Consequences of Spiraea tomentosa invasion in Uropodina mite (Acari: Mesostigmata) communities in wet meadows.

Vegetation cover has been consistently reported to be a factor influencing soil biota. Massive spreading of invasive plants may transform native plant communities, changing the quality of habitats as a result of modification of soil properties, most often having a directional effect on soil microorganisms and soil fauna. One of the most numerous microarthropods in the litter and soil is Acari. It has been shown that invasive plants usually have a negative effect on mites. We hypothesized that invasive Spiraea tomentosa affects the structure of the Uropodina community and that the abundance and species richness of Uropodina are lower in stands monodominated by S. tomentosa than in wet meadows free of this alien species. The research was carried out in wet meadows, where permanent plots were established in an invaded and uninvaded area of each meadow, soil samples were collected, soil moisture was determined and the mites were extracted. We found that Uropodina mite communities differed in the abundance of individual species but that the abundance and richness of species in their communities were similar. S. tomentosa invasion led primarily to changes in the quality of Uropodina communities, due to an increase in the shares of species from forest and hygrophilous habitats. Our results suggest that alien plant invasion does not always induce directional changes in mite assemblages, and conclude that the impact of an alien species on Uropodina may cause significant changes in the abundance and richness of individual species without causing significant changes in the abundance and diversity of their community.

Novel dithiolethione-modified nonsteroidal anti-inflammatory drugs in human hepatoma HepG2 and colon LS180 cells.

PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAID) are promising chemopreventive agents against colon and other cancers. However, the molecular basis mediated by NSAIDs for chemoprevention has not been fully elucidated. Environmental carcinogens induce DNA mutation and cellular transformation; therefore, we examined the effect of NSAIDs on carcinogenesis mediated by the aryl hydrocarbon receptor signaling pathway. In this study, we investigated the activities of a new class of NSAIDs containing dithiolethione moieties (S-NSAID) on both arms of carcinogenesis. EXPERIMENTAL DESIGN: We investigated the effects of the S-NSAIDs, S-diclofenac and S-sulindac, on carcinogen activation and detoxification mechanisms in human hepatoma HepG2 and human colonic adenocarcinoma LS180 cells. RESULTS: We found that S-diclofenac and S-sulindac inhibited the activity and expression of the carcinogen activating enzymes, cytochromes P-450 (CYP) CYP1A1, CYP1B1, and CYP1A2. Inhibition was mediated by transcriptional regulation of the aryl hydrocarbon receptor (AhR) pathway. The S-NSAIDs down-regulated carcinogen-induced expression of CYP1A1 heterogeneous nuclear RNA, a measure of transcription rate. Both compounds blocked carcinogen-activated AhR from binding to the xenobiotic responsive element as shown by chromatin immunoprecipitation. S-diclofenac and S-sulindac inhibited carcinogen-induced CYP enzyme activity through direct inhibition as well as through decreased transcriptional activation of the AhR. S-sulindac induced expression of several carcinogen detoxification enzymes of the glutathione cycle including glutathione S-transferase A2, glutamate cysteine ligase catalytic subunit, glutamate cysteine ligase modifier subunit, and glutathione reductase. CONCLUSIONS: These results indicate that S-diclofenac and S-sulindac may serve as effective chemoprevention agents by favorably balancing the equation of carcinogen activation and detoxification mechanisms.

Xerophilic Alopecosa sulzeri (Pavesi, 1873) (Araneae: Lycosidae)-a new wolf spider species in Poland.

There are 44 species and subspecies of the genus Alopecosa known in Europe, and 13 of them have so far been listed as occurring in Poland. Alopecosa sulzeri (Pavesi, 1873) is a xero- and thermophilic species distributed in the western Palearctic. In Europe, it occurs primarily in the south-east, while it is rare in Central Europe. Between 2007 and 2013, we recorded the species in the central-eastern, north-western and south-western parts of Poland. The sites of A. sulzeri in Poland are located at the northern limit of the geographic range of the species in Europe. Alopecosa sulzeri was caught at four sites in three regions, exclusively in xerothermic grasslands: in the Podlasie Bug Gorge, the Lower Oder Valley and the Trzebnickie Hills. The sites may be relict, or they may provide evidence of the spread of the species from sites located in neighbouring countries. Further spread of stenotopic, xerophilous A. sulzeri in Poland, if continued, is likely to be a slow process, due to the limited number of suitable habitats.

