Long-term efficacy and safety of a new olive oil-based intravenous fat emulsion in pediatric patients: a double-blind randomized study.

BACKGROUND: A new intravenous lipid emulsion (ILE) prepared from a mixture of soybean and olive oils contains only long-chain triacylglycerols, with a low proportion (20%) of polyunsaturated fatty acids and 60% monounsaturated fatty acids. OBJECTIVE: The goal of this randomized, double-blind clinical trial was to assess in children the efficacy and safety of this new ILE compared with a control group receiving a soybean-oil emulsion. DESIGN: Eighteen children received for 2 mo 24% of nonprotein energy (1.80 g kg (-)(1) d(-)(1)) either as the new ILE or a soybean oil-based emulsion. Assessments were performed on days -30, 0, 30, and 60 and the changes (day 60 - day 0) assessed by analysis of variance. RESULTS: There were no significant differences in triacylglycerol, apolipoproteins A-I and B, or HDL cholesterol between the 2 groups, whereas total and LDL cholesterol were higher in the soybean oil group on day 60. The pattern of 20:4n-6 in erythrocyte membranes did not change significantly, nor did the ratio of 20:3n-9 to 20:4n-6. On day 60, 18:1n-9 was significantly higher in the olive oil group, the ratio of Sigma(n)-6 > C(18) + 18:3n-6 to 18:2n-6 was 2.20 +/- 0.09 in the olive oil group and 1.33 +/- 0.16 in the soybean-oil group, and Sigma(n)-3 > C(18) was 3.83 +/- 0.30 in the olive oil group and 4. 03 +/- 0.33 in the soybean-oil group. The peroxidation index was lower after the olive oil treatment. CONCLUSIONS: The olive oil-based emulsion was well tolerated, maintained a normal EFA status, and may be more suitable for prevention of lipid peroxidation than the soybean-oil-based emulsion.

Liver function and plasma antioxidant status in intensive care unit patients requiring total parenteral nutrition: comparison of 2 fat emulsions.

BACKGROUND: Efficacy and safety of an alpha-tocopherol-enriched emulsion incorporating soybean, coconut, olive, and fish oils (SMOF) are compared in terms of biologic parameters to those of soybean oil-based emulsion (LIPOVEN). METHODS: Twenty stressed patients were randomly assigned in a double-blind study to receive at least a 5-day course of total parenteral nutrition. Plasma activities of liver enzymes, C-reactive protein, antioxidant capacity, alpha-tocopherol, retinol, and low density lipoprotein (LDL)-alpha-tocopherol levels were determined. LDL-lipid oxidation is measured after incubation of the LDL in the presence of a prooxidant. RESULTS: The plasma activities of liver enzymes and the phospholipids/apo A1 ratio were increased in both groups. However, in the SMOF group the increases were lower than in the LIPOVEN group and non-significant for the CRP plasma level and the alanineamino-transferase activity. Before parenteral nutrition, the plasma antioxidant status was markedly reduced in both groups. After parenteral nutrition discontinuation, the antioxidant capacity and the amount of LDL-derived oxidation by-products formed were comparable in both groups. There was a significant improvement in plasma lipophilic antioxidant vitamins and LDL-alpha-tocopherol levels only in the SMOF group. CONCLUSIONS: The lower increase of plasma liver enzymes and phospholipids/apo A1 ratio in the SMOF group suggest a better liver function than in the LIPOVEN group. This beneficial effect results in a higher liver mobilization and plasma levels of lipophilic antioxidants. They could, together with higher delivery of omega-3 fatty acids to peripheral tissues, contribute positively to survival rate of stressed patients.

Lead effect on the oxidation resistance of erythrocyte membrane in rat triton-induced hyperlipidemia.

