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)

Low density lipoproteins (LDL), endogenously labelled with 3H in the triglyceride moiety, were isolated from rabbit serum and subsequently incubated in vitro at 37 degrees C with unlabelled preparations of rabbit high density lipoproteins (HDL) or very low density lipoproteins (VLDL). In incubations performed in the presence of phosphate buffer, there was no significant transfer of [3H]triglyceride from LDL to either HDL or VLDL; but when rabbit lipoprotein-free serum (the dialysed 1.21 g/ml infranatant) was added, transfer was apparent to both HDL and VLDL. The triglyceride transferring activity of the lipoprotein-free serum was abolished by heating at 85 degrees C for 10 min; all the transferring activity was found in the fraction which precipitated with ammonium sulphate at a concentration of less than 50% saturation. In direct contrast to the rabbit studies, rat serum failed to show a comparable process of triglyceride transfer. In subsequent experiments, mixtures of labelled LDL and unlabelled VLDL isolated either from rabbits or from rats were incubated with lipoprotein-free rabbit, rat or human serum. The lipoprotein-free serum of both the rabbit and man was effective in promoting transfer of 30--50% of LDL [3H]triglyceride into VLDL, regardless of the species origin of the lipoproteins. By contrast the lipoprotein-free serum of rats was only slightly more effective than buffer alone in promoting such transfers. It has been concluded that rabbit and human serum contains a triglyceride transferring factor of far greater activity than that in rat serum.
Atherosclerosis 1979 Jun
PMID:Species differences in the activity of a serum triglyceride transferring factor. 22 89

Intimal tissue from human atherosclerotic aortae was collected by the Dermatome procedure. The tissue was extraved with 5 mM Tris.HCl buffer containing 0.3 M NaCl and 1 mM EDTA, pH 7.4. The ammonium sulfate precipitate between 0.4--0.8 saturation obtained from the extract was fractionated on a DEAE-cellulose column and the effluent was monitored for lipoprotein lipase inhibition employing purified bovine milk enzyme. The substrate used was an emulsion of purified olive oil and tritiated triolein. Human serum was the source of activator of the substrate. A peak of inhibitory activity was eluted between 0.15--0.17 M NaCl. The major component in the purified material had properties similar to a glycoprotein (lipolipin) which has previously been purified from porcine aorta and shown to inhibit lipoprotein lipase activity. The partially purified human inhibitor decreased both the basal and the serum-stimulated activity of milk lipoprotein lipase. The inhibition was non-competitive with respect to serum. However, high levels of triglyceride substrate appeared to relieve the inhibitory effect. It is postulated that the inhibitor may be involved in an interaction with the emulsified lipid denying the enzyme access to its substrate.
Atherosclerosis 1978 Feb
PMID:The in vitro inhibition of bovine milk lipoprotein lipase by a glycoprotein preparation from human atherosclerotic intima. 64 49

Toxicity preventing activity (TxPA) is a recently identified substance in serum which counteracts the toxic effect of very low density lipoproteins upon endothelial cells in vitro. In two clinical studies, TxPA was low in individuals with angiographically demonstrable coronary artery disease. An atherogenic index which combines TxPA with lipoprotein cholesterol values classifies individuals with coronary artery disease with an accuracy of greater than 93%. TxPA precipitates with 0.15 M trichloroacetic acid and above 3 M (NH4)2SO4. Activity is present in Cohn fractions IV4 and V and is stabilized by antioxidants. TxPA co-elutes with the albumin peak on gel filtration chromatography and as a subcomponent of albumin on ion-exchange chromatography. Isoelectric focusing resolves albumin into two major peaks with pI values of 4.8 and 5.6. The TxPA is identified as the pI 5.6 albumin peak.
Atherosclerosis 1988 Oct
PMID:Purification and identification of very low density lipoprotein toxicity preventing activity. 319 Aug 23

