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LDL Oxidation (ldl + oxidation)
Selected AbstractsSerum paraoxonase activity in patients with type 1 diabetes compared to healthy controlsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2002B. Mackness Abstract Background The oxidation of low-density lipoprotein (LDL) is central to current theories on the initiation and progression of atherosclerosis. Type 1 diabetes is associated with an increase in oxidative stress, which may be responsible for the increased susceptibility to coronary heart disease seen in type 1 diabetes. High-density lipoprotein (HDL) associated paraoxonase (PON1) can retard the oxidation of LDL. Design Paraoxonase activity, concentration and genotype were therefore investigated in 152 people with type 1 diabetes and 282 healthy controls. These parameters were also investigated in the group with type 1 diabetes in relation to the presence of diabetic complications. Results Both PON1 activity and concentration were significantly lower by 16·7% and 19·2% (both P < 0·05) in the type 1 diabetes group. These differences were independent of the PON1 coding region polymorphisms. The distribution of PON1 activity and mass were the same in both populations, i.e. for the PON1-192 polymorphism RR > RQ > QQ and for the PON1-55 polymorphism LL > LM > MM. There were no differences in either the PON1 polymorphisms, PON1 activity and concentration in people with type 1 diabetes in the presence or absence of micro and macro vascular complications of diabetes. Conclusions Low PON1 activity may contribute to the increased atherosclerosis found in type 1 diabetes by reducing the ability of HDL to retard LDL oxidation despite the frequently-found increased HDL in type 1 diabetes when good glycaemic control is established. [source] Protective effects of endomorphins, endogenous opioid peptides in the brain, on human low density lipoprotein oxidationFEBS JOURNAL, Issue 6 2006Xin Lin Neurodegenerative disorders are associated with oxidative stress. Low density lipoprotein (LDL) exists in the brain and is especially sensitive to oxidative damage. Oxidative modification of LDL has been implicated in the pathogenesis of neurodegenerative diseases. Therefore, protecting LDL from oxidation may be essential in the brain. The antioxidative effects of endomorphin 1 (EM1) and endomorphin 2 (EM2), endogenous opioid peptides in the brain, on LDL oxidation has been investigated in vitro. The peroxidation was initiated by either copper ions or a water-soluble initiator 2,2,-azobis(2-amidinopropane hydrochloride) (AAPH). Oxidation of the LDL lipid moiety was monitored by measuring conjugated dienes, thiobarbituric acid reactive substances, and the relative electrophoretic mobility. Low density lipoprotein oxidative modifications were assessed by evaluating apoB carbonylation and fragmentation. Endomorphins markedly and in a concentration-dependent manner inhibited Cu2+ and AAPH induced the oxidation of LDL, due to the free radical scavenging effects of endomorphins. In all assay systems, EM1 was more potent than EM2 and l -glutathione, a major intracellular water-soluble antioxidant. We propose that endomorphins provide protection against free radical-induced neurodegenerative disorders. [source] Betaine Protects Chronic Alcohol and ,-3 PUFA-Mediated Down-Regulations of PON1 Gene, Serum PON1 and Homocysteine Thiolactonase Activities With Restoration of Liver GSHALCOHOLISM, Issue 3 2010Ravi Varatharajalu Background:, Paraoxonase (PON1) is an antioxidant enzyme that prevents LDL oxidation as well as detoxifies homocysteine thiolactone (HCTL), both of which can cause atherosclerosis. Chronic alcohol (ETOH) and high ,-3 polyunsaturated fatty acids (,-3 PUFA) consumption may affect PON1 status presumably via reactive oxygen species by depleting liver glutathione (GSH), whereas betaine may counter their effects. Therefore, we investigated the influence of ETOH, ,-3 PUFA, and betaine on liver GSH, PON1 expression, lipid score, as well as serum PON1 and HCTLase activities. Methods:, Experimental rats belonging to various dietary groups were pair-fed with Lieber-DeCarli low (2.8% the dietary calories as ,3-fatty acids) and high (13.8% the dietary calories as ,3-fatty acids) menhaden fish alcohol-liquid diets with and without betaine (10 g/l diet) for 8 weeks after which liver PON1 mRNA, GSH, lipid score, and serum PON1, HCTLase, and ALT activities were measured. Results:, High ,-3 PUFA decreased liver PON1 mRNA expression, serum PON1, and HCTLase activity by 23% (p < 0.01), 20% (p < 0.05), and 28% (p < 0.05), respectively compared to the low ,-3 PUFA group. ETOH decreased PON1 mRNA expression by 25 and 30% (p < 0.01) with concomitant 27% (p < 0.05) and 38% (p < 0.01), decrease