Nutritional concentration of genistein protects human dermal fibroblasts from oxidative stress-induced collagen biosynthesis inhibition through IGF-I receptor-mediated signaling.

The effects of genistein, a soy isoflavone phytoestrogen and antioxidant, on collagen and DNA biosynthesis (measured by the 5-[3H]proline and the [3H]thymidine incorporation assays), prolidase activity (colorimetric method) and expression (determined by Western immunoblot) of the beta1-integrin receptor, focal adhesion kinase pp125(FAK) (FAK), Src, the insulin-like growth factor-I (IGF-I) receptor, Shc, growth-factor receptor-bound protein 2 (Grb2), son of sevenless protein (Sos) and phosphorylated mitogen activated protein (MAP) kinases, extracellular signal-regulated kinase 1 and 2 (ERK1/ERK2) were examined in normal human dermal fibroblasts (CRL-1474) exposed to oxidative stress. Subconfluent cells were subjected to repetitive stress with 30 microM t-butylhydroperoxide (t-BHP) in combination with 1-100 microM genistein for 1 h per day over the course of 5 days. Also, the cells were treated with t-BHP alone or with t-BHP in combination with 1-100 microM ascorbate. It was found that genistein at 1 microM counteracted the inhibition of collagen biosynthesis evoked by t-BHP in fibroblasts, more effectively than ascorbate at the same concentration. At 10 microM, genistein exerted significantly diminished protective effect on collagen biosynthesis in fibroblasts, while at 100 microM it induced inhibition of this process. The protective effect of genistein on collagen biosynthesis was not related to modulation of prolidase activity or the expression of the beta1-integrin receptor, FAK, Src or Grb2. It was found that genistein, at 1 microM, diminished t-BHP-induced down-regulation of the IGF-I receptor, Shc, Sos and phosphorylated ERK1/ERK2 expression in fibroblasts. Simultaneously, genistein counteracted the antiproliferative activity of the oxidant. These results suggest that the mechanism of the protective effect of genistein on collagen biosynthesis in t-BHP-treated fibroblasts may be due to prevention of disturbances in the IGF-I receptor-mediated, ERK1/ERK2-associated signaling pathway evoked by the oxidant.

ß-diversity decreases with increasing trophic rank in plant - arthropod food chains on lake islands.

Contrasting trophic theories of island biogeography try to link spatial patterns in species distribution and richness with dietary preferences, arguing that the spatial turnover of species among habitat patches changes with trophic rank causing a systematic change in the proportion of plants, herbivores, and predators across habitats of different size. Here we test these predictions using quantitative surveys of plants, spiders, and herbivores as well as of omnivorous and predatory ground beetles on undisturbed Polish lake islands. We found decreased proportions of predators and habitat generalists on larger islands. Environmental niches and niche overlap were highest in predators. Variability in environmental niche width among species increased at higher trophic levels. Our results confirm models that predict a decrease in spatial species turnover (ß-diversity) with increasing trophic level. We speculate that the major trigger for these differences is a reduced dispersal ability in plants at basal trophic ranks when compared to higher trophic levels.

Inhibition of collagen and DNA biosynthesis by a novel amidine analogue of chlorambucil is accompanied by deregulation of ß(1)-integrin and IGF-I receptor signaling in MDA-MB 231 cells.

A novel amidine analogue of chlorambucil N-(2-(4-(4-bis(2-chloroethyl)aminophenyl)butyryl)aminoethyl)-5-(4-amidinophenyl)-2-furanecarboxamide hydrochloride (AB(1)), and the parent drug were compared for their effects on collagen and DNA synthesis in breast cancer MDA-MB 231 cells. IC(50) values for chlorambucil and its amidine analogue for collagen synthesis were found to be about 44 and 19µM, respectively. Increased ability of AB(1) to suppress the protein synthesis, compared to chlorambucil, was found to be related to an inhibition of prolidase activity and expression. The phenomena were probably a result of disruption of ß(1)-integrin and the insulin-like growth factor-I (IGF-I) receptor mediated signaling caused by this compound. Expression of ß(1)-integrin receptor, as well as focal adhesion kinase pp125(FAK) (FAK), growth-factor receptor-bound protein 2 (GRB2), son of sevenless protein 1 (Sos1) and phosphorylated mitogen activated protein kinases (MAPK), extracellular-signal-regulated kinase 1 (ERK(1)) and kinase 2 (ERK(2)) but not Src and Shc proteins was significantly decreased in cells incubated for 24h with 10µM AB(1), compared to controls. Chlorambucil in the same conditions did not evoke any changes in expression of all these signaling proteins, as shown by Western immunoblot analysis. In addition, AB(1) revealed a higher antiproliferative activity than chlorambucil, accompanied by a stronger down-regulation of IGF-I receptor expression. The results were confirmed by [(3)H]thymidine incorporation assay. Incubation of the cells with 10µM AB(1) for 12 and 24h contributed to a decrease in DNA synthesis by about 33 and 46% of the control values, respectively, while in case of chlorambucil by about 23 and 29%, respectively. These data suggest that the amidine analogue of chlorambucil (AB(1)) disturbs MDA-MB 231 cell metabolism more potently than does the parent drug, chlorambucil. The mechanism of this phenomenon may be due to its stronger suppression of ß(1)-integrin and IGF-I receptor signaling.

