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D Bonnefont-Rousselot

Publications and source records attributed to D Bonnefont-Rousselot.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Adaptation of the measurement of plasma and erythrocyte glutathione peroxidase activity on Hitachi 911].

The aim was to automate the assay of plasma and erythrocyte glutathione peroxidase (GSH-Px) activity using the Hitachi 911 (Boehringer Mannheim). There is a need for a reliable and rapid technique for the determination of GSH-Px activity to evaluate 'the oxidative stress'. The technique used was that proposed by the Randox laboratories (Randox Laboratories Ltd, Ransel test, reference: RS-505). The Hitachi 911 was programmed by adapting the manual Randox technique. Repeatability, reproducibility and linearity were satisfactory, and usual values for plasma and erythrocyte GSH-Px activity were determined. Automation of the Ransel test for determination of GSH-Px activity was very useful for serial assays. In addition, the technique is practical and has good interlaboratory reproducibility.

Blood Chemical Analysis↗
PubMed1995

Blood antioxidants (vitamin E and beta-carotene) in long-term low density lipoprotein apheresis.

We measured vitamin E and beta-carotene in the serum and in circulating lipoproteins in a large population of 15 patients with familial hypercholesterolaemia who were undergoing long-term treatment by low density lipoprotein (LDL) apheresis. The technique used for apheresis was dextran sulphate cellulose adsorption. The results showed that before LDL apheresis, patients had high vitamin E and normal beta-carotene levels in the serum and in the VLDL+LDL fraction. There were no relationships between serum levels of vitamin E and beta-carotene and the duration of LDL-apheresis. Low vitamin E and beta-carotene levels in the HDL fraction could be related to the low HDL concentrations in these patients. Vitamin E/cholesterol ratios were similar to those of the normolipaemic controls whereas beta-carotene/cholesterol ratios were lower. After LDL-apheresis treatment, the ratios in the HDL fraction fell whereas the ratios in the serum and in the VLDL and LDL fraction did not change. This study shows that these patients exhibited no deficiency in either serum of VLDL-LDL of vitamin E or beta-carotene after long-term treatment by LDL-apheresis and that the status of these antioxidants in serum was independent of the duration of treatment.

Adolescent↗
PubMed1995

Hydroxyl radical attack of low density lipoprotein decreases its cellular catabolism in the absence of significant lipid peroxidation.

Low density lipoprotein (LDL) has been submitted to oxidative modification induced by gamma radiolysis of water under conditions generating either hydroxyl radical (OH.) alone, or a mixture of superoxide anion and OH.. Treatment of LDL with hydroxyl radical alone did not lead to significant lipid peroxidation as assessed by thiobarbituric acid reactive substances (TBARS) and hydroperoxide measurement and induced only very small change in the electrophoretic mobility of the particle. In contrast, superoxide and hydroxyl radical mixture induced a dose-dependent increase in lipid peroxidation, with a marked elevation of the negative net charge of the LDL. However, in both cases, a similar reduction of the uptake and degradation of modified LDL by the apo B/E receptor pathway of human fibroblasts was observed. This suggests that factors other than lipid peroxidation could play a role in LDL modification and influence their cellular metabolism.

Cells, Cultured↗
PubMed1995

Physicochemical changes in human high-density lipoproteins (HDL) oxidized by gamma radiolysis-generated oxyradicals. Effect on their cholesterol effluxing capacity.

