Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages
AUTOR(ES)
Fogelman, Alan M.
RESUMO
Glutaraldehyde treatment of 125I-labeled low density lipoprotein (125I-native-LDL) produced a modified LDL (125I-glut-LDL) with a molecular weight of 10 × 106 or more. Malondialdehyde treatment of 125I-native-LDL produced a product (125I-MDA-LDL) with a molecular weight not appreciably different from that of the original lipoprotein. However, the electrophoretic mobility of MDA-LDL indicated a more negative charge than native-LDL. 125I-MDA-LDL was degraded by two processes: a high-affinity saturable process with maximal velocity at 10-15 μg of protein per ml and a slower, nonsaturable process. The degradation of 125I-MDA-LDL was readily inhibited by increasing concentrations of nonradioactive MDA-LDL but was not inhibited by acetylated LDL or native-LDL even at concentrations as high as 1600 μg of protein per ml. After exposure of native-LDL to blood platelet aggregation and release in vitro, 1.73 ± 0.19 nmol of malondialdehyde per mg of LDL protein was bound to the platelet-modified-LDL. No detectable malondialdehyde was recovered from native-LDL that had been treated identically except that the platelets were omitted from the reaction mixture.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=348683Documentos Relacionados
- Lymphocyte-conditioned medium protects human monocyte-macrophages from cholesteryl ester accumulation.
- Unmodified low density lipoprotein causes cholesteryl ester accumulation in J774 macrophages.
- Oxidatively modified low density lipoproteins: a potential role in recruitment and retention of monocyte/macrophages during atherogenesis.
- Cholesteryl ester accumulation in macrophages incubated with low density lipoprotein pretreated with cigarette smoke extract.
- Adenine ribo- and deoxyribonucleotide metabolism in human erythrocytes, B- and T-lymphocyte cell lines, and monocyte-macrophages