The anemia observed in severe chronic lead poisoning is in part attributable to alterations in the erythrocyte physicochemical properties. Since they are partly related to the membrane lipid composition, the aim of the present study was to determine the effects of a triton-induced hyperlipidemia on the resistance to oxidation of erythrocyte membranes in lead-treated Wistar rats. Our results showed that triton administration to lead-treated rats induced an increase in erythrocyte choline phospholipid levels together with a significant decrease in the erythrocyte membrane lipid resistance to oxidation. These results led us to suggest that anemia in lead poisoning is linked to interactions between lead present in the membrane and plasma phospholipids. Their increase in rat hyperlipidemia induced by triton resulted in a decrease in the membrane resistance to oxidation and finally in an erythrocyte fragility leading to their destruction.

[In vitro peroxidation of plasma and erythrocyte lipids during WR-1339 induced hyperlipidemia in Wistar rats]. / Peroxydation in vitro des lipides plasmatiques et érythrocytaires au cours de l'hyperlipémie post-triton WR-1339 chez le rat Wistar.

The inhibition of lipoprotein catabolism after triton WR-1339 intravenous administration is associated with an impressive modification in the balance between plasma peroxidable substrates and antioxidants. Treated rat plasma and membrane lipids become peroxiaable when they are incubated with phenylhydrazine in standardized conditions and the production of thiobarbituric acid-reactive substances (lipoperoxidation markers) significantly increases. An accumulation of native lipoproteins which present a decreased alpha-tocopherol on triglycerid ratio and a modification in the plasmatic balance between alpha-tocopherol and ascorbate could explain these observations.

Resistance to oxidation of native lipoproteins and erythrocyte membrane lipids in rats with iron overload.

Iron plays a promoting role in lipid oxidation through several mechanisms. Therefore, hepatic iron deposits in the rat may lead to peroxidative damage and to alterations in the lipoprotein formation. In this report we observed that an iron overload in rats strongly reduced the hepatic lipoprotein secretion but did not affect oxidation resistance of native lipoproteins and erythrocyte lipids in spite of tocopherol and ascorbate deficiencies. Since oxidation resistance depends on the substrate to antioxidant vitamin molar ratio, our results show that an iron overload probably alters the lipoprotein lipid fatty acid composition in rats.

Iron chelation by deferoxamine inhibits lipid peroxidation during cardiopulmonary bypass in humans.

Iron catalysis is involved in oxygen-derived free radical generation and subsequent lipid peroxidation, which have been reported to occur during cardiopulmonary bypass in humans. We assessed the effects of the iron chelator deferoxamine on the susceptibility of circulating low density lipoproteins (LDLs) to induced peroxidation in 20 adult patients (10 controls and 10 treated) undergoing cardiopulmonary bypass for coronary or valve procedures. Deferoxamine was given both intravenously (30 mg/kg body wt, starting 30 minutes before bypass and extending for the next 4 hours) and as an additive to the cardioplegic solution (250 mg/l). Blood samples were taken from both atria before and immediately after the end of cardiopulmonary bypass. Plasma lipid peroxidation was assessed by measuring spectrophotometrically the thiobarbituric acid reactive substances (TBARS) content of selectively isolated LDLs after their exposure to a peroxidizing agent. Before cardiopulmonary bypass, the right and left atrial blood values of LDL-TBARS were not significantly different between the two groups. Cardiopulmonary bypass resulted in a lipid peroxidation of significantly greater magnitude in control than in treated patients. Postbypass right atrial values for LDL-TBARS (expressed in mumol/mmol LDL-phospholipids) were 45.7 +/- 17.2 (mean +/- SEM) in control patients and 6.9 +/- 2.9 in treated patients (p less than 0.02), whereas in the left atrial blood, LDL-TBARS yielded values of 62.7 +/- 20.5 and 10.3 +/- 3.9, respectively (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Low-density lipoprotein ability to generate lipoperoxides in healthy subjects: variations according to age.

Oxidized low-density lipoproteins (LDLs) are recognized to be involved in atherosclerosis development. Since the plasma oxidized LDL assay is inadequate because of the short half-lives of LDLs, measurement of the in vitro ability of LDLs to generate lipoperoxides (LDL-GLs) has been preferred. The present study displays a profile of LDL-GLs in a group of 175 healthy subjects, using a method to measure thiobarbituric acid-reactive substances. We have observed an increased LDL-GL level according to age.

