Compounds > arachidonic-acid-omega-9-hydroperoxide

arachidonic-acid-omega-9-hydroperoxide and 4-hydroxy-2-nonenal

arachidonic-acid-omega-9-hydroperoxide has been researched along with 4-hydroxy-2-nonenal* in 1 studies

Other Studies

1 other study(ies) available for arachidonic-acid-omega-9-hydroperoxide and 4-hydroxy-2-nonenal

Article	Year
Arachidonic acid-derived oxidation products initiate apoptosis in vascular smooth muscle cells. Prostaglandins & other lipid mediators, 2002, Volume: 70, Issue:1-2 The mechanism of arachidonic acid (AA)-induced apoptosis in vascular smooth muscle cells (VSMCs) was studied in the A-10 rat aortic smooth muscle cell line. Treatment of serum-deprived VSMCs with 50 microM AA for 24 h resulted in a loss of cell viability. The apoptotic effect of AA was characterized by annexin V binding, sub-G1 population of cells, cell shrinkage and chromatin condensation. AA-induced VSMC death was attenuated by antioxidants alpha-tocopherol and glutathione, the hydrogen peroxide (H2O2) scavenger catalase and by serum proteins, albumin and gamma globulins. Moreover, the AA peroxidation products, 12(S)-hydroperoxyeicosatetraenoic acid (HPETE), 15(S)-HPETE, 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA) caused VSMC apoptosis. These data suggest an oxidative mechanism of AA-induced VSMC death. The apoptotic effect of AA was pH-dependent, being inhibited by extracellular alkalinization to pH 8.0. AA inhibited serum-stimulated cell cycle progression in quiescent cells, but not in proliferating cells. In conclusion, AA, through its oxidation products causes VSMC apoptosis. Antioxidants, by inhibiting VSMC apoptosis, may prevent consequent pathological events such as atherosclerotic plaque rupture. Topics: Aldehydes; Animals; Antioxidants; Aorta; Apoptosis; Arachidonic Acid; Cell Line; Cell Survival; Culture Media, Serum-Free; DNA; Leukotrienes; Lipid Peroxides; Malondialdehyde; Myocytes, Smooth Muscle; Rats	2002

Article

Year

Arachidonic acid-derived oxidation products initiate apoptosis in vascular smooth muscle cells.

Prostaglandins & other lipid mediators, 2002, Volume: 70, Issue:1-2

The mechanism of arachidonic acid (AA)-induced apoptosis in vascular smooth muscle cells (VSMCs) was studied in the A-10 rat aortic smooth muscle cell line. Treatment of serum-deprived VSMCs with 50 microM AA for 24 h resulted in a loss of cell viability. The apoptotic effect of AA was characterized by annexin V binding, sub-G1 population of cells, cell shrinkage and chromatin condensation. AA-induced VSMC death was attenuated by antioxidants alpha-tocopherol and glutathione, the hydrogen peroxide (H2O2) scavenger catalase and by serum proteins, albumin and gamma globulins. Moreover, the AA peroxidation products, 12(S)-hydroperoxyeicosatetraenoic acid (HPETE), 15(S)-HPETE, 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA) caused VSMC apoptosis. These data suggest an oxidative mechanism of AA-induced VSMC death. The apoptotic effect of AA was pH-dependent, being inhibited by extracellular alkalinization to pH 8.0. AA inhibited serum-stimulated cell cycle progression in quiescent cells, but not in proliferating cells. In conclusion, AA, through its oxidation products causes VSMC apoptosis. Antioxidants, by inhibiting VSMC apoptosis, may prevent consequent pathological events such as atherosclerotic plaque rupture.

Topics: Aldehydes; Animals; Antioxidants; Aorta; Apoptosis; Arachidonic Acid; Cell Line; Cell Survival; Culture Media, Serum-Free; DNA; Leukotrienes; Lipid Peroxides; Malondialdehyde; Myocytes, Smooth Muscle; Rats

2002