The dissociation of (a+c) misfit dislocations at the InGaN/GaN interface.

In hexagonal materials, (a+c) dislocations are typically observed to dissociate into partial dislocations. Edge (a+c) dislocations are introduced into (0001) nitride semiconductor layers by the process of plastic relaxation. As there is an increasing interest in obtaining relaxed InGaN buffer layers for the deposition of high In content structures, the study of the dissociation mechanism of misfit (a+c) dislocations laying at the InGaN/GaN interface is then crucial for understanding their nucleation and glide mechanisms. In the case of the presented plastically relaxed InGaN layers deposited on GaN substrates, we observe a trigonal network of (a+c) dislocations extending at the interface with a rotation of 3° from <1 1 ¯ $\bar 1$ 00> directions. High-resolution microscopy studies show that these dislocations are dissociated into two Frank-Shockley 1/6<2 2 ¯ $\bar 2$ 03> partial dislocations with the I1 BSF spreading between them. Atomistic simulations of a dissociated edge (a+c) dislocation revealed a 3/5-atom ring structure for the cores of both partial dislocations. The observed separation between two partial dislocations must result from the climb of at least one of the dislocations during the dissociation process, possibly induced by the mismatch stress in the InGaN layer.

New light on the photocatalytic performance of NH4V4O10 and its composite with rGO.

Solar-driven photocatalysis has shown great potential as a sustainable wastewater treatment technology that utilizes clean solar energy for pollutant degradation. Consequently, much attention is being paid to the development of new, efficient and low-cost photocatalyst materials. In this study, we report the photocatalytic activity of NH4V4O10 (NVO) and its composite with rGO (NVO/rGO). Samples were synthesized via a facile one-pot hydrothermal method and successfully characterized using XRD, FTIR, Raman, XPS, XAS, TG-MS, SEM, TEM, N2 adsorption, PL and UV‒vis DRS. The results indicate that the obtained NVO and NVO/rGO photocatalysts exhibited efficient absorption in the visible wavelength region, a high content of V4+ surface species and a well-developed surface area. Such features resulted in excellent performance in methylene blue photodegradation under simulated solar light illumination. In addition, the composite of NH4V4O10 with rGO accelerates the photooxidation of the dye and is beneficial for photocatalyst reusability. Moreover, it was shown that the NVO/rGO composite can be successfully used not only for the photooxidation of organic pollution but also for the photoreduction of inorganic pollutants such as Cr(VI). Finally, an active species trapping experiment was conducted, and the photodegradation mechanism was discussed.

Study of the genotoxic potential of iron ions by the SOS chromotest.

Modulation of iron ions induced SOS response by scavengers of reactive oxygen species was studied in SOS chromotest in three strains of Escherichia coli (PQ37, PQ300 and OG400). Iron ions in the absence of reductants induced SOS response generated by reactive oxygen species in a dose dependent manner and this was inhibited in the presence of catalase.

Effects of iron and copper ions on the inducibility of hydrogen peroxide in E. coli.

Inducing capacities of hydrogen peroxide in SOS chromotest were investigated in the absence and in the presence of iron and copper ions. Strain PQ37 of Escherichia coli and two strains with altered protection against oxidative damage (PQ300 and OG400) were employed. The latter two strains were more sensitive to the hydrogen peroxide inducing activity than strain PQ37. At the concentration of 150 nmol/ml and 300 nmol/ml, iron ions induced SOS response. At the concentration range from 30 nmol/ml to 300 nmol/ml iron enhanced the effects produced by H2O2. Results with copper were negative.

Influence of ascorbic acid on cytotoxic activity of copper and iron ions in vitro.

We investigated survival of two kinds of human embryonic cells (CLV102, Lu106) and human melanoma cells (Mel8) exposed to exogenous iron and copper ions in the absence or in the presence of ascorbic acid, catalase and superoxide dismutase. Iron ions produced cytotoxicity towards both kinds of cells dependent on its concentration. Catalase suppressed the cytotoxicity induced by iron ions in Lu106 cells. whereas in CLV102 and Mel8 cells, was ineffective. By contrast, superoxide dismutase abolished the cytotoxicity of iron ions towards CLV102 cells, whereas in Lu106 and Mel8 cells, was ineffective. The mixture of iron ions with ascorbic acid was less cytotoxic than iron ions themselves or ascorbic acid itself, only in CLV102 and Lu106 cells. Ascorbic acid enhanced drastically cytotoxic effect of copper ions in all kinds of cells.

