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Cyclooxygenase pathways

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Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

2014

vol. 61

issue 4

639-649

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.

Biochemical and medical importance of vanadium compounds

100%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

2012

vol. 59

issue 2

195-200

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.

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2 Acta Biochimica Polonica

1 2014

1 2012

2 Baranowska-Bosiacka I.

2 Chlubek D.

2 Gutowska I.

2 Korbecki J.

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Cyclooxygenase pathways

Biochemical and medical importance of vanadium compounds