Amidine analogue of chlorambucil is a stronger inhibitor of protein and DNA synthesis in breast cancer MCF-7 cells than is the parent drug.

A novel amidine analogue of chlorambucil-N-(2-(4-(4-bis(2-chloroethyl)aminophenyl)butyryl)aminoethyl)-5-(4-amidinophenyl)-2-furancarboxamide hydrochloride (AB(1)) and the parent drug were compared for their effects on collagen and DNA biosynthesis in breast cancer MCF-7 cells. IC(50) values for chlorambucil and AB(1) for collagen biosynthesis were found to be about 33 and 13 microM, respectively. The greater potency of AB(1) to suppress collagen synthesis was found to be accompanied by a stronger compared with chlorambucil inhibition of prolidase activity and expression. The phenomenon was related to inhibition of beta(1)-integrin and IGF-I receptor-mediated signaling caused by this compound. The expression of beta(1)-integrin receptor, as well as Src, son of sevenless protein (SOS) and phosphorylated mitogen activated protein (MAP) kinases (MAPK), extracellular-signal-regulated kinase 1 (ERK(1)) and kinase 2 (ERK(2)) but not focal adhesion kinase pp125(FAK) (FAK), Shc, and Grb-2 was significantly decreased in cells incubated for 24 h with 10 microM AB(1) compared to the control, whereas in the same conditions chlorambucil did not evoke any changes in expression of all these signaling proteins, as shown by Western immunoblot analysis. Furthermore, AB(1) induced a stronger down-regulation of the expression of IGF-I receptor and evoked a higher antiproliferative effect. During 12 and 24 h of incubation AB(1) decreased DNA biosynthesis by about 33 % and 51 % of the control, whereas chlorambucil decreased it by about 19 % and 35 %, respectively. These data suggest that the amidine analogue of chlorambucil is a stronger inhibitor of protein and DNA synthesis in MCF-7 cells than is the parent drug.

Erotylidae (Insecta, Coleoptera) of Poland - problematic taxa, updated keys and new records.

New data concerning the occurrence of pleasing fungus beetles (Coleoptera: Erotylidae) in Poland are given, with a focus on rare and difficult to identify Central European taxa. Cryptophilus cf. integer (Heer) (Cryptophilinae) is reported from the Polish territory for the first time based on adult and larval specimens collected in the Wielkopolska-Kujawy Lowland. Identification problems concerning species of Cryptophilus introduced to Europe are discussed. Triplax carpathica Reitter (Erotylinae) is recorded from the Bialowieza Primeval Forest, which is the first known non-Carpathian finding of this species, located in the close proximity of the Polish-Belarussian UNESCO World Heritage Site "Bialowieza Forest". Discussion of Triplax carpathica being conspecific with Siberian Triplax rufiventris Gebler is provided. New Polish localities of several other Erotylidae are reported, and an updated key to Central European species of Triplax is given. The Triplax key is supplemented with dorsal and ventral habitus images of all treated Triplax species. One of the rarest Central European erotyline species Combocerus glaber (Schaller) is recorded from xerothermic grasslands in North-West Poland.

A novel synthetic analogue of a constituent of Isodon excisus inhibits transcription of CYP1A1, -1A2 and -1B1 by preventing activation of the aryl hydrocarbon receptor.

