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Wyświetlanie 1-3 z 3
Tytuł:
Pro-inflammatory properties of cadmium
Autorzy:
Olszowski, Tomasz
Baranowska-Bosiacka, Irena
Gutowska, Izabela
Chlubek, Dariusz
Powiązania:
https://bibliotekanauki.pl/articles/1039631.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
inflammatory mediators and markers
cadmium
Opis:
Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE2 (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles available in Medline, published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.
Źródło:
Acta Biochimica Polonica; 2012, 59, 4; 475-482
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cyclooxygenase pathways
Autorzy:
Korbecki, Jan
Baranowska-Bosiacka, Irena
Gutowska, Izabela
Chlubek, Dariusz
Powiązania:
https://bibliotekanauki.pl/articles/1039189.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cyclooxygenase
prostaglandin
15-deoxy-Δ12,14-prostaglandin J2
receptor desensitization
Opis:
This review compiles the current knowledge on the effects of prostanoids - arachidonic acid metabolites - on their own synthesis, activity and degradation. Interaction mechanisms between the receptors for the relevant compounds are presented, in particular with regard to the cooperation between a thromboxane A2 and prostaglandin I2 receptors. The questions of desensitization and internalization of receptors are discussed. The stages of the inflammatory response and tumor progression are analyzed against the background of the disruption of the synthesis of prostanoids. Special attention is given to the significance of 15-deoxy-Δ12,14-prostaglandin J2 in the regulation of the synthesis of prostanoids and its role as an anti-inflammatory agent. Ultimately, therapeutic approaches as used in various treatments are discussed in the light of the available knowledge.
Źródło:
Acta Biochimica Polonica; 2014, 61, 4; 639-649
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Biochemical and medical importance of vanadium compounds
Autorzy:
Korbecki, Jan
Baranowska-Bosiacka, Irena
Gutowska, Izabela
Chlubek, Dariusz
Powiązania:
https://bibliotekanauki.pl/articles/1039732.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
inflammation
cancer
vanadium
diabetes
insulin-mimetic action
pollution
Opis:
Vanadium belongs to the group of transition metals and is present in the air and soil contaminants in large urban agglomerations due to combustion of fossil fuels. It forms numerous inorganic compounds (vanadyl sulfate, sodium metavanadate, sodium orthovanadate, vanadium pentoxide) as well as complexes with organic compounds (BMOV, BEOV, METVAN). Depending on the research model, vanadium compounds exhibit antitumor or carcinogenic properties. Vanadium compounds generate ROS as a result of Fenton's reaction or of the reaction with atmospheric oxygen. They inactivate the Cdc25B2 phosphatase and lead to degradation of Cdc25C, which induces G2/M phase arrest. In cells, vanadium compounds activate numerous signaling pathways and transcription factors, including PI3K-PKB/Akt-mTOR, NF-κB, MEK1/2-ERK, that cause cell survival or increased expression and release of VEGF. Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein. In addition, vanadium compounds, in particular organic derivatives, have insulin-mimetic and antidiabetic properties. Vanadium compounds lower blood glucose levels in animals and in clinical trials. They also inhibit the activity of protein tyrosine phosphatase 1B. By activating the PI3K-PKB/Akt pathway, vanadium compaunds increase the cellular uptake of glucose by the GLUT4 transporter. The PKB/Akt pathway is also used to inactivate glycogen synthase kinase-3. The impact of vanadium compounds on inflammatory reactions has not been fully studied. Vanadium pentoxide causes expression of COX-2 and the release of proinflammatory cytokines in a human lung fibroblast model. Other vanadium compounds activate NF-κB in macrophages by activating IKKβ.
Źródło:
Acta Biochimica Polonica; 2012, 59, 2; 195-200
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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