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PubMed1981

Effect of dietary level of ascorbic acid on the growth, hepatic lipid peroxidation, and serum lipids in guinea pigs fed polychlorinated biphenyls.

Rats exposed to polychlorinated biphenyls (PCB) or other xenobiotics exhibit an increase in tissue and urinary ascorbic acid, serum cholesterol and hepatic lipid peroxidation. To clarify the physiological role of ascorbic acid in exposure to PCB, we studied the influence of dietary levels of ascorbic acid (30-2,000 ppm) on the growth, serum lipids and hepatic lipid peroxidation in guinea pigs fed 50 ppm PCB-containing diets. The results showed that the growth depression due to PCB was ameliorated by increasing dietary ascorbic acid. The increases in serum cholesterol and phospholipid and in hepatic lipid peroxidation due to PCB were suppressed by larger amounts of ascorbic acid, which inversely correlated with the changes in growth. PCB intake also increased serum levels of cortisol and triglyceride, but these effects were not influenced by dietary level of ascorbic acid. The optimum requirement of ascorbic acid in the guinea pigs fed PCB was 800-2,000 ppm in the diet for the changes in the growth, serum cholesterol and hepatic lipid peroxidation.

Animals↗
PubMed2000

The mechanism of Fe(2+)-initiated lipid peroxidation in liposomes: the dual function of ferrous ions, the roles of the pre-existing lipid peroxides and the lipid peroxyl radical.

The mechanism of Fe(2+)-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe(2+) whenever the second dose of Fe(2+) was added, which indicates that Fe(2+) has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe(2+) could no longer initiate lipid peroxidation and the acceleration of Fe(2+) oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOO(.)), N,N'-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe(2+) oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOO(.) are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe(2+) and can be scavenged by its reaction with Fe(2+). Only when Fe(2+) is oxidized to such a degree that LOO(.) is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe(2+) with LOOH and LOO(.) into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe(2+)-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe(2+) to lipid and the required oxidation of Fe(2+).

Animals↗
PubMed1980

Rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system.

Dialyzed rat liver cytosol (105 000 X g supernatant), when added along with 2.5 mM glutathione, blocked malonaldehyde formation in the NADPH-microsomal lipid peroxidation system, thus protecting against lipid peroxidation. Preheating the cytosol for 10 min at 60 degrees C destroyed its protective ability. Ammonium sulfate fractionation and Sephadex G-100 gel filtration of cytosol indicated that more than one glutathione-dependent protective enzyme was present. Fractions from the G-100 column containing the selenoenzyme glutathione peroxidase failed to protect, but fractions containing the glutathione S-transferases, which have non selenium-dependent glutathione peroxidase activity, did protect. The glutathione S-transferases were purified further with ion exchange chromatography and shown to have protective activity. Thus the rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system is in part due to some of the glutathione S-transferases. The selenium-dependent glutathione peroxidase appears to have no protective effect in this system.

Animals↗
PubMed1994

Appearance of homogeneous smectic multilamellar microenvironments in biomembranes undergoing superoxide-initiated lipid peroxidation: lipid-dienyl radical accumulation and fluidity management in lipid bilayers.

Erythrocyte ghosts were exposed to various levels of oxyradical shock in order to identify the extent of accumulation of peroxidative intermediates. Malondialdehyde reacting end products were the same in all different models. But, the accumulation of dienyl radical species increased with higher intensity of oxyradical shock. These dienyl radicals may rearrange to create a homogeneous smectic multilamellar microenvironment which may be more fluid in terms of the molecular dynamics.

Erythrocyte Membrane↗
PubMed1989

The 21-aminosteroid inhibitors of lipid peroxidation: reactions with lipid peroxyl and phenoxy radicals.

