Non-Conjugated Copoly(Arylene Ether Ketone) for the Current-Collecting System of a Solar Cell with Indium Tin Oxide Electrode.

The mechanism of charge carrier transport in the indium tin oxide (ITO)/polymer/Cu structure is studied, where thin films of copoly(arylene ether ketone) with cardo fluorene moieties are used. This copoly(arylene ether ketone) is non-conjugated polymer which has the properties of electronic switching from the insulating to the highly conductive state. The dependence on the polymer film thickness of such parameters as the potential barrier at the ITO/polymer interface, the concentration of charge carriers, and their mobility in the polymer is studied for the first time. The study of this system is of interest due to the proven potential of using the synthesized polymer in the contact system of a silicon solar cell with an ITO top layer. The parameters of charge carriers and ITO/polymer barrier are evaluated based on the analysis of current-voltage characteristics of ITO/polymer/Cu structure within the injection current models and the Schottky model. The thickness of the polymer layer varies from 50 nm to 2.1 µm. The concentration of intrinsic charge carriers increases when decreasing the polymer film thickness. The charge carrier mobility depends irregularly on the thickness, showing a maximum of 9.3 × 10-4 cm2/V s at 210 nm and a minimum of 4.7 × 10-11 cm2/V s at 50 nm. The conductivity of polymer films first increases with a decrease in thickness from 2.1 µm to 210 nm, but then begins to decrease upon transition to the globular structure of the films at smaller thicknesses. The dependence of the barrier height on polymer thickness has a minimum of 0.28 eV for films 100-210 nm thick. The influence of the supramolecular structure and surface charge field of thin polymer films on the transport of charge carriers is discussed.

(+)-Catechin Stereoisomer and Gallate Induce Oxidative Stress in Rat Aorta.

The goal of the work was to study changes in the activity of the angiotensin-converting enzyme (ACE) and production of reactive oxygen species (ROS) in the aorta of rats after the intraperitoneal injection of stereoisomers of catechin and gallate. The activity of ACE in the aorta sections was determined by measuring the hydrolysis of hippuryl-l-histidyl-l-leucine. The production of ROS in the aorta sections was estimated from the oxidation of dichlorodihydrofluorescein. The time and dose dependences of the effect of catechin stereoisomers and gallate on ACE activity and ROS production in the aorta were studied. It was shown that (+)-catechin and gallate increased the ACE activity and ROS production, and (-)-catechin and (-)-epicatechin did not influence these parameters. The doses of (+)-catechin and gallate that increased the ACE activity to a half-maximal value (AD50) were 0.04 and 0.03 µg/kg, respectively. Fucoidin, a blocker of leukocyte adhesion to the endothelium, reduced the ACE activity to the control level in the aortas of (+)-catechin-treated rats.

Black tea is more effective than green tea in prevention of radiation-induced oxidative stress in the aorta of rats.

In the work, the effect of black tea on oxidative stress induced in the aorta by irradiation was studied. The efficiency of black and green tea types was compared, and the effect of the main green tea components (-)-epigallocatechin galate (EGCG) and (-)-epigallocatechin (EGC) on the aorta was studied. The activity of ACE in rat aorta segments was determined by measuring the hydrolysis of hippuryl-L-histidyl-L-leucine, and the production of ROS was estimated from the oxidation of dichlorodihydrofluorescein. Black tea prevented the radiation-induced activation of the ACE and suppressed increased ROS production in the aorta of irradiated rats. The IC50 value for the suppression of the irradiation-induced increase in ACE activity is 1 ml of black tea brewed at a rate of 0.17 g/100 ml. Black tea is 12 times more effective than green tea. The administration of both catechin derivatives from green tea to rats leads to an increase in the activity of ACE and the formation of ROS in the aorta. The dose that provided half maximum activation of ACE (EC50) on intraperitoneal (i. p.) injection of galloylated catechins was found to be the same, 0.06-0.07 µg/kg of body weight. Upon intragastric gavage of EGCG, the EC50 value was by one order of magnitude higher, 0.8 µg/kg. Black tea was more effective than green tea in prevention a radiation-induced increase of ACE activity and oxidative stress in the aorta. This difference was explained by a low content of galloylated catechins in black tea.

