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At least 19 recordsLinked to original sources
PubMed1979

The mechanism of NADPH-dependent lipid peroxidation. The propagation of lipid peroxidation.

NADPH-dependent lipid peroxidation occurs in two distinct sequential radical steps. The first step, initiation, is the ADP-perferryl ion-catalyzed formation of low levels of lipid hydroperoxides. The second step, propagation, is the iron-catalyzed breakdown of lipid hydroperoxides formed during initiation generating reactive intermediates and products characteristic of lipid peroxidation. Propagation results in the rapid formation of thiobarbituric acid-reactive material and lipid hydroperoxides. Propagation can be catalyzed by ethylenediamine tetraacetate-chelated ferrous ion, diethylenetriamine pentaacetic acid-chelated ferrous ion, or by ferric cytochrome P-450. However, cytochrome P-450 is destroyed during propagation.

Animals↗
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↗
PubMed1978

Relationship between fatty acids and lipid peroxidation in lungs of neonates.

Triglycerides from the lungs of neonatal rats and mice were found to contain large amounts of the polyunsaturated fatty acids, arachidonate (20:4) and docosahexaeonoate (22:6). These fatty acids were diminished or absent in the triglycerides from the lungs of adult rats and mice and both neonatal and adult guinea pigs. No age-related changes were observed in the fatty acid composition of lung phospholipids in any of these species. The presence of arachidonic acid and docosahexaenoic acid in lung triglycerides correlated with the ability of these lungs to peroxidize lipids in vitro in all species. Depletion of lung triglycerides in neonatal rats by fasting abolished this lipid peroxidizing activity.

Age Factors↗
PubMed1979

Inhibition of lipid peroxidation by calcium ions and their protection of steroid hydroxylase activity from peroxidative damage.

Lipid peroxidation of adrenocortical mitochondria and microsomes was greatly stimulated by addition of 1.0 mM or less ferric ions. In the presence of NADPH-yielding system, the formation of corticosterone from endogeneous cholesterol and exogeneous deoxycorticosterone was inhibited as the concentrations of iron increased. Of interest is the fact that 0.5 mM ferric ion-mediated lipid peroxidation was completely abroagated upon addition of 2 mM calcium ions. Accordingly, protected from the peroxidative damage.

Adrenal Cortex↗
PubMed1978

Ethanol-induced hepatotoxicity; experimental observations on the role of lipid peroxidation.

Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.

Animals↗
PubMed1979

Elevation of serum lipid peroxide level associated with doxorubicin toxicity and its amelioration by [dl]-alpha-tocopheryl acetate or coenzyme Q10 in mouse (doxorubicin, toxicity, lipid peroxide, tocopherol, coenzyme Q10).

Elevations of serum lipid peroxide levels were demonstrated in mice after an equitoxic dose of doxorubicin. When BDF1 mice were injected with doxorubicin (20 mg/kg body weight, IP), lipid peroxide levels in sera were elevated 1 day after the injection and the levels declined on subsequent days. 5-Fluorouracil (400 mg/kg body weight, IP) never changed the peroxide levels in serum. Furthermore, it was found that the co-administration of [dl]-alpha-tocopheryl acetate or coenzyme Q10 IM strongly inhibited the doxorubicin-induced elevation of lipid peroxides in serum. The effectiveness of [dl]-alpha-tocopheryl acetate or coenzyme Q10 in reducing the lethality of doxorubicin in mice was also confirmed. These results indicate that the measurement of serum 2-thiobarbituric acid-reacting substances provided a useful measurement of lipid peroxide levels, which may be involved in some way with doxorubicin toxicity, and that the administration of antioxidants provide protection against some of the side effects of doxorubicin.

Animals↗
PubMed1976

Lipid peroxidation and alteration of membrane lipids in isolated hepatocytes exposed to carbon tetrachloride.

