Literature DB >> 3973770

The distribution of ceroid in human atherosclerosis.

M J Mitchinson, D C Hothersall, P N Brooks, C Y De Burbure.   

Abstract

It has been suggested that macrophages in atherosclerotic plaques oxidize the lipid they contain, leading to necrosis in the plaque. Over 200 human aortic and coronary atherosclerotic plaques from 102 human necropsy subjects aged between 5 and 88 were, therefore, examined histologically for the presence of insoluble lipid (ceroid), thought to be a product of lipid oxidation. Ceroid was present in all the plaques but not in areas of diffuse intimal thickening. In early lesions the insoluble lipid was within membrane-bound vesicles in macrophage-like cells, many showing characteristic ring structures suggesting that membrane-associated oxidative systems might be responsible for rendering the lipid insoluble. Staining was increased by an oxidizing agent and abolished by a reducing agent. It is suggested that this distribution supports the concept of lipid oxidation by macrophages within the plaque.

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Year:  1985        PMID: 3973770     DOI: 10.1002/path.1711450205

Source DB:  PubMed          Journal:  J Pathol        ISSN: 0022-3417            Impact factor:   7.996


  15 in total

1.  Mechanism of ceroid formation in atherosclerotic plaque: in situ studies using a combination of Raman and fluorescence spectroscopy.

Authors:  Abigail S Haka; John R Kramer; Ramachandra R Dasari; Maryann Fitzmaurice
Journal:  J Biomed Opt       Date:  2011 Jan-Feb       Impact factor: 3.170

2.  The content of lipoperoxidation products in normal and atherosclerotic human aorta.

Authors:  V V Tertov; V V Kaplun; I A Mikhailova; I V Suprun; A N Orekhov
Journal:  Mol Cell Biochem       Date:  2001-09       Impact factor: 3.396

3.  Ceroid accumulation by murine peritoneal macrophages exposed to artificial lipoproteins: ultrastructural observations.

Authors:  R Y Ball; K L Carpenter; M J Mitchinson
Journal:  Br J Exp Pathol       Date:  1988-02

4.  Ceroid accumulation by murine peritoneal macrophages exposed to artificial lipoproteins.

Authors:  R Y Ball; K L Carpenter; J H Enright; S L Hartley; M J Mitchinson
Journal:  Br J Exp Pathol       Date:  1987-06

5.  Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis.

Authors:  J V Hunt; M A Bottoms; K Clare; J T Skamarauskas; M J Mitchinson
Journal:  Biochem J       Date:  1994-05-15       Impact factor: 3.857

6.  Primary extracellular ceroid type lipopigment. A histochemical and ultrastructural study.

Authors:  M Elleder
Journal:  Histochem J       Date:  1991-06

Review 7.  Why are low-density lipoproteins atherogenic?

Authors:  S G Young; S Parthasarathy
Journal:  West J Med       Date:  1994-02

8.  Oxygen radicals and atherosclerosis.

Authors:  K L Carpenter; C E Brabbs; M J Mitchinson
Journal:  Klin Wochenschr       Date:  1991-12-15

9.  Direct evidence for a protein recognized by a monoclonal antibody against oxidatively modified LDL in atherosclerotic lesions from a Watanabe heritable hyperlipidemic rabbit.

Authors:  H C Boyd; A M Gown; G Wolfbauer; A Chait
Journal:  Am J Pathol       Date:  1989-11       Impact factor: 4.307

10.  Near-Infrared Autofluorescence in Atherosclerosis Associates With Ceroid and Is Generated by Oxidized Lipid-Induced Oxidative Stress.

Authors:  Mazen S Albaghdadi; Ryutaro Ikegami; Mohamad B Kassab; Joseph A Gardecki; Mie Kunio; Mohammed M Chowdhury; Ramzi Khamis; Peter Libby; Guillermo J Tearney; Farouc A Jaffer
Journal:  Arterioscler Thromb Vasc Biol       Date:  2021-05-20       Impact factor: 10.514

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