| First Author | Zhao L | Year | 2005 |
| Journal | Prostaglandins Other Lipid Mediat | Volume | 78 |
| Issue | 1-4 | Pages | 185-93 |
| PubMed ID | 16303615 | Mgi Jnum | J:112785 |
| Mgi Id | MGI:3663556 | Doi | 10.1016/j.prostaglandins.2005.07.003 |
| Citation | Zhao L, et al. (2005) 12/15-Lipoxygenase gene disruption and vitamin E administration diminish atherosclerosis and oxidative stress in apolipoprotein E deficient mice through a final common pathway. Prostaglandins Other Lipid Mediat 78(1-4):185-93 |
| abstractText | Studies in mouse models of atherosclerosis using 12/15-lipoxygenase (12/15-LO) gene disruption and transgenic overexpression demonstrate a pro-oxidative, pro-atherogenic role for this pathway. Vitamin E has been shown to suppress lipid peroxidation and reduce early atherogenesis in several mouse models, although conflicting results from several clinical trials have been reported. ApoE(-/-) and apoE(-/-)/12/15-LO(-/-) mice were maintained on normal chow diet with or without Vitamin E supplement (2000 IU/kg). Plasma Vitamin E, urinary 8,12-iso-iPF(2alpha)-VI and aortic lesion quantitation were assessed. Plasma Vitamin E levels significantly increased upon Vitamin E diet supplementation. 12/15-LO gene disruption resulted in significantly reduced aortic lesions and decreased urinary 8,12-iso-iPF(2alpha)-VI levels in apoE(-/-) mice, similar to Vitamin E administration in the absence of 12/15-LO gene disruption. However, Vitamin E dietary supplementation did not afford additive or synergistic protection in apoE(-/-)/12/15-LO(-/-) mice. These results suggest that early 12/15-LO-mediated lipid peroxidation triggers ensuing non-enzymatic peroxidation that is susceptible to Vitamin E antioxidant action in a common pathway of atherogenesis. |
