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PubMed1981

[Free and esterified cholesterol of the skin in atherogenic hyperlipidemias].

Skin free and esterified cholesterol were assayed using gaseous chromatography following plaque histochromatography separation in 20 control, 36 patients with Type II a hyperlipoproteinemia, 27 with Type II b hyperlipoproteinemia and 19 with Type IV hyperlipoproteinemia. Skin esterified cholesterol was higher in females with Type II a hyperlipoproteinemia without or with xanthomatosis. But the skin esterified cholesterol level was not correlated with skin free cholesterol nor with blood total cholesterol levels, while in males these parameters were well correlated. On the other hand skin cholesterol was assayed in 15 patients with Type II hypercholesterolemia before and after a 6-month treatment with Probucol: there was 10p. 100 reduction of cholesterol level, and a weak decrease in skin free-cholesterol; in contrast, skin esterified cholesterol increased significantly as well as the skin esterified cholesterol/skin total cholesterol ratio (EC/TC). These data suggest a connection between weak vascular risk and skin esterified cholesterol high level (or high EC/TC in skin).

Aged↗
PubMed1980

[Hypolipidaemic agents (author's transl)].

Since clofibrate was discovered, a number of compounds have been made available for the treatment of hyperlipoproteinaemias. Their principal pharmacological and therapeutic properties are summarized in this paper. Other compounds are now under pre-clinical or clinical studies, including probucol which is reviewed in this issue.

Animals↗
PubMedDate not supplied

[Prevention of atherosclerosis with the help of antioxidants].

Recent research findings have suggested a role for pharmacology as well as nutritional antioxidants in the prevention of atherosclerosis. Data from animal studies as well as culture experiments have shown that probucol, which has hypocholesterolemic and antioxidant properties, is able to prevent oxidative modification of low density lipoproteins. Such modification is now believed to play a major part in the initiation and progression of arterial lesions. Nutrients with antioxidant properties such as vitamins C and E, beta-carotene, and monounsaturated fatty acids (when they replace polyunsaturated fatty acids) can reduce the susceptibility of LDL to oxidation. Antioxidant therapy, if proven useful, should be considered an adjunct to lipid-lowering therapy in order to have the greatest impact on coronary heart disease.

Animals↗
PubMed1994

Peroxisome enzyme modification and oxidative stress in rat by hypolipidemic and antiinflammatory drugs.

Changes in the activities of two peroxisomal enzymes (catalase and thiolase), some parameters related to oxidative situations, such as conjugated dienes, zinc, iron, copper and superoxide dismutase after the administration of two known peroxisome proliferators (clofibrate and acetylsalicylic acid), and two drugs pharmacologically related to the former (probucol and diflunisal) have been studied in male Wistar rats. Administration of the drugs was made by p.o. for 15 days. After the treatment the rats were killed, their livers and brains were taken out, and their blood was collected. Peroxisomes were purified by differential centrifugation followed by ultracentrifugation. Total RNA was also extracted and the acyl CoA oxidase mRNA expression was studied. Clofibrate was inactive on both enzymes studied in liver and diflunisal in brain. However, the acyl CoA oxidase mRNA expression increased by clofibrate treatment. Results are justified by the liposolubility and protein-binding properties of the drugs. Otherwise, the present results show the existence of an increased lipid peroxidation, lower value of superoxide dismutase, and variable results for zinc, copper and iron trace elements. These data evidence an oxidative stress situation in plasma of rats treated with these drugs, probably as a consequence of an increase in some beta-oxidation enzymes, which brings about an overproduction of H2O2.

Acetyl-CoA C-Acetyltransferase↗
PubMed1995

Protection against murine cerebral malaria by dietary-induced oxidative stress.

Feeding 20% (w/w) menhaden-fish oil in a standard laboratory chow diet for 4 wk partially protected CBA/CaJ mice from the central nervous system consequences of infection with Plasmodium berghei (ANKA). Full protection (complete survival for 14 days postinfection) could be obtained by feeding a purified pro-oxidant vitamin E-deficient diet containing 4% (w/w) menhaden oil (MO - VE diet). The purified pro-oxidant MO - VE diet also exerted a pronounced suppressive effect against the parasite (depressed 6-day parasitemias). The anitmalarial effect of the MO - VE diet could be prevented by supplementing the diet with vitamin E or with either of 2 synthetic antioxidants, N,N'-diphenyl-p-phenylenediamine or probucol. These results suggest that the fish oil exerts its antimalarial effect by imposing a dietary-induced oxidative stress on the infected host erythrocyte, the parasite, or both. Nutritional manipulation of host oxidative stress status may be a useful adjunct therapy in patients undergoing treatment with pro-oxidant antimalarials such as drugs of the qinghaosu family.