The 21-aminosteroids U74006F and U74500A have been examined for their ability to scavenge the lipid peroxyl (LOO.) and phenoxy (PhO.) radicals. Lipid peroxidation was followed by measuring the formation of linoleic acid hydroperoxide (LOOH; 18:200H) from linoleic acid during incubations in methanol at 37 degrees C. Initiation of lipid peroxidation was by the radical generator 2,2'-azobis(2,4-dimethylvaleronitrile; AMVN), which under the conditions employed, initiated LOOH formation at a constant rate of 22 microM/h with a kinetic chain length of 21. Alpha-tocopherol (alpha TC) nearly completely blocked the chain reaction by scavenging LOO., reducing its formation to that essentially attributable to initiation alone. The average inhibition rate constant kinh for alpha TC at 37 degrees C was calculated as 4.9 x 10(5) M-1 sec-1. U74006F or U74500A also inhibited LOOH formation, reducing its rate to a constant fraction of control in a concentration dependent manner. U74500A was a more potent scavenger of LOO. than U74006F; however, both compounds were considerably less potent than alpha TC based upon their respective kinh's at 37 degrees C. Similarly, alpha TC, U74006F and U74500A scavenged PhO.. As seen with LOO. scavenging, alpha TC was orders of magnitude more reactive toward PhO. than either 21-aminosteroid as judged by their respective second order rate constants (k2). Both U74006F and U74500A were degraded during their reaction with LOO. or PhO. to as yet uncharacterized product(s). The data indicate that while the 21-aminosteroids can scavenge lipid radicals, their activity in this regard is less than expected based upon their ability to inhibit iron dependent lipid peroxidation.

Antioxidants↗
PubMedDate not supplied

[Possible role of hypoxia and lipid peroxidation in the development of a neurosis-like condition in the rat].

The chronic emotional pain stress resulting in a development of neurosis-like state in rats induced an increase of arterial pressure and change of the cardiac rate dynamics under the conditions of functional load. An increase of cardiac mass was also seen without change of masses of the thymus, adrenal glands and the spleen. The rise of activity of cytochromeoxidase and activation of peroxide lipide oxidation (by malonate dialdehyde level) were observed in the cerebral cortex and the hippocampus of neurotized rats. Injection of antioxidant F-801 before each emotional pain stress trial prevented vegetative disturbances, cardiac hypertrophy, and increase of oxidative activity in the brain. The role of peroxide lipide oxidation and that of the factor of hypoxia in development of disturbances caused by neurotization were discussed.

Animals↗
PubMedDate not supplied

[Peculiarities of lipid peroxidation indices in Ligula intestinalis (Cestoda: Pseudophyllidea) and its host--Abramis brama (L.)].

A comparative analysis of indices of peroxidation lipids in tissues of Ligula inteslinalis plerocercoids and in the intermediate fish host, the bream Abramis brama, was performed for the content of common lipids (CL), malonate di-aldehyde (MDA), which is a product of lipid peroxidation (POL), and common antioxidate activity (CAA). The dependence of indices upon size of parasites is recovered. The long-sized parasites had higher rate of MDA and intense CAA. The higher rate of MDA and low one of CAA was observed in the infected fishers comparing to the healthy ones.

Animals↗
PubMed1988

Endotoxin causes hydrogen peroxide-induced lung lipid peroxidation and prostanoid production.

We studied the role of hydrogen peroxide release on endotoxin-induced lung injury in unanesthetized sheep with chronic lung lymph fistulas. We also further defined the relationship between endotoxin injury, lipid peroxidation, and prostaglandin production. Sheep were given endotoxin alone (1 microgram/kg) or pretreated with catalase (32,500 U/kg) or ibuprofen (12.5 mg/kg). Endotoxin alone resulted in an early prostanoid release, lipid peroxidation measured as circulating conjugated dienes both one and four hours after the administration of endotoxin, pulmonary hypertension, hypoxia, and increased protein permeability. Permeability was monitored by lymph flow and lymph protein content. Catalase pretreatment significantly attenuated all of these aspects of the endotoxin response. Ibuprofen prevented the early lung changes and blocked prostanoid release but did not attenuate the increased permeability. In addition, cyclo-oxygenase inhibition had a dual effect on lipid peroxidation, increasing initial conjugated diene levels while suppressing the later release. The initial effect was clearly related to cyclo-oxygenase blockade. The early conjugated diene release appears to be related to arachidonic acid metabolism and does not correspond to the degree of increased permeability. We conclude that H2O2 plays a major role in lung injury after endotoxin.