This paper describes an oxidative process of human high-density lipoproteins (HDL) based upon the action of oxygenated free radicals produced by water radiolysis (OH. and OH./O2.- free radicals at pH 7), monitored by both biochemical and physical markers. Classical biochemical markers (vitamin E, thiobarbituric acid-reactive substances (TBARS), conjugated dienes and differential fluorescence) were studied as a function of the radiation dose (from 0 to 800 Gy; dose rate = 2.7 x 10(-2) Gy.s(-1)). The fluorescence polarization anisotropy (r) was measured with 1,6-diphenylhexatriene (DPH). Vitamin E decrease and formation of lipid peroxidation products (thiobarbituric acid-reactive substances and conjugated dienes) were concomitant in the case of OH. free radicals alone, whereas these products appeared after a small threshold dose when OH. and O2.- free radicals were simultaneously produced in solution. At high radiation doses, TBARS concentrations have reached plateau values (approx. 2 or 7 nmol/mg lipid with OH. or OH./O2.- free radicals, respectively) which were much lower than those obtained after copper oxidation (approx. 15 or 29 nmol/mg lipid after 12 and 24 h incubation, respectively). The free radical-induced oxidative process has led to a rigidification of the HDL and was associated with low values of cholesterol effluxing capacities when these oxidized HDL were incubated with cholesterol-loaded human fibroblasts. Similar results were obtained with copper-oxidized HDL, under our experimental conditions. Consequently, these two kinds of oxidative modification of HDL resulted both in a loss of their capacity to remove cellular cholesterol, which could be explained by the fact that this ability was under the dependence of a HDL optimum fluidity.

Cholesterol↗
PubMed1993

[Peroxidation of human high density lipoproteins by oxygen-derived free radicals].

The involvement of low density lipoprotein (LDL) peroxidation in atherogenesis is now admitted. The oxidation of high density lipoproteins (HDL) could contribute to the atherogenic process, by limiting their capacity to accept cholesterol from cell membranes. In this work, we studied the human HDL peroxidation initiated by OH. or OH./O2.- free radicals generated by gamma radiolysis. This method allows a quantitative and selective production of free radicals, and the resulting oxidation is less drastic than the chemical one. HDL oxidation was followed, as a function of the radiation dose, by the disappearance of endogenous vitamin E, the formation of thiobarbituric acid-reactive substances (TBARS) and the fluorescence at 440 nm. Human HDL turned out to be oxidizable by hydroxyl free radicals and oxygen potentiated this effect. The oxidative modification of HDL, leading to a rigidification of the HDL envelop, could contribute to reduce the ability of HDL to stimulate efflux of cholesterol from tissues.

Free Radicals↗
PubMed1993

Electrophoretic mobility changes of oxidized human low density lipoprotein measured by laser Doppler electrophoresis.

Laser Doppler Electrophoresis was used to detect changes in the surface charge of low density lipoprotein populations exposed to oxidative stress. Before oxidative stress, low density lipoprotein suspensions exhibited homogenous populations of net negative charge but after exposure to hydroxyl and superoxide radicals, peroxyl radicals, or by Cu2+ generated oxidants they exhibited Laser Doppler Electrophoresis changes. The major population of low density lipoprotein became more negatively charged, in agreement with agarose gel electrophoresis. However, Laser Doppler Electrophoresis detected greater heterogeneity of low density lipoprotein, compared to agarose gel electrophoresis. Partially oxidized low density lipoprotein exhibited a less negatively charged subpopulation of particles compared to control samples. This has not been reported previously. Hence, Laser Doppler Electrophoresis is a sensitive method for detecting the appearance of subpopulations of differing surface charge density in oxidatively modified low density lipoprotein. beta-carotene protected low density lipoprotein against oxidative modification even when endogenous vitamin E levels are low. Vitamin E-deficient low density lipoprotein pretreated with beta-carotene exhibited a more narrow negative population when oxidized with peroxyl radicals, compared to control. Native low density lipoprotein pretreated with a mixture of all-trans- and cis-beta-carotene was also protected.

Amidines↗
PubMed1993

[Antioxidative treatment in myocardial reperfusion ischemia].

