Literature DB >> 8024602

Increased plasma and lipoprotein lipid peroxidation in apo E-deficient mice.

T Hayek1, J Oiknine, J G Brook, M Aviram.   

Abstract

Apo E-deficient mice which are highly atherogenic animals were used in order to study their plasma and lipoprotein lipid peroxidation in the absence or presence of oxidative stress. We have demonstrated that plasma from apo E knockout mice demonstrated increased lipid peroxidation both in the absence and in the presence of a free radical generating substance, 2,2-Azobis-(2-amidinopropane) hydrochloride (AAPH). Similarly, low and very low-density lipoprotein (LDL and VLDL) from apo E-deficient mice, but not their high-density lipoprotein (HDL), demonstrated increased lipid peroxidation. We suggest that in apo E-deficient mice, accelerated atherosclerosis is associated with increased lipid peroxidation of plasma, LDL and VLDL, as well as increased susceptibility of these lipoproteins to undergo lipid peroxidation under oxidative stress.

Entities:  

Mesh:

Substances:

Year:  1994        PMID: 8024602     DOI: 10.1006/bbrc.1994.1883

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  28 in total

1.  Matters of the heart transcriptome: a brief history of cardiovascular genomics.

Authors:  Pilar M Labordé-Lahoz
Journal:  Tex Heart Inst J       Date:  2002

2.  The modulating effect of mechanical changes in lipid bilayers caused by apoE-containing lipoproteins on Aβ induced membrane disruption.

Authors:  Justin Legleiter; John D Fryer; David M Holtzman; Andtomasz Kowalewski
Journal:  ACS Chem Neurosci       Date:  2011-10-19       Impact factor: 4.418

Review 3.  Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis.

Authors:  Théophile Godfraind
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2005-12-29       Impact factor: 6.237

4.  Immunohistochemical detection of 4-hydroxy-2-nonenal adducts in Alzheimer's disease is associated with inheritance of APOE4.

Authors:  K S Montine; S J Olson; V Amarnath; W O Whetsell; D G Graham; T J Montine
Journal:  Am J Pathol       Date:  1997-02       Impact factor: 4.307

5.  Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase.

Authors:  M Aviram; M Rosenblat; C L Bisgaier; R S Newton; S L Primo-Parmo; B N La Du
Journal:  J Clin Invest       Date:  1998-04-15       Impact factor: 14.808

Review 6.  LDL oxidation by arterial wall macrophages depends on the oxidative status in the lipoprotein and in the cells: role of prooxidants vs. antioxidants.

Authors:  M Aviram; B Fuhrman
Journal:  Mol Cell Biochem       Date:  1998-11       Impact factor: 3.396

7.  The atherogenic effect of excess methionine intake.

Authors:  Aron M Troen; Esther Lutgens; Donald E Smith; Irwin H Rosenberg; Jacob Selhub
Journal:  Proc Natl Acad Sci U S A       Date:  2003-12-01       Impact factor: 11.205

8.  Polymorphisms of genes in the lipid metabolism pathway and risk of biliary tract cancers and stones: a population-based case-control study in Shanghai, China.

Authors:  Gabriella Andreotti; Jinbo Chen; Yu-Tang Gao; Asif Rashid; Bingshu E Chen; Philip Rosenberg; Lori C Sakoda; Jie Deng; Ming-Chang Shen; Bing-Sheng Wang; Tian-Quan Han; Bai-He Zhang; Meredith Yeager; Robert Welch; Stephen Chanock; Joseph F Fraumeni; Ann W Hsing
Journal:  Cancer Epidemiol Biomarkers Prev       Date:  2008-02-22       Impact factor: 4.254

9.  Up-regulation of apolipoprotein E by leptin in the hypothalamus of mice and rats.

Authors:  Ling Shen; Patrick Tso; David Q-H Wang; Stephen C Woods; W Sean Davidson; Randall Sakai; Min Liu
Journal:  Physiol Behav       Date:  2009-05-28

Review 10.  Alzheimer's Disease Genetic Risk Factor APOE-ε4 Also Affects Normal Brain Function.

Authors:  Amanda M Di Battista; Nicolette M Heinsinger; G William Rebeck
Journal:  Curr Alzheimer Res       Date:  2016       Impact factor: 3.498

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.