Radiation-Induced Transient Currents in Films of Poly(arylene ether ketone) Including Phthalide Moiety.

The electrical properties of thin films of poly(arylene ether ketone) copolymers (co-PAEKs) with a fraction of phthalide-containing units of 3, 5, and 50 mol% in the main chain were investigated by using radiation-induced conductivity (RIC) measurements. Transient current signals and current-voltage (I-V) characteristics were obtained by exposing 20 ÷ 25 µm thick films of the co-PAEKs to monoenergetic electron pulses with energy ranging from 3 to 50 keV in an electric field ranging from 5 to 40 V/µm. The Rose-Fowler-Vaisberg semi-empirical model based on a multiple trapping formalism was used for an analysis of the RIC data, and the parameters of the highly dispersive charge carrier transport were evaluated. The analysis revealed that charge carriers moved in isolation from each other, and the applied electric fields were below the threshold field triggering the switching effect (a reversible high-to-low resistivity transition) in the co-PAEK films. It was also found that the co-PAEK films, due to the super-linear I-V characteristics, are highly resistant to electrostatic discharges arising from the effects of ionizing radiation. This property is important for the development of protective coatings for electronic devices.

Flavonoids decrease the radiation-induced increase in the activity of the angiotensin-converting enzyme in rat aorta.

The basic factor of cardiovascular diseases is atherosclerosis, which is due largely to an increase in the activity of the angiotensin-converting enzyme (ACE) in vessels. Flavonoids diminish the risk of cardiovascular diseases and the flavonoid taxifolin normalizes the activity of ACE. We examined the efficiency of seven flavonoids in preventing an increase in ACE activity in aorta of rats exposed to ionizing radiation. It was shown that the activity of flavones and flavonols decreases with an increase in the number of OH groups in the A and B rings, respectively. The reduction in the activity of flavonoids within the classes correlates with a decrease in their lipophilicity. Flavanonols (taxifolin) are more active than flavonols, and flavonols are more active than flavones.

Effects of taxifolin on the activity of angiotensin-converting enzyme and reactive oxygen and nitrogen species in the aorta of aging rats and rats treated with the nitric oxide synthase inhibitor and dexamethasone.

The action of taxifolin on the angiotensin-converting enzyme (ACE) and the formation of reactive oxygen and nitrogen species (ROS/RNS) in the aorta of aging rats and rats treated with nitric oxide synthase inhibitor (N ω-nitro-L-arginine methyl ester (L-NAME)) or dexamethasone have been studied. The ACE activity in aorta sections was determined by measuring the hydrolysis of hippuryl-L-histidyl-L-leucine, and the ROS/RNS production was measured by oxidation of dichlorodihydrofluorescein. It was shown that taxifolin at a dose of 30-100 µg/kg/day decreases the ACE activity in the aorta of aging rats and of rats treated with L-NAME or dexamethasone to the level of the ACE activity in young control rats. Taxifolin (100 µg/kg/day) was found to also reduce the amount of ROS/RNS in the aorta that increased as a result of L-NAME intake. L-NAME treatment increases the contribution of 5-lipoxygenase and NADPH oxidase to ROS/RNS production in the aorta, while taxifolin (100 µg/kg/day) decreases the contribution of these enzymes to the normal level.

Distribution of the activity of the angiotensin-converting enzyme in the rat aorta and changes in the activity with aging and by the action of L-NAME.