Animals↗
PubMed2000

The effect of dietary treatment on erythrocyte lipid peroxidation, superoxide dismutase, glutathione peroxidase, and serum lipid peroxidation in patients with type 2 diabetes mellitus.

OBJECTIVES: The aim of the present study was to investigate the effect of dietary treatment on serum and erythrocyte lipid peroxidation and erythrocyte antioxidative enzyme activity of patients with Type 2 diabetes. DESIGN AND METHODS: A total of 30 patients with newly diagnosed as Type 2 diabetes were enrolled to the study. A total of 30 healthy subjects served as controls. Diabetic patients were given standard dietary treatment that was composed of 50% to 55% carbohydrate and 30% fat for 2 months. No diet was applied for controls. For both groups serum and erythrocyte lipid peroxidation and erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were obtained at first and at the end of 2 months. RESULTS: Diabetic patients had higher serum and erythrocyte lipid peroxidation than those of controls before dietary treatment(p < 0.05). However, there was no absolute differences in erythrocyte SOD and GSH-Px (p > 0.05). At the end of 2 months of dietary treatment, while diabetics had still higher glucose and erythrocyte lipid peroxidation than controls (p < 0.05), serum lipid peroxidation, erythrocyte SOD, and GSH-Px levels did not differ significantly from those of controls (p > 0.05). In diabetic patients, after 2 months of dietary treatment, whereas serum and erythrocyte lipid peroxidation decreased, erythrocyte SOD and GSH-Px activities showed significant increase (p < 0.05). CONCLUSIONS: Our results showed significant alteration in serum and erythrocyte lipid peroxidation and erythrocyte antioxidant enzyme status of patients with Type 2 diabetes by dietary treatment. However, whether such alterations have clinical importance for diabetic patients needs further investigation.

Adult↗
PubMed1999

Constitutive hsp70 attenuates hydrogen peroxide-induced membrane lipid peroxidation.

Thermal pretreatment improves cardiac recovery from subsequent ischemia/reperfusion. Induction of heat shock proteins (hsps) may contribute to this protection. We have demonstrated that augmentation of the constitutive hsp70 (hsc70) in H9c2 heart myoblasts promotes oxidative resistance. We employed a model oxidant to explore potential target(s) of protection by hsc70. Upon exposure to 54 microM of hydrogen peroxide (H(2)O(2)), hsc70-overexpressing cells exhibited a lower lipid peroxidation than the sham-transfected control. Constitutive hsc70 overexpression, however, did not protect against H(2)O(2)-induced depletion of ATP and glutathione (GSH). Lipid protection also occurred in cells preconditioned at 39 degrees C (selectively induces hsc70) during H(2)O(2) exposure. Interestingly, the protection conferred by hsc70 was comparable in magnitude to that provided by alpha-tocopherol, and was followed with a reduced release of lactate dehydrogenase and a unaltered calcium uptake during H(2)O(2) challenge. Collectively, our observations suggest that hsc70 may preserve membrane function via attenuation of lipid peroxidation during oxidative insult.

Animals↗
PubMed1969

Lipid peroxide formation in microsomes. Relationship of hydroxylation to lipid peroxide formation.