We investigated the effect of a novel synthetic analogue of a constituent from the Chinese medicinal herb Isodon excisus, 3-(3-methoxy-phenyl)-N-(3, 4, 5-trimethoxy-phenyl)-acrylamide (compound 343), on the carcinogen activation pathway mediated by the aryl hydrocarbon receptor (AhR) in human hepatoma HepG2 cells. We found that compound 343 inhibited the upregulation of cytochrome P-450 (CYP) enzyme activity in cells treated with the AhR ligands and potent carcinogens, dimethylbenz[a]anthracene (DMBA) or 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD). Compound 343 also inhibited the DMBA- or TCDD-induced increase in CYP1A1, -1A2 and -1B1 mRNA levels. Carcinogen-induced transcription of CYP genes was also suppressed by compound 343, as measured by a reporter gene controlled by the xenobiotic-responsive element (XRE). This was confirmed by measuring the amount of carcinogen-induced CYP1A1 heterogeneous nuclear RNA. Compound 343 blocked the DMBA- or TCDD-induced activation of the AhR DNA-binding capacity for the XRE, as measured by a chromatin immunoprecipitation assay. Compound 343 also inhibited CYP enzyme activity in microsomes isolated from DMBA- or TCDD-treated cells, as well as the activity of recombinant CYP1A1, -1A2 and -1B1, indicating that compound 343 directly inhibits CYP enzymes. These results indicate that compound 343 is both a potent inhibitor of carcinogen-induced CYP enzyme expression, as well as a direct inhibitor of CYP enzymes.

Differential effects of echistatin and thrombin on collagen production and prolidase activity in human dermal fibroblasts and their possible implication in beta1-integrin-mediated signaling.

Prolidase [E.C. 3.4.13.9] is a cytosolic imidodipeptidase that plays an important role in collagen biosynthesis. The enzyme contributes to the recovery of proline from protein degradation products (mainly collagen) for collagen resynthesis. Prolidase activity and collagen biosynthesis are supposed to be regulated by beta(1)-integrins, which initiate a signaling pathway in which several kinases and intracellular proteins are involved, including focal adhesion kinase pp125(FAK) (FAK), Src, Shc, growth factor receptor bound protein 2 (Grb-2), son of sevenless protein (SOS), Ras, Raf and mitogen-activated protein kinases (MAPK), extracellular-signal regulated kinase 1 (ERK(1)) and kinase 2 (ERK(2)). We studied the effects of echistatin, a well-known disintegrin and thrombin, a serine protease capable of activation of platelet integrin alpha(2)beta(1) receptor on collagen production, prolidase activity, expression of prolidase, beta(1)-integrin receptor, FAK, SOS-protein and phosphorylated MAP-kinases (ERK(1) and ERK(2)) in confluent human dermal fibroblasts. It has been found that treatment of the cells with 100nM echistatin contributes to inhibition of collagen production, as well as prolidase activity and expression compared to control cells. These phenomena were accompanied by a decrease in the expression of FAK, SOS-protein and phosphorylated MAP-kinases, ERK(1) and ERK(2). An opposite phenomenon was observed in fibroblasts treated with 0.1IU thrombin. In this case, a significant increase in collagen production and prolidase activity, accompanied by a distinct raise in the expression of prolidase, FAK and phosphorylated MAP-kinases and a slight increase in expression of SOS compared to controls were found. The results suggest that regulation of prolidase activity and collagen biosynthesis in human dermal fibroblasts may involve beta(1)-integrin-dependent signaling.

Oxidative stress induces IGF-I receptor signaling disturbances in cultured human dermal fibroblasts. A possible mechanism for collagen biosynthesis inhibition.

The effects of oxidative stress on collagen and DNA biosynthesis, beta-galactosidase and prolidase activities, and the expression of prolidase, beta1-integrin receptor, FAK, IGF-IR and MAP-kinases (ERK1, ERK2) were evaluated in human dermal fibroblasts. Subconfluent cells were subjected to repetitive stresses with 30 microM t-BHP for 1 hour per day over the course of 5 days. It was found that oxidative stress induced the inhibition of collagen biosynthesis in these cells in a time-dependent manner. Exposure of the cells to 5 stresses contributed to a decrease in collagen and DNA biosynthesis to about 30% and 50% of the control values, respectively. Prolidase activity and expression were only suppressed in fibroblasts subjected to 1 and 3 stresses. In these cells prolidase activity was decreased by about 20%. As a result of 5 stresses, no further inhibition of prolidase activity occurred; however, expression of the enzyme was slightly increased, as demonstrated by Western blot analysis. It was found that these phenomena were neither related to the expression of beta1-integrin receptor nor to that of FAK. However, the exposure of the cells to 3 and 5 stresses contributed to a distinct decrease in IGF-IR and MAP-kinases (ERK1, ERK2) expression, which is probably responsible for the collagen biosynthesis inhibition.