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Wyświetlanie 1-2 z 2
Tytuł:
THE INFLUENCE OF KETOPROFEN AND ZINC OXIDE NANOPARTICLES ON SERUM COPPER LEVEL IN RATS
Autorzy:
Olbert, Magdalena
Krośniak, Mirosław
Gdula-Argasińska, Joanna
Librowski, Tadeusz
Zygmunt, Małgorzata
Powiązania:
https://bibliotekanauki.pl/articles/956850.pdf
Data publikacji:
2018
Wydawca:
Zakład Opieki Zdrowotnej Ośrodek Umea Shinoda-Kuracejo
Tematy:
inflammation
ketoprofen
serum copper level
zinc oxide nanoparticles
zinc-copper antagonism
Opis:
The role of copper in anti-inflammatory response includes several mechanisms. Antagonism between zinc (Zn) and copper (Cu) and proper balance between the two elements in the organism may affect the course of inflammatory diseases. Copper is a component of Zn/Cu superoxide dismutase (Zn/Cu SOD) and other enzymes involved in the anti-inflammatory response of the organism. To investigate the serum copper level during inflammation and diseases, numerous researches were conducted. Copper deficiency or copper intoxication may lead to biological consequences. Copper deficiency may be caused by various factors, one of them is excessive zinc supplementation. The aim of the study was to investigate the alterations in the serum copper level after 2-week zinc oxide nanoparticles (NPs-ZnO) administration. The second aim was to investigate serum copper level alterations after 2-week NPs-ZnO and single ketoprofen administration. The inflammatory state was induced in each group by the carrageenan injection at the 15th day of the experiment. The results indicate for the decrease in serum copper level in group receiving NPs-ZnO compared to control. Moreover, in groups receiving NPs-ZnO as well as ketoprofen, a decrease in serum copper level was observed. We may conclude that NPs-ZnO administration and also ketoprofen administration acts as anti-inflammatory agents and may induce a decrease in serum copper level.
Źródło:
Medicina Internacia Revuo; 2018, 28, 110; 11-22
0465-5435
Pojawia się w:
Medicina Internacia Revuo
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Metal responsive transcription factor 1 (MTF-1) regulates zinc dependent cellular processes at the molecular level
Autorzy:
Grzywacz, Agata
Gdula-Argasińska, Joanna
Muszyńska, Bożena
Tyszka-Czochara, Małgorzata
Librowski, Tadeusz
Opoka, Włodzimierz
Powiązania:
https://bibliotekanauki.pl/articles/1038990.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
metal responsive-transcription factor 1
cell signaling
inflammation
NF-κB
Opis:
Metal responsive transcription factor 1 (MTF-1) is a zinc dependent transcription factor which is involved in the regulation of intracellular signaling pathways. MTF-1 regulates the expression of two streams of genes functioning in metal homeostasis and anti-oxidative response. MTF-1 acts in the process of binding of toxic metal ions in the cell, due to the activation of the expression of metallothioneins (MTs). Additionally, MTF-1 regulates transcription of genes involved in the sequestration of zinc and its intracellular transport. Disruption of zinc and MT homeostasis has an indispensable influence on the development of several pathological states. Moreover, by increasing MT activity, MTF-1 can effectively protect cells from oxidative and hypoxic stresses. The mechanism of MTF-1 action in cells includes the regulation of the proper immune response through activation/repression of anti- and pro-inflammatory cytokines. MTF-1 function in immune response is related to nuclear factor-κB (NF-κB) activity. Synthesis of insulin is also related to the activity of this transcription factor and zinc balance. Insulin transport also depends on zinc. In pancreatic β-cells, several types of the zinc transporters are found. Zinc transporters coordinated action is crucial for the synthesis and secretion of insulin. Disturbances in the regulation of signaling pathways connected with MTF-1 function can entail further alterations in zinc intracellular status and this growing imbalance can promote the pathophysiology of degenerative disorders.
Źródło:
Acta Biochimica Polonica; 2015, 62, 3; 491-498
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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