Adaptive response towards adriamycin in vitro: circumvention with verapamil.

In an attempt to identify mechanisms of adaptive response to adriamycin (ADR), we have earlier isolated ADR-resistant cell lines CHO/R and ME18/R by short-term pulse exposures of parent cell lines to this drug, followed by single-cell cloning. The results presented in this study have shown that the development of resistance to ADR was accompanied by cross-resistance to vinblastine and methotrexate. The resistance of tested cell lines towards ADR was substantially reversed by verapamil (VPL) at non-toxic concentrations. VPL abolished also the capability of these cell lines to express adaptive response after treatment of the cells with a conditioning dose of ADR. From the results of our study, we conclude that similar characteristics play a role in the mechanism of the phenomenon of adaptive response as in the mechanism of pleiotropic multidrug resistance.

Capability of adriamycin and busulfan to induce adaptive response in vitro.

The capability to induce an adaptive response by low doses of busulfan (BS) or adriamycin (ADR) was studied in two kinds of mammalian cells with acquired or inherent resistance to ADR (ME18/R and V3) cultured in vitro. The results indicate the presence of an adaptive response to ADR in both kinds of used cells pretreated with a low priming dose of ADR. In the same kind of cells no adaptive response to BS after priming with a low dose of this drug was found.

Studies on the nature of cytotoxic effects induced by dihydralazine.

The effects of scavengers on the cytotoxicity of dihydralazine were evaluated. Pretreatment of two kinds of mammalian cells cultured in vitro with catalase or sodium dismutase abolished partially or almost totally the effects of the drug. Hydroxyl radicals scavengers dimethylsulphoxide and D-mannitol minimized the cytotoxic response of both kinds of cells.

Studies on adaptation to adriamycin in cells pretreated with hydrogen peroxide.

Various investigations have reported the occurrence in bacterial and mammalian cells of an adaptive response to the toxic effects of oxidants or agents that cause oxidation via redox reactions. In our previous study, it was shown that several cell lines pretreated with a low dose of hydrogen peroxide (H2O2) exhibited an adaptive response to subsequent high doses of adriamycin (ADR), whereas other cell lines did not. Based on the observation that the cell lines utilized differed in their sensitivity towards adriamycin, we undertook the present investigation with the goal of evaluating possible relationships between the levels of antioxidant enzymes and sensitivity towards adriamycin. Another aim was to determine relationships between the inducibility of these enzymes and the occurrence of adaptation. We utilized African Green monkey kidney (V3), human embryo (CLV98), human melanoma (ME18), and Chinese hamster ovary (CHO) cell lines and experimentally developed adriamycin-resistant human melanoma (ME18/RN) and Chinese hamster ovary (CHO/RN) cell sublines. Cytotoxicity was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and trypan blue exclusion. The levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were determined in the same kind of experiment as that revealing the occurrence of adaptation. The rank order established for catalase activities was similar to that for sensitivity towards adriamycin. Aberrant increases in the tested enzymes were demonstrated in experimental groups of all kinds of cells. We conclude that in our cell systems catalase is a major determinant of adriamycin resistance. Whether the occurrence of the adaptive response under study is dependent on the contribution of catalase, itself dependent on the degree of resistance to the drug, is discussed.

Studies on the nature of genotoxic and cytotoxic effects induced by hydralazine.

The nature of genotoxic and cytotoxic effects induced by hydralazine was analyzed taking into account possible protection of cells by catalase, superoxide dismutase and dimethyl sulfoxide. For the experiments designed to evaluate the influence of scavengers on the genotoxicity expressed as the SOS induction factor the E. coli PQ37 strain was used. The cytotoxic effects were investigated in V3 cells cultured in vitro. The genotoxicity and cytotoxicity of hydralazine were suppressed by catalase in a dose-dependent manner but they were enhanced by superoxide dismutase. No protective effect of dimethyl sulfoxide was observed. Our results indicate that H2O2 plays an essential role in the genotoxicity and cytotoxicity of hydralazine.

Comparison of the induction of SOS repair in Escherichia coli PQ37 and PQ243 by antineoplastic agents.