Increased ability of LDL from normolipidemic type 2 diabetic women to generate peroxides.

BACKGROUND: We assessed the ability of LDL from 30 type 1 diabetic patients (18 men, 12 women), 65 type 2 diabetic patients (35 men, 30 women), and 35 controls (19 men, 16 women) to generate peroxides. The men and women in the diabetic groups were studied separately and matched for age, body mass index, duration of diabetes, glycohemoglobin, and conventional lipid characteristics according to the presence or absence of hyperlipidemia. METHODS: The ability of LDL to form peroxides was assessed by measuring the thiobarbituric acid-reactive substances corrected for LDL-cholesterol [ratio of malondialdehyde (MDA) to LDL-cholesterol]. LDL particle size was expressed as the ratio of LDL-cholesterol to apolipoprotein B (LDL-cholesterol/apoB). RESULTS: The MDA/LDL-cholesterol ratio was higher in type 1 and type 2 diabetic patients with hyperlipidemia than in controls. The MDA/LDL-cholesterol ratio was also higher in type 2 normolipidemic women than in controls (P <0.01). The LDL-cholesterol/apoB ratio was lower in type 2 diabetic women than in type 2 diabetic men (P <0.05). The MDA/LDL-cholesterol ratio was negatively correlated with the LDL-cholesterol/apoB ratio (r = -0.78, P <0.001) in hyperlipidemic type 1 (not type 2) diabetic patients. In normolipidemic type 2 diabetic patients, the MDA/LDL-cholesterol ratio was also negatively correlated with the LDL-cholesterol/apoB ratio (r = -0.75, P <0.001) because of the highly significant negative correlation in type 2 diabetic women (r = -0.89, P <0.01). CONCLUSIONS: LDL from well-controlled type 2 diabetic women is smaller and more prone to form peroxides. This could explain why diabetic women are at greater risk of cardiovascular disease.

Weak resistance to oxidation of native lipoproteins in Wistar rats.

We report an impressive decline in plasma lipid resistance to oxidation during Triton-WR-1339-induced hyperlipidemia in rats. This decline is associated with a modification in the balances between alpha-tocopherol and lipids and alpha-tocopherol and ascorbate. These results are consistent with a weak resistance of accumulated native lipoproteins in plasma to oxidation, during a 6-hour time course, and they suggest a misunderstood role of lipoprotein catabolic enzymes: to improve this characteristic. Conclusively, the results lead us to propound Triton-induced hyperlipidemia as an original model for studying the balance impairment between antioxidants and oxidizable substrates.

Vitamin E and coronary heart disease in Tunisians.

BACKGROUND: Vitamin E (VE) is thought to be effective in preventing atherosclerosis. However, to date no consistent relationship has been identified between VE and coronary heart disease (CHD). This study was designed to assess the degree of association between VE and CHD in a sample of the Tunisian population. METHODS: Sixty-two angiographically confirmed coronary atherosclerotic patients and 65 age- and sex-matched controls were included. VE was measured in plasma and in the LDL fraction by HPLC. Cholesterol, triglycerides, and phospholipids were measured by enzymatic methods. RESULTS: A trend toward a meaningful decrease of plasma VE was observed in affected patients compared with controls (P: = 0.06). VE concentrations standardized for cholesterol and lipid concentrations were significantly lower (P: <0.02) in coronary patients than in controls (4.35 +/- 1.03 vs 4.82 +/- 1.23 mmol/mol for cholesterol-adjusted VE and 2.35 +/- 0.56 vs 2.66 +/- 0.65 mmol/mol for lipid-adjusted VE, respectively). In the LDL fraction, only cholesterol-standardized VE was significantly lower in cases than controls (3.84 +/- 1.13 vs 4.41 +/- 1.16 mmol/mol). This association between VE and CHD remained unchanged independent of age, sex, smoking habit, hypertension, and diabetes. In CHD patients, lower lipid-adjusted VE was associated with enhanced LDL susceptibility to oxidation but without alteration of the serum fatty acid profile. CONCLUSIONS: These results support the hypothesis that VE plays a role in preventing atherosclerosis.