UVB-induced vitamin E radical does not propagate lipid peroxidation in low density lipoproteins

1993 ◽  
Vol 15 (5) ◽  
pp. 527
Author(s):  
Elena A. Serbinova ◽  
Lester Packer
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Low Density Lipoproteins ◽  
Low Density

Mécanisme moléculaire de l'effet protecteur de la vitamine E dans l'athérosclérose

2002 ◽  
Vol 80 (7) ◽  
pp. 662-669 ◽  
Author(s):  
Abdelouahed Khalil
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Vascular Diseases ◽  
Epidemiologic Studies ◽  
Low Density Lipoproteins ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Prooxidant Effect

Oxidation of low-density lipoproteins constitutes the first step of a very complex process leading to atherosclerosis. Vitamin E, and principally alpha-tocopherol, is considered as the principal inhibitor of lipid peroxidation. Some studies showed the beneficial role of vitamin E in the prevention and reduction of atherosclerosis and its associated pathologies. However, other in vitro studies advance a prooxidant role of vitamin E. The results of the epidemiologic studies are difficult to generalize without taking account of the clinical randomized tests. In this work, we reviewed the principal studies devoted to the role of vitamin E and discussed the assumption of a prooxidant effect of this molecule.Key words: vitamin E, low-density lipoproteins (LDL), lipid peroxidation, cardio-vascular diseases.

Increased Lipid Peroxidation in Serum and Low-Density Lipoproteins Associated with Aging in Humans

2002 ◽  
Vol 72 (5) ◽  
pp. 315-320 ◽  
Author(s):  
Jale Balkan ◽  
Öznur Kanbagli ◽  
Güldal Mehmetçik ◽  
Ümit Mutlu-Türkoglu ◽  
Gülçin Aykaç-Toker ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Ldl Cholesterol ◽  
Serum Vitamin ◽  
Lipid Peroxide ◽  
Low Density Lipoproteins ◽  
Elderly Subjects ◽  
Low Density ◽  
Diene Conjugates ◽  
Diene Conjugate

This study was carried out in 140 healthy subjects who were divided into three subgroups of age: young (21–40 years), mature (41–60 years), and elderly ( 61–85 years) to investigate lipid peroxides and the antioxidant system in serum and low-density lipoproteins (LDL). Serum levels of cholesterol and LDL-cholesterol increased with age. The elderly group was found to have higher polyunsaturated fatty acid (PUFA) levels, thiobarbituric acid reactive substances (TBARS), diene conjugates, and lower cholesterol-adjusted vitamin E levels and antioxidant activity (AOA) as compared to the young group. No age-related difference was detected in serum vitamin C levels. Age correlated positively with serum cholesterol, LDL-cholesterol, PUFA, TBARS, diene conjugates, and negatively with cholesterol-adjusted vitamin E levels and AOA. In addition, endogenous LDL diene conjugate levels and the susceptibility of LDL to copper-induced lipid peroxidation increased in elderly subjects as compared with young subjects. In addition, positive correlations were detected between age and LDL endogenous diene conjugate levels and TBARS formation after copper incubation. However, the susceptibility of whole serum to copper-induced lipid peroxidation did not change in young and elderly subjects. Our results show that endogenous lipid peroxide levels in serum and LDL, and the susceptibility of LDL to copper-induced oxidation, increased with aging in humans.

Favorable effects of Globularia alypum on cardiometabolic markers in high fructose-fed rats

2020 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Yasmina Bahlil ◽  
Djamil Krouf ◽  
Zoheir Mellouk ◽  
Nawal Taleb-Dida ◽  
Akila Guenzet
Keyword(s):  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Low Density Lipoproteins ◽  
Standard Diet ◽  
Low Density ◽  
Content Type ◽  
High Fructose Diet ◽  
Globularia Alypum ◽  
High Fructose ◽  
Antioxidant Defense Systems

Purpose This study aims to examine whether Globularia alypum (Ga) lyophilized aqueous leaves extract treatment improves cardiometabolic syndromes such as hyperglycemia, lipid profiles and oxidative damage resulting from a high-fructose diet induced in hypertriglyceridemic rats. Design/methodology/approach A total of 24 male Wistar rats weighing 80 ± 5 g were first randomly divided into 2 groups. A total of 12 control rats (C) were fed a standard-diet (St-D) and 12 high fructose (HF) rats were fed a high-fructose diet (HF-D) containing St-D in which cornstarch was substituted by fructose (61.4%). After 15 weeks of feeding, body weight (BW) was about 320 ± 20 g and hypertriglyceridemia was noted in HF vs C group (2.69 ± 0.49 mmol/L) vs (1.25 ± 0.33 mmol/L). Each group of rats was then divided into two equal groups (n = 6) and fed during four weeks either a St-D or HF-D, treated or not with 1% of Ga extract (C-Ga) and (HF-Ga). After 28 days, fasting rats were anesthetized and blood and tissues were removed to measure biochemical parameters. Findings The results showed no significant differences in BW and insulinemia between all groups. Ga extract supplementation reduced glycemia (−36%), glycosylated hemoglobin (−37%), Homeostasis Model of Assessment-Insulin Resistance index (−34%) and triacylglycerol’s contents in plasma (−33%), very low density lipoproteins–low density lipoproteins (VLDL-LDL) (−48%), liver (−52%) and aorta (−39%); total cholesterol concentrations in aorta was 3.7-fold lower in HF-Ga vs HF group. Ga treatment reduced lipid peroxidation in plasma, VLDL-LDL, red blood cells (RBC), liver, muscle and kidney by improving superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) in RBC and catalase (CAT) activity in kidney (p < 0.05). Moreover, Ga ameliorates glutathione (GSH) production in RBC (+41%) and kidney tissues (+35%). Originality/value Ga extract ameliorated cardiometabolic syndrome by its hypotriglyceridemic effect and prevented development of insulin resistance. It reduces lipid peroxidation by enhancing non-enzymatic (GSH) and enzymatic (SOD, GPx and CAT) antioxidant defense systems in high-fructose hypertriglyceridemic rats. Therefore, supplementation of Ga leaves extract as an adjuvant could be used for the treatment of hypertriglyceridemia and the prevention and/or the management of cardio-metabolic adverse effects.

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