1. Aminopyrine strongly inhibits NADPH-induced lipid peroxide formation in rat liver microsomes, but ascorbate-induced peroxidation is inhibited to a smaller extent. 2. Aminopyrine oxidation is stimulated by Mg(2+) but inhibited by Ca(2+). Concentrated solutions (10mm) of iron-chelating agents inhibit aminopyrine oxidation, but the more dilute solutions (0.5mm) of chelators that block lipid peroxide formation do not inhibit aminopyrine oxidation. Microsomes prepared from sucrose-EDTA homogenates rapidly oxidize aminopyrine, but do not form lipid peroxide when incubated with ascorbate or NADPH. 3. Aminopyrine oxidation is strongly inhibited by p-chloromercuribenzoate, less by iodoacetamide and weakly by N-ethylmaleimide. The site of action of these compounds is considered to be a ferredoxin-type protein. GSH and cysteine also inhibit. 4. Other drugs oxidized by microsomes such as caffeine, phenobarbitone and hexobarbitone had either no or little effect on lipid peroxide formation, but codeine inhibited. 5. Most aliphatic hydrocarbons, alcohols, ketones and aldehydes did not affect lipid peroxide formation, but chloroform and carbon tetrachloride inhibited. 6. Many aromatic compounds inhibited lipid peroxide formation. Only aromatic acids were without any effect and phenols and amines were very strong inhibitors. 7. Induction of lipid peroxide formation in microsomes by incubation with ascorbate or NADPH or by treatment with ionizing radiation leads to a sharp decline in the ability of microsomes to oxidize aminopyrine or hydroxylate aniline. 8. It is considered that the two processes of hydroxylation and lipid peroxide formation are closely linked in microsomes. They probably depend on the same electron-transport chain, and peroxide formation, which involves membrane disintegration, may be part of the normal membrane remodelling process.

Aminopyrine↗
PubMedDate not supplied

[The effect of lipid peroxidation on the lipid and phospholipid composition of mitochondrial membranes during thermal incubation].

Alterations in the content of lipids and phospholipids were studied in rat liver mitochondrial membranes after long-term heating at 37 degrees, pH 7.4, using FeSO4-ascorbate as inductors of lipid peroxidation. Under these conditions, activation of lipid peroxidation in mitochondrial membranes led to a marked increase in the rate of hydrolysis of phosphatidylethanolamine and lysophosphatidylethanolamine, to elevated synthesis of phosphatidylserine, sphingomyelin, phosphatidic and lysophosphatidic acids, diglycerides and cholesterol esters as well as to inhibit hydrolysis of phosphatidylcholine, cardiolipin and their lyso-derivatives.

Animals↗
PubMedDate not supplied

Lipid peroxidation of intravenous lipid emulsions and all-in-one admixtures in total parenteral nutrition bags: the influence of trace elements.

An iodometric titration was used to assess the influence of a daily portion of trace elements on lipid peroxidation of pure lipid emulsions and lipid-containing all-in-one (AIO) admixtures by measuring the peroxide value (PV; mmol peroxides/L). A pure lipid emulsion (Intralipid 20%; Pharmacia & Upjohn, Dubendorf, Switzerland) was stored in ethylvinylacetate bags under light protection (LP) at 40 degrees C with and without trace elements. In absence of trace elements the PV of Intralipid 20% was significantly lower (day 14: 2.77 vs 18.04; p < .001). After the same time period with the same storage conditions the drop in pH was two times higher in presence of trace elements (1.54 vs 0.77). In an AIO admixture with LP stored at 2 degrees C to 8 degrees C, trace elements increased the PV from 0.04 to 0.19 mmol/L (day 29; p < .01). The drop in pH was 0.01 and 0.02 units, respectively. When stored at 20 degrees C to 30 degrees C and exposed to daylight, the PV of the AIO admixture containing trace elements reached 1.92 compared with 0.52 in their absence (day 19; p < .001) with a pH drop of 0.03 and 0.11, respectively (day 29). Although trace elements led to a much higher drop in pH in pure lipid emulsions, no obvious influence on the pH of AIO admixtures was demonstrated. To minimize lipid peroxidation, AIO admixtures should be stored light-protected and refrigerated without trace elements. The latter should be added immediately before administration or should be given separately.

Fat Emulsions, Intravenous↗
PubMed1979

[Lipid peroxides and atherosclerosis. The content of lipid peroxidation products in the blood in ischemic heart disease].

It was established that the content of primary (acylhydroperoxide) and secondary (intermollecular "seams" in aminophospholipids) products of lipid peroxide oxidation in blood of patients with ischemic heart disease is increased against the background of hyperlipidemia and hypercholesterolemia. It is suggested that intensification of lipid peroxide oxidation may play a role in the pathogenesis of atherosclerosis.

Adult↗