in liver GSH levels in low and high ,-3 PUFA groups, respectively. Correspondingly, serum PON1 activity decreased by 23% (p < 0.05) and 58% (p < 0.01) while serum HCTLase activity decreased by 25% (p < 0.05) and 59% (p < 0.01) in the low and high ,-3 PUFA ETOH groups, respectively. Betaine restored liver PON1 mRNA expressions in low and high ,-3 PUFA ETOH groups with parallel restorations of PON1 activity and liver GSH. Concomitantly, betaine reduced hepatosteatosis accompanied by alleviation of liver injury caused by chronic alcohol and high ,-3 PUFA. Conclusions:, Based on these results, we conclude that dietary betaine not only atheroprotective by restoring liver GSH that quenches free radicals, but also may alleviate liver injury by reducing hepatosteatosis. [source] Melatonin inhibits oxidative modification of low-density lipoprotein particles in normolipidemic post-menopausal womenJOURNAL OF PINEAL RESEARCH, Issue 3 2000Akihiko Wakatsuki In this study, we investigated the short-term effect of melatonin on the susceptibility of low-density lipoprotein (LDL) to oxidation in normolipidemic post-menopausal women. Fifteen post-menopausal women received 6.0 mg melatonin daily for 2 wk. Blood samples were obtained before and after the treatment and the plasma levels of total cholesterol, total triglyceride, high-density lipoprotein (HDL)-cholesterol, LDL-cholesterol, LDL-triglyceride, and LDL-apolipoprotein B were determined. LDL oxidation was performed by incubation with copper ions and was analyzed by monitoring the kinetics of conjugated diene formation and measuring the concentration of thiobarbituric-acid-reactive substances (TBARS). LDL-apolipoprotein B derivatization was analyzed by measuring trinitrobenzene sulfonic acid (TNBS) reactivity. Melatonin treatment significantly increased the plasma triglyceride levels (P<0.05), but did not significantly alter the plasma levels of total cholesterol, HDL-cholesterol, or LDL-lipids. The kinetics analysis of conjugated diene production revealed that melatonin treatment significantly prolonged the lag time of conjugated diene formation (from 64.71±11.89 to 70.15±10.52 min, P<0.05). The oxidation rate and the amount of conjugated diene, however, did not change significantly. The TBARS concentration was significantly reduced by melatonin treatment (from 49.31±7.57 to 38.69±23.90 nM/mg LDL, P<0.05). Furthermore, melatonin treatment significantly reduced the copper-induced decrease of TNBS reactivity (from 79.43±6.19 to 86.50±9.07% at 1 hr and from 71.03±6.74 to 76.31±4.99% at 2 hr, P<0.05). These results indicate that melatonin treatment may reduce LDL susceptibility to oxidative modification in normolipidemic post-menopausal women. [source] Inhibitory effects of Hibiscus sabdariffa L extract on low-density lipoprotein oxidation and anti-hyperlipidemia in fructose-fed and cholesterol-fed ratsJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 15 2004Chang-Che Chen Abstract Hibiscus sabdariffa L extract (HSE) is an aqueous extract of Hibiscus sabdariffa L flowers that is used as a local soft drink and medical herb in Taiwan. Oxidation of low-density lipoprotein (LDL) has been shown to increase the incidence of atherosclerosis. In this study, we determined the antioxidative activity of HSE on LDL oxidation by examining relative electrophoretic mobilities (REM) and thiobarbituric acid-reactive substances (TBARS). The data revealed an inhibitory effect of HSE on Cu2+ -mediated REM and TBARS. HSE exhibited a remarkable ability to reduce cholesterol degradation and ApoB fragmentation. Overall, HSE showed a high potency to inhibit the production of oxidized LDL induced by copper and, specifically, to reduce serum triglycerides in high-fructose diet (HFD) fed rats and serum cholesterol in high-cholesterol diet (HCD) fed animals. The levels of LDL and the ratio of LDL-cholesterol (LDL-C) to HDL-cholesterol (HDL-C) were reduced by HSE in both hyperlipidaemia models. Based on these findings, we suggest that HSE may be used to inhibit LDL oxidation and to prevent various types of hyperlipidaemia in HFD- or HCD-fed rats. Copyright © 2004 Society of Chemical Industry [source] Cranberry proanthocyanidins associate with low-density lipoprotein and inhibit in vitro Cu2+ -induced oxidation,JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 14 2001Mandy L Porter Abstract Antioxidant activity of six fractions of cranberry phenolic compounds was determined by inhibition of Cu2+ -induced low-density lipoprotein (LDL) oxidation. The phenolic composition of each fraction was determined by high-performance liquid chromatography. The phenolic fractions were mixed with aliquots of modified human serum prior to LDL isolation. The serum was modified to remove very-low-density lipoprotein