h reperfusion was used for the determination of neurons surviving using haematoxylin/eosin staining. The average neuronal density in the CA1 region of hippocampus in the sham-operated rats, in ischemised rats without pre-treatment and in ischemised rats with statin pre-treatment was 47.03 ± 3.09/0,025 mm2, 9.05 ± 2.46/0,025 mm2 and 16.45 ± 2.78/025 mm2, respectively. A significant neuroprotective effect was observed in the pre-treated ischemic group (P 2, 28.2 ± 2.053/025 mm2, 30.3 ± 4.816/025 mm2, respectively. A highly significant difference in c-Fos positivity (P P > 0.05). These findings indicate that simvastatin provides protection against CA1 hypoxic neuronal injury, which is independent of c-fos activation. We can conclude that simvastatin neuroprotection may be mediated by multiple mechanisms as can be expected based on its pleiotropic effects