Lipid peroxidation, determined by malondialdehyde formation, occurs at a low, but detectable, rate in parenchymal cells isolated from livers of fasted rats. Pretreatment of rats with phenobarbital increased malondialdehyde formation about 2-fold, probably because of the increased amount of endoplasmic reticulum. Lipid peroxidation was increased in the cells by the addition of either NADPH or CCl4, and the effect of the two agents together was more than additive. Phenobarbital pretreatment increased peroxidation due to exposure of the cells to CCl4 but not that associated with NADPH addition. The amount of CCl4 producing a 50% increase in malondialdehyde formation was about 3-fold less for cells from phenobarbital-treated rats than for those from control rats. Decreased cytochrome P450 levels in isolated hepatocytes produced by prior treatment of rats with allylisopropylacetamide enhanced lipid peroxidation from endogenous substrates but did not affect lipid peroxidation caused by the addition of NADPH. Allylisopropylacetamide markedly lowered lipid peroxidation caused by CCl4 in proportion to the loss of cytochrome P450. Malondialdehyde production associated with metabolism of endogenous substrates in the cells, or resulting from incubation of the cells with NADPH was not accompanied by changes in the fatty acid or protein content of three membranous fractions (microsomal mitochondrial, and cell debris) isolated from homogenates of these cells. Exposure of liver cells to CCl4, however, caused major losses in all fatty acids and of protein from the microsomal fraction, but only polyunsaturated fatty acids were decreased in the cellular debris fraction. Incubation with NADPH and CCl4 together enhanced malondialdehyde formation, but caused no further decrease in fatty acid content in these two fractions. Mitochondrial fatty acids were not decreased by any treatments described.

Animals↗
PubMed1979

[Lipid peroxides and atherosclerosis. The enzymatic detoxication of lipid peroxides in the blood in ischemic heart disease due to coronary artery arteriosclerosis].

It was established that in blood of patients with ischemic heart disease due to atherosclerosis of the coronary arteries (the diagnosis was verified in selective coronaroangiography) the content of acylhydroperoxides grows while the activity of glutathione-peroxidase II decreases. In blood of patients with no damage to the coronary vessels (according to the results of angiography), glutathione-peroxidase II activity does not differ significantly from the values in the control group. The decrease of glutathione-peroxidase II activity was most marked in patients with ischemic heart disease and hypercholesterolemia. It is suggested that the increase in the peroxide content in blood of patients with ischemic heart disease may be due to the sharp decrease in the activity of glutathione-peroxidase II.

Adult↗
PubMed1979

Lipid peroxidation and its inhibition by tinoridine, II. Ascorbic acid-induced lipid peroxidation of rat liver mitochondria.

Incubation of rat liver mitochondrial suspension with ascorbic acid and Fe2+ resulted in the formation of malondialdehyde and a decrease in the turbidity of the suspension. The maximum amount of malondialdehyde formed during the peroxidation reaction was estimated to be 1 mol per approximately 6 mol of mitochondrial phospholipids. Tinoridine and alpha-tocopherol at the concentration of 5 micron and 1 mM, respectively, completely inhibited the peroxidative disintegration of mitochondria. From the relationship between the concentration of tinoridine and the amount of malondialdehyde formed, it was demonstrated that 1 mol of tinoridine prevents the formation of about 6 mol of malondialdehyde. These findings suggest that there is a limit in the chain reaction of the lipid peroxidation of mitochondria and that the limit is the membrane sphere which is capable of releasing 6 molecules of malondialdehyde and contains about 36 molecules of the constitutive phospholipids.

Animals↗
PubMed1976

Lactoperoxidase-catalyzed lipid peroxidation of microsomal and artificial membranes.

Lactoperoxidase, in the presence of H2O2, I-, and rat liver microsomes, will peroxidize membrane lipids, as evidenced by malondialdehyde formation. Fe3+ assists in the formation of malondialdehyde. Fe3+ can be added at the end of the reaction period as well as at the beginning with equal effectiveness, suggesting that it only acts to assist in the conversion of lipid peroxides, previously formed by lactoperoxidase, to malondialdehyde. The addition of EDTA to the microsomal reaction mixture results in a 40% decrease in malondialdehyde formation. The antioxidant butylated hydroxytoluene will completely block the formation of malondialdehyde. Malondialdehyde formation is not dependent upon the production of superoxide, singlet oxygen, or hydroxyl radicals. Peroxidation of membrane lipids by this system is equally effective in both intact microsomes and in liposomes, indicating that iodination of microsomal protein is not required for lipid peroxidation to occur.