Oral contraceptives (OCs) have been shown to induce antiethinyl estradiol antibodies in some women which may be detected as circulating immune complexes by precipitation in ammonium sulphate at 25% saturation (CIC.AS). A reevaluation of the presence of CIC.AS in 644 women either receiving sex steroid hormones or not was made, and the respective role of estrogens and progestogens investigated, together with the influence of the dose. The study confirmed that CIC.AS levels were significantly different in controls (442 +or- 246 mcg/ml serum), healthy gonadal hormone users (754 +or- 700 mcg) and users with thrombosis (1331 +or- 1099 mcg/ml). These results indicated that: 1) CIC.AS could be induced by synthetic estrogens as well as progestogens but not by nonsynthetic hormones; 2) the induction of CIC.AS seemed poorly dose-related; and 3) the induction was not correlated with the duration of use; 4) high CIC.AS levels occurred as soon as 3 weeks after the beginning of synthetic gonadal hormone use in reactive women and persisted throughout treatment and decreased slowly when discontinued; and 5) CIC.AS was detected more frequently (64.7%) in women with thrombosis than in healthy users (32.2%), P0.001. The importance of the immunologic changes as a risk factor in thrombosis in OC users was evaluated in comparison with other predisposing factors and tobacco smoking.
Atherosclerosis 1982 Sep
PMID:Blood changes in sex steroid hormone users. Circulating immune complexes induced by estrogens and progestogens and their relation to vascular thrombosis. 715 Mar 97

The increasing possibility that homocysteine might be involved in atherosclerosis in non-homocysteinuric subjects has required the measurement of low concentrations of this aminothiol in biological samples. The procedure described here represents an improvement of different HPLC methods. We utilized an isocratic HPLC system with fluorescence detection of plasma total homocysteine derivatized after reaction with ammonium 7-fluoro-benzo-2-oxa-1,3-diazole-4-sulphonate. With the help of the rapidly eluting internal standard N-acetyl-cysteine, the method ensures very good recovery (approximately 100%), reproducibility and precision (within-assay: 2.31%; day-to-day: 2.8%) in the physiological concentration range. This procedure allowed us to validate various animal models of hyperhomocysteinemia such as dietary folic acid deficiency in rat and acute methionine loads in rat and hamster. Using this method, we also confirmed that men have higher plasma total homocysteine levels than women. Due to its simplicity and reliability, our procedure is suitable for routine analysis of total homocysteine and other aminothiols (cysteine, cysteinyl-glycine and glutathione) in biological samples, as required in clinical and research laboratories.
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PMID:Hyperhomocysteinemia induced by folic acid deficiency and methionine load--applications of a modified HPLC method. 881 64

Plant compounds ammonium salt of glycyrretic acid (AGA) and 18-dehydroglycyrretic acid (18-DHGA) effectively reduced the concentration of total cholesterol, triglycerides, and atherogenic lipoproteins in blood serum of rabbits with modeled cholesterol atherosclerosis. They reduced significantly the content of malonic dialdehyde and raised the activity of superoxide dismutase in the animals' organs. Due to their powerful hypolipidemic and antioxidant effect AGA and 18-DHGA significantly reduced the surface of the atherosclerotic changes of the aorta. Both compounds considerably excel polisponin in the indicated properties.
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PMID:[The hypolipidemic and antiatherosclerotic properties of the ammonium salt of glycyrrhetic acid and of 18-dehydroglycyrrhetic acid]. 902 13

This paper describes an operationally simple, rapid hydrogenation of unsaturated sterols and bile alcohols in a domestic microwave oven. This has been achieved by the addition of catalytic amounts of Pd/C in methylene chloride/propylene glycol solvents in the presence of ammonium formate followed by microwave irradiation. It is suggested that this methodology will be helpful in the identification of saturated and unsaturated sterols with different side-chain structures in rare diseases: sitosterolemia, cerebrotendinous xanthomatosis (CTX), as well as atherosclerosis and diabetes mellitus. Sterols, such as cholesterol, campesterol, sitosterol, and bile alcohols with unsaturated side chains, were converted to their reduced congeners with high yield and purity.
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PMID:Rapid hydrogenation of unsaturated sterols and bile alcohols using microwaves. 917 33

