Disease relevance of Oxidised ATP

• Inhibition of simian virus 40 DNA replication by specific modification of T-antigen with oxidized ATP [1].
• Oxidized ATP protection against anthrax lethal toxin [2].
• Both Brilliant Blue G and oxidized ATP inhibited the release of [3H]GABA caused by ATP application; the Brilliant Blue G-sensitive, P2X7 receptor-mediated fraction, was much larger after ischemia than after normoxia [3].
• The reaction of the E. coli chaperonin GroEL (cpn 60) with the ATP analogue 2',3' oxidised ATP (oATP) has been studied [4].
• Results showed that the P2X(7) receptor agonist 2',3'-O-(4-benzoyl)benzoyl-ATP induced ERK1/2 phosphorylation in human astrocytoma cells overexpressing the recombinant rat P2X(7) receptor (rP2X(7)-R), a response that was inhibited by the P2X(7) receptor antagonist, oxidized ATP [5].

High impact information on Oxidised ATP

• Blocking of the P2Z receptor by oxidized ATP also inhibited multinucleated giant cell generation stimulated by concanavalin A or rIFN-gamma without decreasing monocyte migration or membrane adhesion molecule expression [6].
• Membrane permeabilization and cytotoxicity were fully blocked by pretreatment of the cells with oxidized ATP, a compound recently shown to block P2Z receptors covalently in macrophages [6].
• Aminoacyl-tRNA synthetases: affinity labeling of the ATP binding site by 2', 3' -ribose oxidized ATP [7].
• Both ATP-induced DC permeabilization and apoptosis were inhibited by oxidized ATP, a P(2Z)/P2X(7)-specific antagonist [8].
• Interleukin-2 partially relieved inhibition by oATP [9].

Chemical compound and disease context of Oxidised ATP

• Purine-induced gliosis could be reversed by the non-selective P2X/P2Y receptor antagonist pyridoxalphosphate-6-azophenyl-2', 4'-disulphonic acid (PPADS), but not by oxidized ATP (an antagonist of the P2X(7) receptor), in line with previous studies of our laboratory suggesting the involvement of a P2Y receptor subtype [10].
• The role of lysine residues 297 and 306 in nucleoside triphosphate regulation of E. coli CTP synthase: inactivation by 2',3'-dialdehyde ATP and mutational analyses [11].

Biological context of Oxidised ATP

• The P2Z-receptor agonist 3'-O-'(4-benzoylbenzoyl)-ATP (BzATP) was twofold more potent than ATP in eliciting cytolysis, which was preceded by a sustained high intracellular Ca2+ concentration; pretreatment with oxidized ATP prevented both the increase in the intracellular Ca2+ concentration and cell death [12].
• The most compelling evidence has been the observation that inhibitors of ionotropic nucleotide (P2X) receptors, including periodate-oxidized ATP (oATP), attenuate a subset of endotoxin-induced effects such as activation of NF-kappaB and up-regulation of inducible NO synthase [13].
• Ability of P2X7less FSDCs or of oxidized ATP-inhibited FSDCs to stimulate Ag-specific TH lymphocytes was severely decreased although Ag endocytosis was minimally affected [14].
• Furthermore, flow cytometric analysis indicates that exposure to oxidized ATP or treatment with LPS reversibly decreases cell cycle progression, without increasing the percentage of apoptotic cells [15].
• 3. The effect of BzATP on Akt phosphorylation in rat cortical astrocytes was significantly reduced by the P2X(7) receptor antagonist Brilliant Blue G and the P2X receptor antagonist iso-pyridoxal-5'-phosphate-6-azophenyl-2',4'-disulfonic acid, but was unaffected by trinitrophenyl-ATP, oxidized ATP, suramin and reactive blue 2 [16].

Anatomical context of Oxidised ATP

• The covalent blocker oxidized ATP (oATP), an inhibitor of P2X and P2Z receptors, prevented Ca2+ influx and plasma membrane depolarization, but had no effect on Ca2+ release from stores [9].
• Pretreatment of hepatocytes with oxidized ATP, a P2z-receptor antagonist, or complexation of ATP(4-) (the agonist for the P2z-receptor) with an excess of Mg2+, prevented ATP o-induced cell death [12].
• The effects of ATP were mimicked by submillimolar concentrations of 3-O-(4'-benzoyl)-benzoyl-benzoyl-ATP, and were inhibited by pretreatment of mast cells with a selective blocker of human and mouse P2X(7) receptor, 1[N,O-bis(5-isoquinolinesulphonyl)-N-methyl-l-tyrosyl]-4-phenylpiperazine, as well as oxidized ATP [17].
• The effects of oxidized ATP (oATP) on responses triggered by extracellular adenosine 5'-triphosphate (ATPe) were investigated in the mouse macrophage-like cell line J774 [18].
• ATP-induced efflux of 86Rb+ from erythrocytes was inhibited by extracellular Na+ and oxidized ATP, as well as by KN-62, an antagonist specific for the human P2X7 receptor [19].

Associations of Oxidised ATP with other chemical compounds

• 2) The effect was inhibited by oxidized ATP and the isoquinoline KN-62, two known P2X7 receptor antagonists [20].
• The P2zR-mediated PLD activity was distinguished from phorbol ester-stimulated PLD activity because the latter was slowly activated (t(1/2) > 15 min), unaffected by oxidized ATP or KN-62, and completely inhibited by bisindolylmaleimide [21].
• The deleterious effects of BzATP-treated microglia were prevented by nonselective P2X antagonists (PPADS and oxidized ATP) and by the more selective P2X(7) antagonist Brilliant Blue G [22].
• Furthermore, removal of extracellular Mg2+ enhanced the ATP- and BzATP-stimulated increases in [Ca2+]i. BzATP stimulated PLD in a concentration- and time-dependent manner that could be abolished by removal of extracellular Ca2+ and was inhibited by suramin, PPADS, and oxidized ATP [23].
• Addition of P2X inhibitors, such as periodate-oxidized ATP (oATP) or pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid tetrasodium, significantly reduced LOS-induced apoptosis [24].

Gene context of Oxidised ATP

• In addition, oxidized-ATP treatment (which inhibits P2X7) of macrophages blocks LPS-induced NO production, NF-kappaB and ERK-1/2 activation [25].
• IL-1beta efflux from shed vesicles was enhanced by ATP stimulation and inhibited by pretreatment with the P2X(7) antagonist oxidized ATP, thus indicating a crucial involvement of the pore-forming P2X(7)R in the release of the cytokine [26].
• P2 receptor inhibitors, including oxidized ATP, blocked NO synthase (NOSII) up-regulation and NO production induced by infection with M. tuberculosis or bacille Calmette-Guérin, or treatment with LPS or TNF-alpha [27].
• Addition of ATP also induced a rapid loss of CD23 from the surface of wild-type DC (t(1/2 )< 120 s), and this loss was inhibited by oxidized ATP and KN-62 which are known P2X7 receptor antagonists [28].
• Inhibition of chemokine expression in rat inflamed paws by systemic use of the antihyperalgesic oxidized ATP [29].

Analytical, diagnostic and therapeutic context of Oxidised ATP

• To further support a role for ATP receptors in spontaneous cell death, addition to the macrophage cell cultures of oxidized ATP, a selective inhibitor of ionotropic purinergic receptors, or the ATP-hydrolysing enzyme apyrase, also reduced spontaneous death [30].

References