Animals↗
PubMedDate not supplied

[Role of lipid peroxides in the pathogenesis of arteriosclerosis. Detoxication of lipid peroxides by the glutathione-peroxidase system in the aorta].

In aorta of intact rabbits the high activity of glutathione-peroxidase, which detoxicates lipoperoxides, was observed. In aorta of animals with pronounced experimental atheromatosis the enzyme activity did not distinctly differ from the control values. The animals with high initial content of glutathione-peroxidase in aorta were shown to be less subjected to the impairment in alimentary atherosclerosis.

Animals↗
PubMed1979

Lipid peroxidation of the microsomal fraction and extracted microsomal lipids from DAB-induced hepatomas.

NADPH- and ascorbic acid-induced microsomal lipid peroxidation was almost absent in subcutaneously implanted DAB-induced hepatomas D23, D30 and D192A, and present at greatly reduced levels in DAB-induced primary hepatomas when compared with normal liver controls. Fatty acid analysis of the microsomal lipid from passaged tumours demonstrated adequate levels of substrate in the phospholipid fractions to support lipid peroxidation. Lipid extracted from hepatoma microsomal fractions was shown to undergo ascorbic acid-induced lipid peroxidation, but to a lesser extent that the corresponding liver extract. This may be partially explained by a decrease in the phospholipid content of hepatoma microsomal membranes. However, phospholipid extracted from microsomal fractions of hepatoma and liver supported lipid peroxidation to a similar extent. The possible role of the non-lipid component of the membrane in the process of lipid peroxidation is discussed.

Animals↗
PubMed1975

Superoxide, hydrogen peroxide, and singlet oxygen in lipid peroxidation by a xanthine oxidase system.

1. Xanthine oxidase acting aerobically upon acetaldehyde was found to cause the peroxidation of linolenate. This was demonstrated by increased absorbance at 233 nm due to diene conjugation and by the detection of a lipid peroxide spot on the thin layer chromatograms. 2. Superoxide dismutase inhibited this lipid peroxidation, as did catalase, thus indicating that both O2- and H2O2 were essential intermediates. Scavengers of singlet oxygen also inhibited the peroxidation of linolenate, whereas scavengers of hydroxyl radical did not. These effects, which were observed in the absence of iron salts, led to the proposal that O2- and H2O2 can directly give rise to a singlet oxygen, as follows: O2- + H2O2 leads to OH- + OH. + O2. 3. This proposal was further supported through the use of 2,5-dimethylfuran, as an indicating scavenger of singlet oxygen. Thus, when this compound was exposed to a known source of singlet oxygen, it gave a product which was detectable by thin layer chromatography. This product was also observed when 2,5-dimethylfuran was exposed to the xanthine oxidase system, in which case its accumulation was prevented by superoxide dismutase or by catalase, but not by scavengers of hydroxyl radical.

Acetaldehyde↗
PubMed1975

Lipid peroxidation in isolated hepatocytes.