Perfusion-induced myocardial ischaemia is observed in several situations: chronic coronary insufficiency, unstable angina, myocardial infarction, and during coronary angioplasty or bypass surgery. Oxygen-derived free radicals are liberated in large quantities during myocardial reperfusion ischaemia. Though very toxic in experimental studies, the responsibility of these free radicals in myocardial injury remains to be demonstrated clinically. Oxidant stress, characterised by an imbalance between the free radical attack and insufficient cellular defense seems partially responsible for reperfusion arrhythmias and post-ischemic stunning. On the other hand, its role is less evident in prolonged myocardial ischaemia causing irreversible myocardial lesions such as infarction. Antioxidant therapy is under evaluation in clinical trials. There are several options: some prevent the formation of free radicals by inhibiting the biochemical reactions which may produce them or by limiting the intervention of the neutrophils--the "fulcrum" of free radicals formations. Other antioxidant therapies inactivate free radicals as they are formed by promoting their degradation or their neutralisation. Experimental data is profuse and discordant. The models are very different. The first clinical trials are under way using either specific antioxidant molecules or molecules having other beneficial effects: in the latter case, the benefit of the antioxidant action is more difficult to demonstrate. Antioxidant therapy could play a role in surgical myocardial protection, especially of transplant organs, in very early forms of ischaemia. It could also prevent the pejorative hemodynamic consequences of myocardial stunning of the border zones of infarction, so enabling patients to survive a difficult period. The results of on-going studies should clarify the role of antioxidant therapy in reperfusion-induced myocardial ischaemia.

Antioxidants↗
PubMed1993

Oxidation of low-density lipoproteins by OH. and OH./O2-. free radicals produced by gamma radiolysis.

The aim of this study was to analyze quantitatively the oxidative modification of low-density lipoproteins (LDLs) induced by OH. free radicals produced by gamma radiolysis, in the absence or in the presence of oxygen (action of OH. free radicals, or simultaneous action of OH. and O2-. free radicals, respectively). The effects of increasing radiation doses on aqueous LDL solutions have been monitored by several parameters: a decrease in endogenous vitamin E, the formation of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes, the appearance of a differential fluorescence (excitation wavelength = 360 nm), and an increase in the relative electrophoretic mobility. Initial radiation yields (decrease in vitamin E, formation of TBARS) have been determined at pH 7 as a function of LDL concentration (from 0.75 to 9 g liter-1). From the comparison of these yields with those of OH. and O2-. free radicals produced by water radiolysis, we have deduced reaction mechanisms for the initiation of oxidation of LDLs by OH. and OH./O2-. free radicals.

Gamma Rays↗
PubMed1992

[Oxidative stress in 29 HIV seropositive patients. Two-year results of a double-blind trial of diethyldithiocarbamate versus placebo].

Among 29 seropositive subjects who had participated in the HIV 87 therapeutic trial (Mérieux laboratories), the oxidative stress was evaluated at 24 months in 16 treated with diethyldithiocarbamate (dithiocarb) and in 13 who had received the placebo. No significant difference was found between these two groups, whereas the existence of an oxidative stress has been confirmed in seropositive subjects compared with controls.

Adult↗
PubMed1992

Effect of pH on low-density lipoprotein oxidation by O2-./HO2. free radicals produced by gamma radiolysis.

This study aimed to analyze quantitatively the initiation and the consequences of low-density lipoprotein (LDL) peroxidation by O2-./HO2. free radicals produced by gamma radiolysis. The action of increasing radiation doses on aqueous LDL solutions has been monitored simultaneously by several parameters: a decrease in endogenous vitamin E, the formation of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes, the appearance of a differential fluorescence (excitation wavelength = 360 nm), and an increase of the relative electrophoretic mobility. Initial radiation yields (decrease in vitamin E, formation of TBARS) have been determined at pH 7 and pH 5.7 as a function of LDL concentration (from 0.75 to 9 g liter-1). From the comparison of these yields with those of O2-. radicals produced by water radiolysis, we have deduced reaction mechanisms for LDL peroxidation initiated by O2-./HO2. free radicals.

Dose-Response Relationship, Drug↗
PubMed1992

Simple method for quantifying alpha-tocopherol in low-density+very-low-density lipoproteins and in high-density lipoproteins.