Animal Feed↗
PubMed1994

S 12340: a potent inhibitor of the oxidative modification of low-density lipoprotein in vitro and ex vivo in WHHL rabbits.

Oxidative modification of low-density lipoprotein (LDL) is thought to play a key role in the formation of foam cells and in the initiation and progression of the atherosclerotic plaque. After evaluation of a large number of original drugs, S 12340 was found to be the most potent compound in inhibiting in a dose-dependent manner the human LDL oxidative modification induced either by copper ions or by cultured endothelial cells. Both the electrophoretic mobility and the thiobarbituric acid reactive substances returned to almost normal values in the presence of 0.5 microM of S 12340. Watanabe heritable hyperlipidemic rabbits were treated orally for 3 days or for 1 month with S 12340 to evaluate the potential protective effect of the compound on LDL oxidative modification induced ex vivo. Purified LDL from placebo and treated rabbits were submitted to oxidation, and S 12340 was effectively able to protect LDL in a dose-dependent manner and at doses as low as 10 mg/kg/day. Purified LDL from animals sacrificed at various times after oral administration of S 12340 were protected against oxidation for at least 6 h after the last administration of the compound. These findings are in good agreement with the plasma and LDL levels of S 12340 in these WHHL rabbits. S 12340, probucol and vitamin E were all able to decrease the optical density of the 1,1-diphenyl-2-picrylhydrazyl solution, demonstrating their free radical scavenging properties. The pharmacological properties of the compound suggest that S 12340 may be of potential interest for a new therapeutic approach to atherosclerosis.

Animals↗
PubMed1995

[Role of cholesterol esters in triglyceride transport].

Biosynthesis of cholesterol esters in the blood flow and their function are determined by the fact that these compounds are the sole endogenously synthesized molecules whose hydrophobicity is higher than that of triglycerides transferred by the blood. Within the structure of intermediate density lipoproteins, cholesterol esters substitute for triglycerides during association of apoprotein B-100 with the C-terminal lipid-binding domain. Substitution of the liquid-crystalline phase of triglycerides for the corresponding phase of cholesterol esters results in a significant alteration of the apoprotein B-100 conformation and the formation of low density lipoproteins. Within the structure of low density lipoproteins, the N-terminal domain (apoprotein B-100 ligand) acquires an active conformation and an ability to interact with cell membrane receptors, thereby facilitating their absorption of low density lipoproteins. Cholesterol synthesis in the blood is an independent step in triglyceride transport. Inhibition of cholesterol ester synthesis into high density lipoproteins and their conversion into intermediate density lipoproteins is unaccompanied by the acquisition by apoprotein B-100 of a final conformation or by the formation of low density lipoproteins. Remnants of intermediate density lipoproteins having an intermediate conformation of apoprotein B-100 and the inactive position of the domain ligand are accumulated in the blood. This results in the development of IIb type hyperlipoproteinemia. Resumption of conversion of cholesterol esters from high density lipoproteins into intermediate density lipoprotein remnants normalizes the triglyceride transport. The final conformation of apoprotein B-100 can be modelled by substituting triglycerides in intermediate density lipoprotein remnants for another substance whose hydrophobicity is similar to that of cholesterol esters (dolichol, probucol).(ABSTRACT TRUNCATED AT 250 WORDS)

Anticholesteremic Agents↗
PubMed1998

Some natural and synthetic antioxidants as stabilizers of beta-carotene conversion into vitamin A.

The effect of antioxidants (vitamins C and E, quercetin, probucol, butylated hydroxytoluene) on the oxidation of beta-carotene and its conversion into retinal under the influence of beta-carotene 15,15'- dioxygenase (CDO) from rat intestinal mucosa was studied. The activity of CDO decreased in the presence of oxidants. Antioxidants protected both the substrate and the enzyme. The extent of the protection depended on the antioxidant type. The combined injection of antioxidants and beta-carotene to animals completely or partially prevented the inhibition of the intestinal CDO which was caused by products of non-enzymatic oxidation of beta-carotene. Vitamins C and E, which protected the enzyme--substrate complex in vivo and in vitro, were found to be the most efficient protectors of beta-carotene conversion into retinal.

