diphenylhexatriene and Arteriosclerosis

diphenylhexatriene has been researched along with Arteriosclerosis* in 2 studies

Other Studies

2 other study(ies) available for diphenylhexatriene and Arteriosclerosis

ArticleYear
Decreased plasma membrane fluidity in the development of atherosclerosis in cholesterol-fed rabbits.
    Atherosclerosis, 1988, Volume: 70, Issue:1-2

    Rabbits were fed a diet supplemented with 3% peanut oil or 3% peanut oil plus 0.5% cholesterol. Aortas from rabbits fed the cholesterol supplemented diet for 2 weeks were free of grossly visible lesions; however, aortas from rabbits fed this diet for 10 weeks exhibited extensive lesion development. Lesions were not observed in aortas of rabbits fed the high-fat supplemented diet. The fluorescence anisotropy of DPH was significantly (P = 0.0001) increased in plasma membranes isolated from aortas of rabbits fed the high-fat plus cholesterol vs. high-fat supplemented diet; the increase in fluorescence anisotropy observed after only 2 weeks on diet (0.201 +/- 0.002 vs. 0.144 +/- 0.002) was similar to that observed after 10 weeks on diet (0.244 +/- 0.002 vs. 0.193 +/- 0.001). The data support the hypothesis that plasma membrane fluidity [is decreased in atherosclerosis and indicate the decrease in membrane fluidity] occurs early in the development of the disease.

    Topics: 5'-Nucleotidase; Animals; Arteriosclerosis; Cell Membrane; Cholesterol, Dietary; Diphenylhexatriene; Fluorescence Polarization; Male; Membrane Fluidity; Nucleotidases; Rabbits; Subcellular Fractions

1988
Decreased microsomal membrane fluidity in the development of cholesterol-induced atherosclerosis in the rabbit.
    Experimental and molecular pathology, 1986, Volume: 45, Issue:3

    The hypothesis was examined that arterial microsomal membrane fluidity is decreased in atherosclerosis. To investigate this hypothesis, the fluorescence anisotropy (r) of 1,6-diphenylhexa-1,3,5-triene was measured in aortic microsomes isolated from normal and atherosclerotic rabbits. A decrease in membrane fluidity, as indicated by a significant increase in r, was observed in microsomes from atherosclerotic rabbits. Notably, the increase in r occurred prior to macroscopic lesion development. The data support the hypothesis that membrane fluidity is decreased in atherosclerosis and indicate that this decrease occurs early in the atherogenic process. The hypothesis that decreased microsomal membrane fluidity contributes to the increased activity of acyl-CoA:cholesterol acyltransferase (ACAT) in atherosclerosis was also investigated. The hypothesis was rejected on the basis that enrichment of microsomes from normal rabbits with exogenous cholesterol to achieve r values equal to that of microsomes from atherosclerotic rabbits did not result in comparable ACAT activity.

    Topics: Animals; Aorta; Arteriosclerosis; Cholesterol; Cholesterol, Dietary; Diphenylhexatriene; Fluorescence Polarization; Male; Membrane Fluidity; Microsomes; Rabbits; Sterol O-Acyltransferase

1986