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

Conditions associated with impaired nitric oxide (NO) activity and accelerated atherosclerosis have been shown to be associated with a reduced bioavailability of tetrahydrobiopterin (BH4). We therefore hypothesized that BH4 supplementation may improve endothelial dysfunction of chronic smokers. Forearm blood flow (FBF) responses to the endothelium-dependent vasodilators acetylcholine (ACh; 0.75, 1.5, and 3.0 microg/100 mL tissue/min) or serotonin (5-HT; 0.7, 2.1, and 6.3 ng/100 mL tissue/min), to the inhibitor of endothelial nitric oxide synthase (NOS) N(G)-monomethyl-L-arginine (L-NMMA; 2, 4, and 8 micromol/min), and to the endothelium-independent vasodilator sodium nitroprusside (SNP; 0.1, 0.3, and 1.0 microg/100 mL tissue/min) were measured by venous occlusion plethysmography in controls and chronic smokers. Drugs were infused into the brachial artery, and FBF was measured before and during concomitant intra-arterial infusion of BH4, tetrahydroneopterin (NH4; another reduced pteridine), or the antioxidant vitamin C (6 and 18 mg/min). In control subjects, BH4 had no effect on FBF in response to ACh, 5-HT, and SNP. In contrast, in chronic smokers, the attenuated FBF responses to ACh and 5-HT were markedly improved by concomitant administration of BH4, whereas the vasodilator responses to SNP were not affected. L-NMMA-induced vasoconstriction was significantly reduced in smokers compared with controls, suggesting impaired basal NO bioactivity. BH4 improved L-NMMA responses in smokers while having no effect on L-NMMA responses in controls. Pretreatment with vitamin C abolished BH4 effects on ACh-dependent vasodilation. In vitro, NH4 scavenged superoxide created by the xanthine/xanthine oxidase reaction equipotent like BH4 but failed to modify ACh-induced changes in FBF in chronic smokers in vivo. These data support the concept that in addition to the free radical burden of cigarette smoke, a dysfunctional NOS III due to BH4 depletion may contribute at least in part to endothelial dysfunction in chronic smokers.
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PMID:Tetrahydrobiopterin improves endothelium-dependent vasodilation in chronic smokers : evidence for a dysfunctional nitric oxide synthase. 1066 24

A synthetic heparin-mimicking polyaromatic anionic compound RG-13577 (polymer of 4-hydroxyphenoxy acetic acid and formaldehyde ammonium salt, Mr approximately 5800) exhibits specific binding to vascular smooth muscle cells (SMCs) and inhibits their proliferative response to growth promoting factors. Receptor binding of (14)C-RG-13577 was efficiently competed by apolipoprotein E3 (apoE), lactoferrin, and the LRP (LDL receptor-related protein) receptor associated 39 kDa protein (RAP). Unlike cell surface binding of apoE, binding of RG-13577 to SMCs was not affected by heparin, heparan sulfate degrading enzymes, or low density lipoprotein (LDL). Moreover, wild-type and heparan sulfate-deficient Chinese hamster ovary (CHO) cells, as well as normal- and LDL receptor negative- human skin fibroblasts bind RG-13577, but not apoE, to a similar extent. On the other hand, homozygous mouse embryonic fibroblasts deficient in the LDL receptor-related protein (LRP) expressed a markedly reduced binding of RG-13577 as compared to normal mouse embryonic fibroblasts. These results indicate that RG-13577 and related compounds bind to the LRP receptor on the surface of vascular SMCs. Addition of lactoferrin to cultured SMCs protected the cells against the antiproliferative effect of compound RG-13577, suggesting that this inhibition is mediated by RG-13577 binding to LRP receptors on the SMC surface. Altogether, we have identified a series of synthetic polyaromatic anionic molecules that exhibit specific binding to LRP and thereby exert an antiproliferative effect on vascular SMCs. These compounds are applied to suppress SMC proliferation associated with restenosis and accelerated atherosclerosis.
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PMID:A synthetic heparin-mimicking polyanionic compound binds to the LDL receptor-related protein and inhibits vascular smooth muscle cell proliferation. 1118 Apr 2


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