We assessed the distribution of alpha-tocopherol in serum lipoprotein samples after separating the lipoprotein fractions by either sequential ultracentrifugation or selective precipitation with sodium phosphotungstate-magnesium chloride reagent. alpha-Tocopherol concentrations were determined by reversed-phase high-performance liquid chromatography. After ultracentrifugation, we found that in men, low- and very-low-density serum lipoproteins (LDL-VLDL) contained 53.6% of alpha-tocopherol vs 46.4% in high-density lipoproteins (HDL). In women, serum LDL-VLDL contained 45.6% alpha-tocopherol after ultracentrifugation vs 54.4% in HDL. After selective precipitation, the proportions of alpha-tocopherol in men were 56.1% in LDL-VLDL vs 43.9% in HDL, and in women, 45.4% in LDL-VLDL vs 54.6% in HDL. After selective precipitation, alpha-tocopherol recovery from whole lipoprotein fractions was 97% to 100% vs 80% after ultracentrifugation, thus allowing more accurate alpha-tocopherol quantification than after separation by ultracentrifugation.

Adult↗
PubMedDate not supplied

Could antioxidant supplementation reduce antiretroviral therapy-induced chronic stable hyperlactatemia?

OBJECTIVE: To determine if asymptomatic stable chronic hyperlactatemia in human immunodeficiency virus (HIV)-infected patients under highly active antiretroviral therapy (HAART, including nucleoside analog reverse transcriptase inhibitors (NRTI)) could be improved by antioxidant supplementation. DESIGN: To match two groups of patients taking NRTI for at least 24 months: 15 without and 15 with antioxidant supplementation (vitamin E, beta-carotene, N-acetylcysteine, selenium, Gingko biloba extracts and nutritional supplements). For both the groups, the supplementation by antioxidants or its lack was carefully assessed. Venous lactatemia, blood oxidative stress markers (plasma lipid peroxidation, enzymatic and non-enzymatic antioxidants), CDC revisited classification, CD4 count and viral load, NRTI (with or without stavudine) and other antiretroviral drugs used, lipoatrophy, central fat accumulation were assessed. RESULTS: Patients were not statistically different with respect to the CDC classification, CD4 count, viral load and characteristics of antiretroviral therapy. Blood oxidative stress markers, i.e. vitamin E, vitamin A and beta-carotene tended to be higher in the supplemented group. The difference observed in venous lactate concentration between the two groups was significant (1.37 +/- 0.10 vs. 1.82 +/- 0.19 mmol/l in the supplemented and non-supplemented groups, respectively P = 0.04). CONCLUSION: Antioxidant supplementation improves the asymptomatic stable chronic hyperlactatemia observed in HIV-infected patients taking HAART including NRTI for a long time. Controlled studies are needed to demonstrate the efficacy of this supplementation on mitochondrial toxicity observed during HAART and the possible usefulness of its combination with mitochondrial cofactors like carnitine, riboflavine, coenzyme Q, alpha-lipoic acid.

Adipose Tissue↗
PubMedDate not supplied

[Oxidation of lipoproteins and mechanism of action of antioxidants : contribution of gamma radiolysis].

Water gamma radiolysis leads to a selective and quantitative production of radical species, which allows the study of the one-electron oxidation or reduction of several biological systems, especially lipoproteins. Well defined quantities of*OH, O2*-/HO2* or RO2*. free radicals can thus be specifically produced by radiolysis of water or of ethanol. Such radical species can initiate one-electron oxidation reactions on compounds dissolved in water or in ethanol. Given the oxidative hypothesis of atherosclerosis, it is classically admitted that the oxidation of low density lipoproteins (LDL) but also of high density lipoproteins (HDL) is involved in the development of the atherosclerotic process. Nevertheless, the initiation mechanisms of this oxidation are still poorly defined. Therefore, gamma radiolysis is a method of choice for the study of the mechanisms of oxidation of LDL and HDL by oxygenated free radicals (*OH, O2*-, HO2*, RO2*). Gamma radiolysis allows to obtain oxidized lipoproteins with a very well defined oxidation status, and is a less drastic method than other currently used oxidation procedures such as those using for example copper ions. Finally, gamma radiolysis is also especially appropriate to study the mechanisms of action of antioxidant molecules, either in pure solutions or as inhibitors of lipid peroxidation in lipoproteins in vitro.

Free Radicals↗