Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative modification of low-density lipoproteins (LDLP) may play an important role in the pathogenesis of atherosclerosis. The work deals with the study of the inhibiting effect of tris(2-hydroxyethyl)ammonium orthocresoxyacetate (cresacin) on Cu+2-induced oxidation of human LDLP in vitro. The degree of LDLP oxidation was judged according to the accumulation of diene conjugates in the incubation medium. Inhibition of the degree of LDLP oxidation was found to be dependent on the dose of cresacin. The level of products forming during LDPL oxidation and reacting with thiobarbituric acid was also determined. Like in the previous case, the dose-dependent effect of inhibition of LDLP peroxidation by cresacin was also observed. It is concluded that cresacin is an effective inhibitor of LDLP oxidative modification in vitro.
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PMID:[Tris(2-hydroxyethyl)ammonium ortho-cresyl acetate inhibits oxidative modification of the low density lipoproteins]. 946 May 96

LDLP and VLDLP have different biological functions: phylogenetically older LDLP transfer FA that serve as substrates for intracellular production of energy and ATP while VLDLP transfer FA--precursors of cell membranes and eicosanoids. The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. VLDLP consist of palmitic and oleic VLDLP and LDLP of linoleic and linolenic LDLP. The contribution of LDLP to the development of HLP atherosclerosis and atheromatosis is negligible. LDLP form palmitic and oleic VLDLP with hydrated LDLP density. Blockade of LDLP absorption by apoB endocytosis and deficit of poly-FA constitute the etiological basis of atherosclerosis. Its pathogenetic basis is the excess of palmitic VLDLP with LDPL density in the intercellular space that block absorption of linoleic LDLP with all transferred SC poly-FA. Atheromatosis is clinically and prognostically most significant symptom of atherosclerosis associated with accumulation of ligand-free VLDLP and LDLP in arterial intima of the elastic type as the local pool of interstitial tissue for intravascular pool of intercellular medium. Type 2 diabetes mellitus in aged patients is a symptom of atherosclerosis resulting from SC poly-FA deficit and GLUT4 incompetence. Insulin-dependent cells differ in the degree of insulin resistance. Non-alcoholic fatty liver disease, synthesis of a physiological palmitic TG by hepatocytes and excessive formation of palmitic VLDLP in liver integrate pathogenesis of atherosclerosis and hepatic steatosis. The main pathogenetic factor is the excess of palmitic s-FA and palmitic TG.
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PMID:[Low and very low density lipoproteins: pathogenetic and clinical significance]. 2365 66