They point to end of inflammatory process
does their "suppression or absence" points to the severity of leukemic process?
Lipoxins are the most recent addition to the family of bioactive products generated from Arachidonic Acid (AA). They have a number of proinflammatory and anti-inflammatory actions. Lipoxins are short lived endogenously produced nonclassic eicosanoids whose appearance in inflammation signals the resolution of inflammation. They are abbreviated as LX, an acronym for lipoxygenase (LO) interaction products. At present two lipoxins have been identified; lipoxin A4 (LXA4) and lipoxin B4 (LXB4). (wikipedia) During inflammation, cells die by apoptosis. As part of resolution, lipoxins signal macrophages to the remains of these cells (phagocytosis).[6] During the acute inflammatory process, the proinflammatory cytokines such as IFN-γ and IL-1β can induce the expression of anti-inflammatory mediators such as lipoxins and IL-4, which promote the resolution phase of inflammation.[7]
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Should Inhibitor of PARP-1 affect cellular levels of superoxide ? and what would be the effect in patient taking anti-oxide.
Can conceptually use of Inhibitor of PARP-1, inhibit the MTOR inhibitors since it impact Mitochondrial Glycolytic state?
And the answer comes from Chantal Ethier et al
"Phosphorylation of the mTORC1 target S6 is decreased as well as the phosphorylation of the mTORC2 component Rictor on Thr1135. Finally, Akt phosphorylation on Ser473 is lost and then, cell death by necrosis occurs. Inhibition of PARP-1 with the potent PARP inhibitor AG14361 prevents all of these events. Moreover, the antioxidant N-acetyl-L-cysteine (NAC) can also abrogate all the signaling events caused by MNNG exposure suggesting that reactive oxygen species (ROS) production is involved in PARP-1 activation and modulation of mTOR signaling. In this study, we show that PARP-1 activation and PAR synthesis affect the energetic status of cells, inhibit the mTORC1 signaling pathway and possibly modulate the mTORC2 complex affecting cell fate."
Other interactions?
Histone deacetylase inhibitor potentiated the ability of MTOR inhibitor to induce autophagic cell death in Burkitt leukemia/lymphoma
Li Hua Dong1†Go to article!
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