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A Hadjian

Publications and source records attributed to A Hadjian.

14 recordsLinked to original sources

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects.

The purpose of this study was to investigate the effect of eicosapentaenoic and docosahexaenoic acids on plasma lipids and lipoproteins, lipid peroxidation and antioxidant status in healthy humans. A total of 19 healthy volunteers consumed 6 g/day Maxepa fish oil for 3 weeks (1.8 g n-3 fatty acids/day). At baseline and at day 21, we evaluated plasma lipoproteins, plasma and low-density lipoprotein fatty acids, lipid peroxidation markers (malondialdehyde concentration, low-density lipoprotein peroxidation in vitro), and the content of a number of antioxidants (reduced and oxidized glutathione in whole blood, plasma and erythrocyte glutathione peroxidases, plasma vitamin E and beta carotene). Plasma concentrations of total cholesterol, triglycerides, phospholipids, low-density lipoprotein cholesterol and low-density lipoprotein size did not differ significantly after 3 weeks of supplementation. Adding the fish oil to the diet increased the concentration of n-3 very-long-chain polyunsaturated fatty acids and decreased the concentration of n-6 fatty acid and oleic acid in plasma and low-density lipoprotein. Eicosapentaenoic and docosahexaenoic acid supplementation caused elevated values of the high-density lipoprotein cholesterol due to an increment of the high-density lipoprotein 2 fraction and reduced low-density lipoprotein peroxidation rate in vitro. However, we observed an imbalance between oxidizable substrates and antioxidants with an increased lipid peroxidation, whereas the content of reduced glutathione and beta carotene decreased without any variation in vitamin E. Association of antioxidants with n-3 PUFA could prevent lipid peroxidation and enhance the antiatherogenic effects of n-3 polyunsaturated fatty acids.

Adult↗

Malondialdehyde kit evaluated for determining plasma and lipoprotein fractions that react with thiobarbituric acid.

The determination of thiobarbituric acid reactants (TBARs) is a widely used method for investigating overall lipid peroxidation. An assay kit that could be used with plasma and lipid fractions would facilitate standardization of the method. The results reported here indicate that the malondialdehyde (MDA) kit manufactured by Sobioda (Grenoble, France) complies with criteria of good analytical practices. The detection limit was 0.11 mumol of MDA per liter of plasma. The within-run (CV = 1.8-3.3%) and between-run (CV = 3.3-4.4%) precisions were acceptable. The analytical recovery of MDA after supplementing human plasma samples with tetraethoxypropane standards varied from 88% to 100%. The mean (SD) lipoperoxide concentration determined in 32 healthy adults, ages 20-40 years, was 2.51 (0.25) mumol/L. No significant sex-related difference was noted: 2.57 (0.28) in men vs 2.44 (0.20) mumol/L in women. Applying the method to lipid fractions showed that lipoprotein fractions contain relatively little MDA: 0.07 (0.03) mumol/L of plasma for very-low-density lipoproteins and 0.19 (0.10) mumol/L for low-density lipoproteins.

Adolescent↗

Effect of an acute zinc depletion on rat lipoprotein distribution and peroxidation.

The aim of this study was to determine the extent to which zinc depletion leads to lipoprotein modifications by measuring both lipoprotein-fraction distribution and peroxidation in zinc-depleted rats. The animals were divided into three groups and fed for 8 wk a zinc-adequate diet (100 ppm) ad libitum (AL), a zinc-deficient diet (0.2 ppm) ad libitum (ZD), or a zinc-adequate diet according to the pair feeding method (PF). Trace-element status, tissular lipids, and lipoprotein-fraction study were performed. The MDA production by the lipoprotein fraction was measured before and after induced peroxidation. Cholesterol and phospholipids were increased in ZD rats. An important increase of VLDL and IDL was observed and a significant enhanced production of MDA by the LDL was related to zinc deficiency. From this observation, we may conclude that LDL fractions of ZD rats are more susceptible to induced oxidative damage. These results suggest that in zinc deficiency, the lipoprotein fragility is an aggravating factor of peroxidation and the dyslipoproteinemia may lead to an atherogenic risk.

Animals↗

Zinc deficiency does not enhance LDL uptake by P 388 D1 macrophages in vitro.

The aim of the study was to investigate the effect of zinc depletion on the susceptibility of Wistar rat low-density lipoproteins (LDL) to peroxidation and their uptake by macrophages, before and after in vitro oxidation. The rats were fed for 7 wk a Zn-adequate diet (100 ppm) ad libitum (AL), a Zn-deficient diet (0.2 ppm) ad libitum (ZD), or a Zn-adequate diet according to the pair-feeding method (PF). Zinc status was determined and, for each group, blood was pooled, and LDS were isolated and labeled with 125Iodine. An aliquot of each LDL sample was oxidized using FeII 10 microM/ascorbate 250 microM. Oxidized and nonoxidized (native) LDL were incubated with P 388 D1 macrophages, and their rates of uptake and degradation by macrophages were measured. Before oxidation, LDL uptake and degradation were not modified by the diet, suggesting that Zn deficiency did not modify rat LDL in vivo. After oxidation, both LDL uptake and degradation were significantly enhanced in the three groups. Nevertheless, we did not observe a significant effect of Zn deficiency. This observation suggests that, in our experimental conditions, Zn deficiency did not modify LDL catabolism.

Analysis of Variance↗

[Focalized matrix proteolysis and inflammation].

The zinc metalloproteinases (MMPs or matrixins) are capable of damaging most of the constituents of the extra-cellular matrix and the basement membrane. The matrix proteolysis is the result of an imbalance both in the turnover of these constituants and in the ratio of the tissue inhibitors of metalloproteinases (TIMPs) versus metalloproteinases. After a brief description of the nature and structure of MMPs and TIMPs, this article reports on recent progress concerning the intra and extra-cellular activation mechanisms of proenzymes (proMMPs) which bring into play a series of proteolytic activations involving different proteinase families. Two points are stressed: 1) the main sites of focalized matrix proteolysis regulation, illustrated in the cellular interaction of inflammation, and 2) the wide phenotypic variety of MMPs and TIMPs.

Amino Acid Sequence↗