Six alkylating antineoplastic drugs (Cyclophosphamide, Chlorambacil, Busulfan, Melphalan. Streptozotocin and Lomustine) and two reference compounds (methyl methanesulphonate and N-methyl-N'-nitro-N-nitrosoguanidine) were investigated in the SOS Chromotest using the Escherichia coli strain PQ37 (wilde-type) and derived strain (PQ243), which carries the same markers as PQ37 and additionally tagA alkA. As a measure of the SOS induced activity induction factors of sflA::lacZ expression were determined. The strain PQ243 was more sensitive towards all compounds inducing SOS DNA repair then the strain PQ37 Cyclophosphamide was detected as negative in the strain PQ243 in the presence of an exogenous metabolic activation system. Lomustine was inactive both in the mutant strain and in the wild-type strain in the presence of S9 mix fraction as well as in the absence of it. Melphalan and Busulfan (without or with S9 mix) were shown to be positive exclusively in the strain PQ243. Based on these results, we discuss the usefulness of the strain PQ243 in the monitoring of the genotoxicity of drugs and in the genetic analysis of their mode of action.

Protective role of reactive oxygen species scavengers against toxicity of 3-chloropyridine and 2-chloropyridine N-oxide.

The nature of biological effects of substituted pyridines and their N-oxides is a matter for discussion. Our previous study demostrated that 3-chloropyridine is cytotoxic and clastogenic. No cytotoxic activity was observed with 2-chloropyridine tested in the same dose range. In this study experiments were performed to assess cytotoxicity and clastogenicity of 2-chloropyridine N-oxide and 3-chloropyridine N-oxide. In the dose range from 800 to 3200 mug 2-chloropyridine/ml, N-oxide showed a dose-dependent cytotoxicity and clastogenicity. In the same dose range, 3-chloropyridine N-oxide was found to be non-cytotoxic and non-clastogenic. The nature of the effects induced by 3-chloropyridine and 2-chloropyridine N-oxide was analysed on the basis of possible protection by scavengers of reactive oxygen species. The cytotoxicity of both compounds was effectively suppressed by catalase and hydroxyl radicals scavengers. Pretreatment of V(3) cells with dimethyl sulfoxide or catalase provided protection against the ability of both compounds to induce chromosomal aberrations. From the data of this study we conclude that cytotoxicity and clastogenicity of 3-chloropyridine and 2-chloropyridine N-oxide are linked to the generation of reactive oxygen species.

Role of pyridine N-oxide in the cytotoxicity and genotoxicity of chloropyridines.

During metabolic processes, substituted pyridines may undergo N-oxidation and decomposition. It is a matter of discussion whether these processes influence the reactivity of this class of compounds. To elucidate this problem, the cytotoxicity and clastogenicity of two selected Chloropyridines on cultured V(3) cells was assessed in the absence and in the presence of pyridine N-oxide. For this purpose two cytotoxicity assays in parallel with chromosomal analysis were performed. In the dose range from 400 to 3200 mug/ml, 3-chloropyridine showed a dose-dependent cytotoxicity and clastogenicity towards V(3) cells, whereas in the same dose range 2-chloropyridine was found to be non-cytotoxic and non-clastogenic. Pyridine N-oxide (200 mug/ml) showed protective effects against 3-chloropyridine-induced cytotoxicity and clastogenicity. Under analogous experimental conditions cytotoxic and clastogenic effects were induced by 2-chloropyridine. From these studies it appears that the expression of toxicity by halogenated pyridines differing in the position of the halogen moiety may be influenced in different ways by the potential metabolite.

Evaluation of potential carcinogenic properties of Tolpa Peat Preparation in vitro.

For the evaluation of the potential carcinogenic properties of TPP the Syrian hamster embryo cell transformation test was employed. TPP did not induce morphological cell transformation in these cells.

The protective role of pyridine N-oxide in cytotoxicity and genotoxicity of hydrogen peroxide and adriamycin.

Scavenging and cytotoxic activity of pyridine N-oxide was investigated in cultured V3 and CHO cells. Pyridine N-oxide was effective in suppressing the cytotoxic effects induced in these systems both by hydrogen peroxide and adriamycin and preventing the production of chromosomal aberrations by these compounds. On the other hand superoxide dismutase inhibited the cytotoxic activity of pyridine N-oxide.

Evaluation of the SOS chromotest for detection of genotoxic drugs.

In the present investigation, the SOS Chromotest with E. coli PQ37 was evaluated. The potential of the test to identify genotoxic properties of different cytostatics was examined. Only intercalating agents showed good activity. The SOS Chromotest appeared to be less effective than the Salmonella mutagenicity test in the detection of alkylating agents.

Evaluation of mutagenic and genotoxic properties of TPP.

For evaluation of mutagenic and genotoxic properties of Tolpa Peat Preparation (TPP) four selected short-term tests were employed. TPP has been found to be neither mutagenic nor genotoxic.