Animals↗
PubMed1998

Long-term effect of low-density lipoprotein apheresis in a patient with heterozygous familial hypercholesterolemia: follow-up study using coronary angiography.

A 62-year-old man with old myocardial infarction and familial hypercholesterolemia was treated by both probucol and low-density lipoprotein (LDL) apheresis. Coronary angiography was performed before and after 3.5 years of LDL apheresis treatment, and no new lesion or progression of coronary atherosclerosis was observed. LDL apheresis drastically reduced the serum total cholesterol. However, it is still unclear whether LDL apheresis effectively prevented the recurrence of cardiac events and the progression of coronary atherosclerosis in this patient.

Anticholesteremic Agents↗
PubMed1998

[Anti-atherogenic drugs].

Rupture of an instable plaque, characterized by a large lipid-rich central core, inflammatory cells, and a thin fibrous cap, causes sudden thrombus formation and acute coronary syndromes (ACS). Lipid lowering therapy by HMG-CoA reductase inhibitors leads to reduction of cardiovascular complications, but has very small effect on the degree of stenosis of ACS. Oxidizing metabolites generated at the site of coronary angioplasty can induce chain reactions that may lead to restenosis. Probucol improves the restenosis rate after coronary angioplasty if given before PTCA (percutaneous transluminal coronary angioplasty). These results will provide a better understanding of drug action, help explain certain drug interactions, and facilitate the choice of a drug for ACS.

Acute Disease↗
PubMed1998

Time trends in the use of cholesterol-lowering agents in older adults: the Cardiovascular Health Study.

OBJECTIVES: To describe recent temporal patterns of cholesterol-lowering medication use and the characteristics that may have influenced the initiation of cholesterol-lowering therapy among those aged 65 years or older. SUBJECTS AND METHODS: A cohort of 5201 adults 65 years or older were examined annually between June 1989 and May 1996. We added 687 African American adults to the cohort in 1992-1993. We measured blood lipid levels at baseline and for the original cohort in the third year of follow-up. We assessed the use of cholesterol-lowering drugs at each visit. RESULTS: The prevalence of cholesterol-lowering drug use in 1989-1990 was 4.5% among the men and 5.9% among the women; these figures increased over the next 6 years to 8.1% and 10.0%, respectively, in 1995-1996. There was a 4-fold increase in the use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors during the 6 years of follow-up, from 1.9% of all participants in 1989-1990 to 7.5% in 1995-1996. The use of bile acid sequestrants, nicotinic acid, and probucol declined from initial levels of less than 1% each. Among the participants who were untreated in 1989-1990, but eligible for cholesterol-lowering therapy after a trial of dietary therapy according to the 1993 guidelines of the National Cholesterol Education Panel, less than 20% initiated drug therapy in the 6 years of follow-up, even among subjects with a history of coronary heart disease. Among participants untreated at baseline but eligible for either cholesterol-lowering therapy or dietary therapy, initiation of cholesterol-lowering drug therapy was directly associated with total cholesterol levels, hypertension, and a history of coronary heart disease, and was inversely related to age, high-density lipoprotein cholesterol levels, and difficulties with activities of daily living. Other characteristics that form the basis of the 1993 National Cholesterol Education Panel guidelines-diabetes, smoking, family history of premature coronary heart disease, and total number of risk factors-were not associated with the initiation of cholesterol-lowering drug therapy. CONCLUSIONS: Given the clinical trial evidence for benefit, those aged 65 to 75 years and with prior coronary heart disease appeared undertreated with cholesterol-lowering drug therapy.

Aged↗
PubMed2000

Lipid-lowering for lower limb atherosclerosis.