The activity of the angiotensin-converting enzyme (ACE) of the inner surface (the endothelium surface) of rat aorta sections has been studied depending on their distance from the aortic arch, age of rats, and the duration of treatment of rats with the NO synthase inhibitor, N (ω)-nitro-L-arginine (L-NAME). The activity of ACE of aorta sections was determined by measuring the hydrolysis of hippuryl-L-histidyl-L-leucine and was expressed as picomoles of Hip-His-Leu hydrolyzed per minute per square millimeter of the endothelium surface. It was found that the ACE activity considerably varies along the aorta of young rats. This variability decreases with increasing age of rats and by the action of L-NAME. The average ACE activity in the aorta increases with the age of rats and with increasing time of L-NAME treatment. Enalapril normalizes the distribution of the ACE activity along the aorta and decreases the average ACE activity. The changes in the distribution of the ACE activity along the aorta and in the average ACE activity in the aorta with increasing age of the rat and by the action of L-NAME may play a role in the development of atherosclerosis of vessels on aging and the inhibition of formation of nitric oxide.

Low doses of ethanol decrease the activity of the angiotensin-converting enzyme in the aorta of aging rats and rats treated with a nitric oxide synthase inhibitor and dexamethasone.

In the present study, the activity of ACE (angiotensin-converting enzyme) in the aorta of senescent rats and rats treated with the NOS (NO synthase) inhibitor L-NAME (NG-nitro-L-arginine methyl ester) or dexamethasone and the effect of low doses of ethanol (0.2-1.2 g/kg of body weight, daily for 8-12 days) on this activity were studied. We found that ACE activity increased with age and in response to L-NAME and dexamethasone treatment. Ethanol at a dose of 0.4 g/kg of body weight per day decreased ACE activity in the aorta of aged rats and of rats treated with L-NAME or dexamethasone to the level of activity in young control rats. The optimal ethanol dose (the dose inducing a maximum decrease in ACE activity) increased with increasing doses of dexamethasone: 0.4 g/kg of body weight per day at 30 µg of dexamethasone/kg of body weight and 0.8 g/kg of body weight per day at 100 µg of dexamethasone/kg of body weight. It was also found that optimal doses of ethanol increased the number of cells in the thymus of rats treated with dexamethasone. The optimal dose of ethanol of 0.4 g/kg of body weight per day, which induced a maximum decrease in ACE activity in rat aorta, corresponded to a dose of 30 g of ethanol/day, which, according to epidemiological data, produces a maximum decrease in the incidence of cardiovascular disease in humans. In conclusion, the decrease in ACE activity in vessels may be one of the main mechanisms of the beneficial effects of low doses of ethanol on human health.

Determination of reactive oxygen and nitrogen species in rat aorta using the dichlorofluorescein assay.

A method for the determination of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in macroscopic sections of vessels has been developed on the basis of the dichlorofluorescein (DCF) assay. DCF was measured by fluorescence in extracts of vessels. The main artifact of the method is the oxidation of dichlorodihydrofluorescein (DCFH(2)) which is released from vessels together with DCF during the extraction procedure. This problem was resolved by decreasing pH during the extraction. The optimal conditions and the time for aorta incubation with DCFH(2)-DA and for the extraction of DCF from aorta have been determined. The ROS/RNS production in different aorta segments and the dependence of ROS/RNS production on rat age have been studied. It was shown that thoracic aorta sections produced the same amounts of ROS/RNS and the intermediate between the thoracic and the abdominal aorta part produced ROS and RNS by 14% more than the thoracic aorta. It was found that ROS/RNS production in aorta increases with rat age: the doubling time of ROS/RNS production rate is 113 days from birth.

Modification of multidrug resistance of tumor cells by ionizing radiation.