and chylomicrons that may bind phenolic compounds. Only fractions 5 and 6 that contained proanthocyanidins (PAs) significantly increased the lag time of LDL oxidation, and the lag time for fraction 6 was significantly higher than for fraction 5. The mass distribution of PAs in these fractions was obtained by matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry, a technique that allows rapid characterisation of the molecular weight distribution in mixtures of oligomeric compounds. Fraction 5 contained trimers through heptamers, whereas fraction 6 contained pentamers through nonamers. In addition, fraction 6 contained PA oligomers with more doubly linked, A-type interflavan bonds. Results indicate that PAs specifically associate with LDL in modified serum and increase the lag time of Cu2+ -induced oxidation. Differences between fractions 5 and 6 in PA structure and effects on LDL oxidation suggest that the degree of polymerisation and the nature of the interflavan bond influence antioxidant properties. © 2001 Society of Chemical Industry [source] Cover Picture , Mol.MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 12 2008Nutr. Selected topics of issue 12 are: Procyanidin effects on oesophageal adenocarcinoma cells strongly depend on flavan-3-ol degree of polymerization Daily Intake of thiamine correlates with the circulating level of endothelial progenitor cells and the endothelial function in patients with type II diabetes Fungal siderophores function as protective agents of LDL oxidation and are promising anti-atherosclerotic metabolites in functional food Identification of four IgE-reactive proteins in raspberry (Rubus ideaeus L.) [source] Mechanisms and Effects of Green Tea on Cardiovascular HealthNUTRITION REVIEWS, Issue 8 2007Arpita Basu PhD Green tea, rich in antioxidant and anti-inflammatory catechins, especially epigallocatechin gallate (EGCG), has been shown to reduce surrogate markers of atherosclerosis and lipid peroxidation, particularly LDL oxidation and malondialdehyde concentrations, in several in vitro, animal, and limited clinical studies. Epidemiological observations in Southeast Asian countries indicate an inverse correlation exists between habitual consumption of green tea beverages and the incidence of cardiovascular events. A few short-term clinical studies have reported its effects in attenuating biomarkers of oxidative stress and inflammation among smokers, and an ability to decrease postprandial lipemia in hypercholesterolemic subjects has also been suggested. However, further investigations are needed to confirm the potential role of green tea beverages and the safety of green tea supplements in reducing body fat, as well as other biomarkers of cardiovascular disease risks. [source] Antioxidative activity of sulfur-containing compounds in Allium species for human LDL oxidation in vitroBIOFACTORS, Issue 1-4 2004Hiroyuki Nishimura Abstract Sulfur-containing compounds contributing to health promotion in Allium species are produced via enzymic and thermochemical reactions. Sulfur-containing amino acids and volatile organosulfur compounds were prepared for an antioxidative assay. The inhibitory activity of S-alk(en)yl-L-cysteines and their sulfoxides, volatile alk(en)yl disulfides and trisulfides, and vinyldithiins in Allium species against lipid hydroperoxide (LOOH) formation in human low-density lipoprotein (LDL) was examined. It was elucidated that the alk(en)yl substituents (methyl, propyl, and allyl) and the number of sulfur atoms in the compounds were important for the antioxidative activity. 3,4-Dihydro-3-vinyl-1,2-dithiin, which is produced by a thermochemical reaction of allyl 2-propenethiosulfinate, exhibited the highest antioxidative activity of human LDL among sulfur-containing compounds. [source] Cardiovascular Protective Effects of ResveratrolCARDIOVASCULAR THERAPEUTICS, Issue 3 2004Silvia Bradamante ABSTRACT Resveratrol (3,4,,5-trihydroxy-trans-stilbene), a phytoalexin found in grape skins, peanuts, and red wine, has been reported to have a wide range of biological and pharmacological properties. It has been speculated that at low doses (such as consumed in the common diet) resveratrol may have cardioprotective activity. In this article we describe recent in vitro and in vivo studies in animal models. The results of these studies suggest that resveratrol modulates vascular cell function, inhibits LDL oxidation, suppresses platelet aggregation and reduces myocardial damage during ischemia-reperfusion. Although the reported biological data indicate that resveratrol is a highly promising cardiovascular protective agent, more studies are needed to establish its bioavailability and in vivo cardioprotective effects, particularly in humans. [source] | ||||||||||||||||