BACKGROUND: Raised lipid levels, including cholesterol, are important risk factors in the development of lower limb arterial disease (atherosclerosis). OBJECTIVES: The objective of this review was to assess the effects of lipid lowering therapy in patients with lower limb atherosclerosis. SEARCH STRATEGY: The reviewers searched the Cochrane Peripheral Vascular Diseases Group trials register, Embase, reference lists of relevant articles, and contacted trial investigators in Europe and pharmaceutical companies. SELECTION CRITERIA: Randomised trials of lipid-lowering therapy in patients with lower limb atherosclerosis. The main outcomes were mortality, non-fatal events, direct tests of disease progression, indirect measurements of disease, and subjective measures. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data and assessed trial quality independently. The reviewers contacted investigators to obtain information needed for the review that could not be found in published reports. MAIN RESULTS: There were nine eligible trials, but two were excluded because of poor methodology. The seven remaining trials involved a total of 698 participants from seven different countries. Men and women participated in all but one trial and were generally middle aged to elderly. The follow-up period varied from four months to three years. The overall quality of the included trials was high. The trials were heterogeneous in terms of inclusion criteria, type of drugs used and outcomes measured. Lipid-lowering therapy produced a marked but non-significant reduction in mortality (odds ratio 0.21, 95% confidence interval 0. 03 to 1.17), but little change in non-fatal events (odds ratio 1.21, 95% confidence interval 0.80 to 1.83). In two trials there was a significant overall reduction in disease progression on angiogram (odds ratio 0.47, 95% confidence interval 0.29 to 0.77). The changes in ankle brachial pressure index and walking distance were inconsistent, although trials showed a general improvement in symptoms that could not be combined in a meta-analysis. Side effects were generally mild, with the exceptions of liver toxicity produced by betapyridil and the adverse effect of probucol on lipoprotein profile. REVIEWER'S CONCLUSIONS: Lipid-lowering therapy may be useful in preventing deterioration of underlying disease and alleviating symptoms. These results cannot determine whether one lipid-lowering regimen is better than another.

Arteriosclerosis↗
PubMed2004

HMG CoA reductase inhibitors (statins) for dialysis patients.

BACKGROUND: Cardiovascular disease accounts for more than half the number of deaths among dialysis patients. The role of HMG CoA reductase inhibitors (statins) in the treatment of hyperlipidemia in dialysis patients is unclear and their safety has not been established. OBJECTIVES: To assess the benefits and harms of statins in peritoneal dialysis (PD) and hemodialysis patients (HD). SEARCH STRATEGY: We searched MEDLINE (1966-July 2003), EMBASE (1980-July 2003), the Cochrane Central Register of Controlled trials (CENTRAL, in The Cochrane Library - issue 2, 2004), the Cochrane Renal Group's specialized register (April 2004) and handsearched reference lists of textbooks, articles and scientific proceedings. SELECTION CRITERIA: Randomized controlled trials (RCTs) and quasi-RCTs comparing statins with placebo, no treatment or other statins in dialysis patients. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Statistical analyses were performed using the random effects model after testing for heterogeneity. The results were expressed as weighted mean difference (WMD) for continuous outcomes and relative risk (RR) for dichotomous outcomes with 95% confidence intervals (CI). MAIN RESULTS: Six studies involving 357 participants were identified - three studies had both continuous ambulatory peritoneal dialysis (CAPD) and HD participants, two included only HD participants and one study only included CAPD participants. Studies were all of short duration and morbidity and mortality were not assessed. Average total cholesterol decreased significantly with statins compared to placebo in all dialysis patients (WMD -53.70 mg/dL (1.40 mmol/L), 95% CI -66.95 to -40.54). Similarly, average LDL cholesterol decreased significantly with statins in comparison to placebo in all patients (WMD -55.40 mg/dL (1.44 mmol/L), 95% CI -69.90 to -40.90) as did average triglycerides (-33.72 mg/dL (0.37 mmol/L), 95% CI -54.16 to -13.28). There was a significant increase in average HDL cholesterol levels (WMD 4.84 mg/dL (0.13 mmol/L), 95% CI 0.28 to 9.40) with statins compared to placebo in HD but not in CAPD patients. One trial compared statins to the hypolidemic agent probucol and found no significant differences between the two treatment groups. REVIEWERS' CONCLUSIONS: Statins used for 12 weeks decreased cholesterol levels in dialysis patients similar to the general population. Included studies were of short duration and therefore the efficacy of statins in decreasing the cardiovascular, cerebrovascular events and mortality rates is still unclear. The safety of statins needs to be addressed in the current ongoing clinical trials.

