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PubMedDate not supplied

Lipid peroxidation intensity and lipid status parameters in the estimation of the severity of ischemic heart disease.

Atherosclerotic changes on the coronary arteries are the basis of the ischemic heart disease. It is assumed that the initial changes in this process occur as a consequence of the lipid peroxidation in the vessel wall. We estimated this process through the level of malondialdehyde (MDA) in the serum of 86 patients in whom selective coronary angiography was done for the suspected ischemic heart disease. According to the number of the stenotic coronary arteries (stenosis greater than 50%), we divided the patients into four groups: the control group with normal coronary angiography finding, simple, double or triple vessel coronary disease. In all the patients we also estimated the other parameters of the lipid status (cholesterol, triglycerides, LDL, HDL, Apo-AI, Apo B) and atherogenic indices Apo-AI/Apo B, LDL/HDL and HDL/total cholesterol. No significant changes were observed in the lipid parameters between the control and experimental group. However, mean MDA level in the whole experimental group was 3.89 mumol/L, 3.93 mumol/L in triple vessel coronary disease, 3.83 mumol/L in double vessel and 3.92 mumol/L in single vessel disease group. The difference between all the experimental and the control group was highly significant (p < 0.001). We concluded that the level of MDA--lipid peroxidation index had the better correlation with the disease status than the other parameters of lipid status and the sensitive atherogenic indices.

Adult↗
PubMed1990

Increased levels of lipid peroxides in aged rat brain as revealed by direct assay of peroxide values.

Lipid peroxide concentrations in brain tissues of young and aged rats were determined by a direct method for measuring peroxide values. Three different brain regions were analyzed for lipid peroxides. The peroxide levels increased in all three regions of aged as compared to those of young rats, while lipid peroxides in plasma appeared to be stable along with age. Lipid peroxides in cerebrum and cerebellum increased 1.6-2.0 times in aged brains compared with young ones, and about 3-fold in the brain stem. Increased levels of lipid peroxides in aged brains seem not merely due to increased pools of precursor polyene fatty acids, but rather due to altered protection systems for lipid peroxidase formation.

Aging↗
PubMed1984

Evidence for the accumulation of peroxidized lipids in membranes of senescing cotyledons.

Fluorescent products of lipid peroxidation accumulate with age in microsomal membranes from senescing cotyledons of Phaseolus vulgaris. The temporal pattern of accumulation is closely correlated with a rise in the lipid phase transition temperature reflecting the formation of gel phase lipid. Increased levels of fluorescent peroxidation products are also detectable in total lipid extracts of senescent cotyledons. Lipoxygenase activity increases with advancing age by about 3-fold on a fresh weight basis and 4-fold on a dry weight basis indicating that the tissue acquires elevated levels of lipid hydroperoxides. As well, levels of glutathione and superoxide dismutase activity decline on a dry weight basis as the cotyledons age, rendering the tissue more susceptible to oxidative damage. Catalase activity rises initially and then declines during senescence, but peroxidase activity rises steeply. Thus, apart from this increase in peroxidase, which would scavenge H(2)O(2) only if appropriate cosubstrates were available, the defense mechanisms for coping with activated oxygen species (O(2) (-), H(2)O(2), OH) are less effective in the older tissue. The observations support the contention that formation of gel phase lipid in senescing membranes is attributable to lipid peroxidation and suggest that the reactions of lipid peroxidation are utilized by the cotyledons to mediate deteriorative changes accompanying the mobilization and transport of metabolites from the storage tissue to the developing embryo.

Journal Article↗
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↗
PubMedDate not supplied

[The effect of cadmium chloride and hydrogen peroxide on the lipid peroxidation and fractional composition of lipids in hepatocytes of rats].

The isolated hepatocytes were incubated in the medium, containing cadmium chloride or hydrogen peroxide. Influence of the latter on the intensity of lipid peroxidation and contents of some lipids fractions, as well as viability of hepatocytes in these conditions has been studied. It is shown that under such cultivation conditions the activation of lipid peroxidation in the hepatocytes takes place. Its activation in presence of cadmium chloride was one of the factors of the membranes damage. The changes in the content of some fractions of lipids were similar both under the incubations of the cells with cadmium chloride and hydrogen peroxide. This allows one to suppose that cadmium chloride causes changes in the lipid composition of membranes as a result of intensification of lipid peroxidation.

