Disease relevance of CHEBI:15655

• In conclusion, this study shows that 13-HPODE activates PPARalpha in rat Fao but not in human HepG2 hepatoma cells [1].
• The compound 13-L-hydroperoxylinoleic acid (LOOH) triggered the death of clonal rat pheochromocytoma PC12h cells (LD50 = about 8 microM) [2].

High impact information on CHEBI:15655

• 13-HPODE augmented TNF alpha-induced mRNA accumulation and transcriptional activation of VCAM-1 in HAECs [3].
• Lineweaver-Burk analysis of the effect of OPP on pseudoperoxidase kinetics suggested that OPP was competitive with 13-HPODE [4].
• It has been proposed that 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid [13(S)-HPODE]-mediated formation of 4-oxo-2(E)-nonenal and 4-hydroxy-2(E)-nonenal arises from a Hock rearrangement [5].
• Several types of oxidative stress such as exposure to hydrogen peroxide, 13-L-hydroperoxylinoleic acid, and xanthine + xanthine oxidase triggered apoptotic nuclear condensation and DNA fragmentation in normal PC12 cells [6].
• Hydrogen peroxide, 13-L-hydroperoxylinoleic acid, and xanthine + xanthine oxidase induced a significant loss of delta psi m simultaneously with cell death [6].

Biological context of CHEBI:15655

• Oxygen consumption measurements showed that the luteolin-7-G/iron ion complexes react with oxygen molecules in competition with 13-HPODE acid, and free iron ions exclusively react with 13-HPODE acid [7].
• Low concentrations of HNE influenced the electron paramagnetic resonance (EPR) signal of 13(S)-hydroperoxy-9(Z), 11 (E)-octadecadienoic acid (13-HPODE)-generated Fe3+-LOX-1 slightly, but higher concentrations completely eliminated the EPR signal indicating an active site hindered from access by 13-HPODE [8].
• This study was conducted to check whether the primary lipid peroxidation product of linoleic acid, 13-hydroperoxy-9,11-octadecadienoic acid (13-HPODE), might be involved in the PPARalpha-activating effect of oxidized fats [1].
• The addition of 13(S)-HpODE stimulated a concentration-dependent increase in EGF-dependent phosphorylation of SHP-2 and its association with EGFR [9].
• 13(S)-HpODE augments epidermal growth factor signal transduction by attenuating EGF receptor dephosphorylation [10].

Anatomical context of CHEBI:15655

• The aim of the present study was to investigate the relaxations to 13-HODE and its hydroperoxyprecursor (13-HPODE) and to examine the role of the endothelial cells [11].
• In segments with endothelium, both cyclo-oxygenase inhibitors again abolished the relaxations to 13-HODE, but only diminished those to 13-HPODE [11].
• 5. In the splenic artery 13-HPODE and 13-HODE induced contractions above 3 microM which were blocked by the thromboxane receptor antagonist, daltroban.(ABSTRACT TRUNCATED AT 250 WORDS)[11]
• However, the formation of heptanone-etheno-dGuo adducts in calf thymus DNA was reduced when compared with the 13(S)-HPODE [12].
• The effect of 13-L-hydroperoxylinoleic acid (LOOH) on both Xenopus oocytes and neurotransmitter receptors synthesized in the oocytes was studied by electrophysiological and ion flux measurement [13].

Associations of CHEBI:15655 with other chemical compounds

• 4. Prostacyclin biosynthesis, as measured by radioimmunoassay, increased upon incubation with 13-HODE and 13-HPODE (10 microM) [11].
• Micelle and acid-soap formation of linoleic acid and 13-L-hydroperoxylinoleic acid being substrates of lipoxygenase-1 [14].
• When the MnPs were reacted with 13(S)-HPODE in the presence of Mn(II), H2O2 and tert-nitrosobutane (t-NB), the ESR spectrum contained a sharp triplet of acyl radical (aN = 0.81 mT) [15].
• Furthermore, the cystatin C-expressing cell line also resisted other oxidative stresses, including glutamate- and 13-L-hydroperoxylinoleic acid (LOOH)-induced cell death [16].

References