Cholesterol↗
PubMed1997

Whole plasma oxidation assay as a measure of lipoprotein oxidizability.

Lipoprotein oxidation induced in vitro in whole plasma is expected to be a more relevant model of the lipoprotein oxidation in the arterial wall than the in vitro oxidation of single isolated lipoproteins, e.g., low density lipoprotein (LDL). However, it is unclear, whether the oxidizability of whole plasma may serve as an adequate measure of the oxidizability of plasma lipoproteins. We measured the oxidizability of whole plasma diluted 150-fold as an absorbance increase at 234 nm known to reflect the level of conjugated dienes in the samples. Plasma oxidation was induced by Cu(II), 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH), lipoxygenase or myeloperoxidase+H2O2. Oxidizability of human plasma measured in the presence of Cu(II) was found to correlate with the oxidizability of LDL measured in the common Cu(II)-based LDL oxidation assay. The plasma oxidizability also correlated positively with plasma oxidizable fatty acid and negatively with plasma antioxidant content. Supplementation of human plasma with different antioxidants (albumin, urate, ascorbate, bilirubin, alpha-tocopherol and ubiquinol-10) in vitro decreased its oxidizability. Supplementation of Watanabe heritable hyperlipidaemic rabbits with different antioxidants (vitamin E, ubiquinone-10, probucol, carvedilol) in vivo lowered the oxidizability of rabbit plasma in comparison with rabbits fed standard diet. When plasma from hyperlipidaemic patients with or without coronary heart disease and from age-matched healthy controls was studied, the plasma oxidizability was found to be highest in the patients with coronary heart disease and lowest in the controls. Taken together, these data indicate that the plasma oxidation assay (i) provides information similar to that obtained using the common LDL oxidation assay, (ii) upgrades the latter, taking into account the effect of hydrophilic antioxidants on lipoprotein oxidation and characterizing the oxidizability of all plasma lipoproteins, and (iii) offers important practical advantages, such as fast and simple sample processing, low amount of plasma required and avoidance of artefactual oxidation during lipoprotein isolation. We propose the measurement of plasma oxidizability at 234 nm as an adequate practical index of the oxidizability of plasma lipoproteins.

Amidines↗
PubMed1992

The prevention of atherosclerosis with antioxidants.

Recent research findings have suggested a role for pharmacologic as well as nutritional antioxidants in the prevention of atherosclerosis. Data from animal studies as well as cell culture experiments have shown that the drug probucol, which has hypocholesterolemic and antioxidant properties, is able to prevent oxidative modification of low density lipoproteins (LDL). Such modification is now believed to play a major part in the initiation and progression of arterial lesions. Nutrients with antioxidant properties such as vitamins C and E, beta-carotene, and mono-unsaturated fatty acids (when they replace polyunsaturated fatty acids) can reduce the susceptibility of LDL to oxidation. Antioxidant therapy, if proven useful, should be considered an adjunct to lipid-lowering therapy in order to have the greatest impact on coronary heart disease.

Animals↗
PubMed2003

Oxidized low-density lipoprotein and high-density lipoprotein cholesterol modulate coronary arterial remodeling: an intravascular ultrasound study.

BACKGROUND: Oxidized low-density lipoprotein (oxLDL) not only plays an important role in plaque formation, but also impairs the endothelium-dependent relaxation. Constrictive remodeling rather than intimal hyperplasia mainly contributes to restenosis after balloon angioplasty. Probucol (powerful antioxidant) reduced restenosis rate by improving constrictive remodeling. Thus, oxLDL may modulate coronary arterial remodeling. HYPOTHESIS: The study was designed for using intravascular ultrasound to test the hypothesis that arterial constrictive remodeling (CR) was associated with oxLDL in patients with coronary artery disease. METHODS: Intravascular ultrasound was performed in 36 patients with de novo atherosclerotic coronary. Remodeling was defined and evaluated as follows: remodeling index (RI) = lesion vessel area (VA)/(proximal reference VA + distal reference VA)/2. Constrictive remodeling (CR) was defined as remodeling index (RI) < 0.9. Neutral and expansive remodeling (NER) was defined as RI > or = 0.9. The level of plasma ox-LDL was measured by sandwich ELISA using the monoclonal antibody (DLH3)-recognized oxidatively modified lipoproteins and the antihuman apoprotein B monoclonal antibody. RESULTS: Neutral and expansive remodeling was found in 24 lesions, and CR in 12 lesions. Remodeling index was significantly lower in the CR group than in the NER group (0.8 +/- 0.1 vs. 1.0 +/- 0.1, p < 0.001). The level of oxLDL in the CR group was significantly higher than that in the NER group (24.0 +/- 12.1 vs. 16.4 +/- 6.2 U/ml, p < 0.05). The level of high-density lipoprotein-cholesterol (HDL-C) in the CR group was significantly lower than that in the NER group (40.5 +/- 4.8 vs. 46.2 +/- 10.6 mg/ml, p < 0.05). There was a statistically significant correlation between the value of HDL-C/ ox-LDL and the RI (r = -0.48, p < 0.005). CONCLUSIONS: Oxidized LDL and HDL-C were associated with arterial remodeling in de novo atherosclerotic lesions.