Animals↗
PubMedDate not supplied

Effects of vitamin E deficiency and nitrogen dioxide exposure on lung lipid peroxidation: use of lipid epoxides and malonaldehyde as measures of peroxidation.

The effect of vitamin E deficiency in male Sprague-Dawley rats upon lipid peroxidation in lung tissue was examined by measuring malonaldehyde and lipid epoxide production. In addition to controls, some animals were also exposed to 3 +/- 0.1 ppm NO2 continuously for 7 d in order to study the effects of oxidant stress on lung lipid peroxidation and vitamin E content. The observed changes in malonaldehyde and epoxide content could serve as good indices of lipid peroxidation, particularly under conditions of vitamin E deprivation. The responses measured indicated an inverse relation in the lung between tissue vitamin E content and quantity of lipid peroxidation products. Measurement of lipid epoxides served as a reliable indicator of lung tissue lipid peroxidation. Finally, NO2 inhalation appeared to elicit a response characterized by increased assimilation of vitamin E into lung tissue.

Animals↗
PubMed1991

[A study of lipid peroxidation in neonates--(1) Daily change of serum lipid peroxides in full term neonates].

Lipid peroxide has been highlighted as a possible marker of cell destruction by oxygen derived free radical reactions. We, therefore, examined serum lipid peroxides, malondialdehydes (MDA) in 106 healthy full term neonates (aged 0.5 to 317 hrs, averaged 79.3 +/- 69.9 hrs). Their lipid peroxides in capillary blood were determined by the luminescence method (Yagi method). Based on our data, we conclude as follows: 1) MDA concentrations were influenced by the serum bilirubin concentrations. We, therefore, adjusted our data according to the serum bilirubin concentrations. 2) We found significantly higher values of MDA (4.76 +/- 1.35 nmol.ml-1) than those in adult (3.12 +/- 0.35 nmol.ml-1). In fact, these values increased gradually on the second day, and the high values were maintained until the fifth day. 3) The values of MDA and total bilirubin concentrations in the vaginally delivered neonates were significantly higher than those delivered by Cesarean section (P less than 0.05). 4) There were no correlations between the values of MDA and values of other serum lipid and bilirubin.

Humans↗
PubMed1993

Differential effects of extracellular calcium on lipid peroxidation dependent (ethacrynic acid and allyl alcohol) and lipid peroxidation independent (disulfiram)-induced cytotoxicity in normal and vitamin E-deficient rat hepatocytes.

Hepatocytes have been isolated from normal and vitamin E-deficient rats in which the hepatic vitamin E level was less than 6% that of controls. The hypothesis was tested that extracellular calcium ameliorates chemical-induced cell killing because it decreases the extent of vitamin E loss induced by oxidative stress: such a retarding effect of calcium on cytotoxicity should be lost in hepatocytes from vitamin E-deficient rats. In normal hepatocytes, allyl alcohol and ethacrynic acid induced oxidative stress as indicated by GSH depletion, lipid peroxidation and cell death. Extracellular calcium retarded the induction of lipid peroxidation and cell death without affecting the GSH depletion. In vitamin E-deficient cells, extracellular calcium had lost its protective effect on ethacrynic acid- and allyl-alcohol induced cytotoxicity; it did not affect the GSH depletion and subsequent induction of lipid peroxidation and cell death by ethacrynic acid. However, in vitamin E-deficient hepatocytes, extracellular calcium even potentiated the cytotoxicity of allyl alcohol; under those conditions it also increased GSH loss. Neither in normal, nor in vitamin E-deficient hepatocytes, extracellular calcium had an effect on disulfiram-induced cytotoxicity, i.e. cell death in the absence of lipid peroxidation. These results support the hypothesis that the protecting effect of extracellular calcium on cytotoxicity, associated with lipid peroxidation in normal hepatocytes, is mediated by its protection against intracellular vitamin E loss.

1-Propanol↗
PubMed1998

Linoleic acid peroxidation--the dominant lipid peroxidation process in low density lipoprotein--and its relationship to chronic diseases.