PURPOSE: The effect of ionizing radiation on multidrug resistance (MDR) of human larynx cancer HEp-2 cells has been investigated. We studied the dependence of the radiation effect on radiation dose, time after irradiation and cell density. METHODS: MDR was determined from an increase in cell sensitivity to daunorubicin, taxol and vincristine by the inhibitors of multidrug resistance cyclosporin A and avermectin B(1), and from the suppression by cyclosporin A of the transport of rhodamine 123 out of the cells. The cells were irradiated with X-ray beams (dose rate 1.12 Gy min(-1)) at room temperature. RESULTS: It was shown that, at 8 and 16 h after irradiation with doses up to 4 Gy, the multidrug resistance of cells increases, and at 24 h it decreases to the control level. The effect was maximal by 16 h after irradiation with a dose of 1 Gy. Both, the contribution of active transport to the rate of rhodamine 123 efflux from cells and their resistance to vincristine, increased. The effect of irradiation on multidrug resistance of HEp-2 cells depended on the density of cells on the substrate, being maximal at a density of 80,000-100,000 cm(-2). CONCLUSION: The irradiation-induced changes in the MDR of tumor cells should be taken into account when combining radiotherapy with chemotherapy. It was assumed that the dependence of multidrug resistance of HEp-2 cells on radiation dose and cell density is determined by changes in the amount of reactive oxygen species in the cells.

Detection of reactive oxygen species induced by radiation in cells using the dichlorofluorescein assay.

The goal of this study was to determine the amount of reactive oxygen species (ROS) that arises inside cells irradiated in medium containing blood serum using the 2'7'-dichlorofluorescein (DCF) assay. DCF fluorescence in cells and medium was recorded on an MF44 Perkin Elmer fluorimeter, and fluorescence in cells only was recorded on a Partec flow-through cytometer. Human larynx tumor HEp-2 cells and lympholeukosis P388 cells were irradiated with X rays at a dose rate of 1.12 Gy/min. The factors (temperature, pH, serum concentration) affecting the oxidation of 2'7'-dichlorofluorescin (DCFH) to DCF were studied, and errors in the dichlorofluorescein assay of ROS were minimized. The amount of ROS registered by the DCF assay in cells was found to depend on the concentration of serum in the medium during irradiation. In the presence of 10% serum, radiation had no effect on the amount of detectable ROS. The effect of radiation on the formation of intracellular ROS was almost completely abolished if the irradiated medium was removed immediately after radiation exposure. The increase in the formation of ROS in cells irradiated in medium with a low serum content is due mainly to the radiolytic products of water that arise in medium and oxidize DCFH located in cells.

Antitumor effect of avermectins.

The effect of a mixture of naturally occurring aversectin C and avermectin B(1) on the growth of ascites and solid experimental tumors of mice was studied. It was shown for the first time that avermectins possess a pronounced antitumor action. When added at nontoxic doses, they significantly suppressed the growth of ascites Ehrlich carcinoma and P388 lympholeukemia and solid Ehrlich and 755 carcinomata. With some administration regimens, avermectins suppressed the tumor growth by 70-80%. Avermectins were most effective when injected intraperitoneally. It was also shown that avermectins enhanced the vincristine-induced suppression of the growth of Ehrlich carcinoma, melanoma B16, and P388 lympholeukemia. Avermectins produced this effect only when injected after vincristine.

Avermectins inhibit multidrug resistance of tumor cells.

The modification of the sensitivity of Hep-2 and P388 tumor cells to taxol and vincristine, substrates of multidrug resistance proteins, by naturally occurring avermectins and the effect of avermectins on the accumulation of calcein in cells and the efflux of rhodamine 123 were studied. While avermectins did not affect the sensitivity of tumor cells to hydrogen peroxide and cisplatin, they significantly enhanced the sensitivity of cells of both wild-type and resistant strains to taxol and vincristine. The coefficients of modification for resistant strains were substantially higher. Avermectins suppressed the efflux of rhodamine 123 from cells and increased the accumulation of calcein in cells. The relative inhibitory activity of avermectins depended on the cell type and on the substrate of multidrug resistance proteins whose transport they suppressed (vincristine, taxol, rhodamine 123, calcein acetoxymethyl ester). The least active was avermectin B1 or ivermectin; the most active avermectins varied depending on the substrate and the cell type. In the case of vincristine transport, the most active avermectin was almost by one order of magnitude more effective than the traditional inhibitor of multidrug resistance cyclosporin A. This property of avermectins can be used in tumor therapy by combining application of avermectins with antitumor preparations, the substrates of multidrug resistance proteins.