Chi-Square Distribution↗
PubMed2004

Oligodendrocytes are susceptible to apoptotic cell death induced by prion protein-derived peptides.

Neurodegenerative prion diseases, characterized by a progressive dementia, are associated with the accumulation of abnormal forms of the prion (PrPc) protein, potentially due to an aberrant regulation of PrPc biogenesis and/or topology. One of these forms, termed ctmPrP, displays a transmembrane conformation and might trigger neuronal cell death in Gerstmann-Straüssler-Scheinker (GSS) syndrome and other prion-associated diseases in humans. Although the primary target cells involved in the progression of prion diseases remain unidentified, it was recently suggested that modifications of the oligodendroglial cells occur early in prion diseases. In the present study, we demonstrate that a putative transmembrane domain of the human PrPc, i.e., amino acids 118-135, induces oligodendrocyte (OLG) death in vitro in a time- and dose-dependent manner. The process leading to OLG death and induced by the PrP[118-135] peptide was characterized by DNA fragmentation, cytoskeletal disruption, and caspase activation. Protection against the PrP[118-135] peptide-induced OLG apoptosis by several antioxidant molecules, such as probucol, propylgallate, and promethazine, suggests that oxidative injuries contribute to the PrP[118-135] cytotoxicity to OLGs. These results suggest a potential pathophysiological role of the ctmPrP- and/or PrP fragment-mediated OLG cytotoxicity in spongiform encephalopathies.

Animals↗
PubMed2002

Macrophages take up triacylglycerol-rich emulsions at a faster rate upon co-incubation with native and modified LDL: An investigation on the role of natural chylomicrons in atherosclerosis.

Chylomicrons play a role in atherosclerosis, however, because the mechanisms involved in the cell uptake of these particles are not fully understood, investigations were carried out using a radioactively labeled protein-free triacylglycerol-rich emulsion incubated with peritoneal macrophages obtained from normal and apoE-knockout mice. Experiments were done in the presence of substances that inhibit several endocytic processes: EDTA for low density lipoprotein receptor, fucoidan for scavenger receptor, cytochalasin B for phagocytosis, and a lipopolysaccharide for lipoprotein lipase. In addition, triacylglycerol-rich emulsions were also prepared in the presence of native or modified radioactively labeled low density lipoprotein particles that are known to accumulate in the arterial intima. Probucol was also used to prevent the possible role played by an antioxidant in triacylglycerol-rich emulsion uptake. We have shown that triacylglycerol-rich emulsion alone is taken up by a coated-pit-dependent mechanism, mediated by macrophage secretion of apolipoprotein E. Furthermore, native, aggregated, acetylated, and moderately macrophage-oxidized low density lipoprotein stimulate the uptake of a triacylglycerol-rich emulsion through several mechanisms such as an actin-dependent pathway, scavenger receptors, and lipolysis mediated by lipoprotein lipase. On the other hand, in spite of the interaction of low density lipoprotein forms with a triacylglycerol-rich emulsion, the cellular triacylglycerol-rich emulsion uptake is impaired by copper-oxidized low density lipoprotein, possibly due to its diminished affinity towards lipoprotein lipase. We have also shown that macrophages take up aggregated low density lipoprotein better than the acetylated or oxidized forms of low density lipoprotein.

Animals↗