Intracellular lipid peroxidation was initiated by the addition of ADP-complexed ferric iron to isolated rat hepatocytes and the reaction monitored by the thiobarbituric acid method or by measurement of the formation of conjugated dienes. Both the production of malondialdehyde (thiobarbituric-acid-reacting substances) and of conjugated dienes was dependent, on the ADP-Fe-3+ concentration in a dose-related fashion. Malondialdehyde formation stopped spontaneously within 20 min after the initiation of the reaction and the plateau reached was also related to the ADP-Fe-3+ concentration. Control experiments revealed that more than 90% of the malondialdehyde accumulating during the incubation period could be ascribed to intracellular production. The cellular NADPH/NADP+ ratio was always high and only slightly decreased upon ADP-Fe-3+-induced lipid peroxidation which, however, was associated with a marked decrease in the cellular glutathione concentration. The rate of accumulation of malondialdehyde as well as the final level reached during ADP-Fe-3+-initiated lipid peroxidation was increased by the addition of chloral hydrate. This apparent stimulatory effect could, however, be ascribed to the inhibition of the mitochondrial oxidation of the malondialdehyde formed during cellular lipid peroxidation, thus allowing more malondialdehyde to accumulate during the process. ADP-Fe-3+-induced cellular lipid peroxidation was associated with a decrease in the concentration of glutathione. Also, lowering of the intracellular glutathione level by the addition of diethyl maleate or by simply preincubating the hepatocytes (up to 50 min) promoted the ADP-Fe-3+ malondialdehyde production and formation of conjugated dienes. Furthermore, when cellular glutathione concentration had been lowered by preincubation of the hepatocytes, significant malondialdehyde production could be observed even at ADP-Fe-3+ concentrations which were too low to induce measurable lipid peroxidation in fresh hepatocytes. It is thus concluded that glutathione has an important role in the cell defence against lipid peroxidation and suggested that the isolated hepatocytes provide a suitable experimental model system for the characterization of this and other possible cellular defence mechanisms and how they are affected by the nutritional status of the donor animal.

Adenosine Diphosphate↗
PubMed1978

The role of lipid components of the diet in the regulation of the fatty acid composition of the rat liver endoplasmic reticulum and lipid peroxidation.

The fatty acid compositions of the lipids and the lipid peroxide concentrations and rates of lipid peroxidation were determined in suspensions of liver endoplasmic reticulum isolated from rats fed on synthetic diets in which the fatty acid composition had been varied but the remaining constituents (protein, carbohydrate, vitamins and minerals) kept constant. Stock diet and synthetic diets containing no fat, 10% corn oil, herring oil, coconut oil or lard were used. The fatty acid composition of the liver endoplasmic reticulum lipid was markedly dependent on the fatty acid composition of the dietary lipid. Feeding a herring-oil diet caused incorporation of 8.7% eicosapentaenoic acid (C(20:5)) and 17% docosahexaenoic acid (C(22:6)), but only 5.1% linoleic acid (C(18:2)) and 6.4% arachidonic acid (C(20:4)), feeding a corn-oil diet caused incorporation of 25.1% C(18:2), 17.8% C(20:4) and 2.5% C(22:6) fatty acids, and feeding a lard diet caused incorporation of 10.3% C(18:2), 13.5% C(20:4) and 4.3% C(22:6) fatty acids into the liver endoplasmic-reticulum lipids. Phenobarbitone injection (100mg/kg) decreased the incorporation of C(20:4) and C(22:6) fatty acids into the liver endoplasmic reticulum of rats fed on a lard, corn-oil or herring-oil diet. Microsomal lipid peroxide concentrations and rates of peroxidation in the presence of ascorbate depended on the nature and quantity of the polyunsaturated fatty acids in the diet. The lipid peroxide content was 1.82+/-0.30nmol of malonaldehyde/mg of protein and the rate of peroxidation was 0.60+/-0.08nmol of malonaldehyde/min per mg of protein after feeding a fat-free diet, and the values were increased to 20.80nmol of malonaldehyde/mg of protein and 3.73nmol of malonaldehyde/min per mg of protein after feeding a 10% herring-oil diet in which polyunsaturated fatty acids formed 24% of the total fatty acids. Addition of alpha-tocopherol to the diets (120mg/kg of diet) caused a very large decrease in the lipid peroxide concentration and rate of lipid peroxidation in the endoplasmic reticulum, but addition of the synthetic anti-oxidant 2,6-di-t-butyl-4-methylphenol to the diet (100mg/kg of diet) was ineffective. Treatment of the animals with phenobarbitone (1mg/ml of drinking water) caused a sharp fall in the rate of lipid peroxidation. It is concluded that the polyunsaturated fatty acid composition of the diet regulates the fatty acid composition of the liver endoplasmic reticulum, and this in turn is an important factor controlling the rate and extent of lipid peroxidation in vitro and possibly in vivo.

Animals↗