Modern separation and identification methods enable detailed insight in lipid peroxidation (LPO) processes. The following deductions can be made: (1) Cell injury activates enzymes: lipoxygenases generate lipid hydroperoxides (LOOHs), proteases liberate Fe ions--these two processes are prerequisites to produce radicals. (2) Radicals attack any activated CH2-group of polyunsaturated fatty acids (PUFAs) with about a similar probability. Since linoleic acid (LA) is the most abundant PUFA in mammals, its LPO products dominate. (3) LOOHs are easily reduced in biological surroundings to corresponding hydroxy acids (LOHs). LOHs derived from LA, hydroxyoctadecadienoic acids (HODEs), surmount other markers of LPO. HODEs are of high physiological relevance. (4) In some diseases characterized by inflammation or cell injury HODEs are present in low density lipoproteins (LDL) at 10-100 higher concentration, compared to LDL from healthy individuals.

Aging↗
PubMedDate not supplied

Lipid peroxidation in autoimmune systemic vasculitides. Effect of corticoid treatment on lipid peroxidation. Antioxidant protection with vitamin E.

The effect of treatment with prednisone on lipid peroxidation and on lipid metabolism generally and the effect of vitamin E on plasma lipid peroxidation were studied in a group of patients with autoimmune systemic vasculitides. Vitamin E total plasma antioxidant capacity was determined to ascertain the antioxidant efficiency of vitamin E. Treatment with prednisone was found to induce disturbances of the lipid metabolism at the level of total cholesterol and of triglycerides. The increased values of the LDL/HDL ratio showed an increased risk of vascular disturbance in the patients investigated. The high level of lipid peroxides associated with a reduced activity of the endogenous antioxidant system was found to be uninfluenced by treatment with prednisone. Treatment with vitamin E reduced the process of lipid peroxidation but the endogenous deficiency of the antioxidant capacity prevented it to resume its normal values. In spite of the antiinflammatory and antioxidant treatment the high level of lipid peroxides might induce a self-maintained chronic process which, in time, might lead to the aggravation of the degenerative vascular changes.

Adult↗
PubMed1991

Peroxide-dependent and -independent lipid peroxidations catalyzed by chelated iron.

Oxidation of linoleic acid (LA) in tetradecyltrimethylammonium bromide micelles was induced by ferrous- and ferric-chelates in the presence of linoleic acid hydroperoxide (LOOH). Ferrous-chelates also induced lipid peroxidation in the presence of H2O2, but ferric-chelates did not, thought they could generate OH-radicals in the presence of H2O2, resulting in deoxyribose degradation. Of the chelators tested, nitrilotriacetic acid (NTA) chelated with iron showed the highest activity for induction of H2O2- and LOOH-dependent lipid peroxidations and H2O2-dependent deoxyribose degradation. NTA with ferrous ion, but not with ferric ion, also initiated oxidation of LA after a short lag period in the absence of peroxides such as H2O2 and LOOH, but other chelators with ferrous ion did not. The peroxide-independent lipid peroxidation and associated oxidation of ferrous-NTA to ferric-NTA progressed in two steps: an induction step in a lag period and then a propagation step. Ferrous ion complexed with NTA was autoxidized pH-dependently and synchronously with oxygen uptake. The rates of both reactions increased with increase of pH, but were not related to the length of the lag period, which was also dependent on pH, and was shortest at pH 4.2. The EPR spectrum of the ferric-NTA complex prepared directly from ferric salt was different from that of the complex prepared from ferrous salt, confirming that some ferric-type active oxygen participated in induction of peroxide-independent lipid peroxidation. From these results, we propose a possible mechanism of lipid peroxidation induced by ferrous-NTA without peroxides. The finding that iron-NTA had the highest activity for induction of the oxidations of LA and deoxyribose is discussed in relation to the carcinogenic and nephrotoxic effects of this chelating agent.

Catalysis↗
PubMed2003

DNA damage caused by lipid peroxidation products.

Lipid peroxidation is a process involving the oxidation of polyunsaturated fatty acids (PUFAs), which are basic components of biological membranes. Reactive electrophilic compounds are formed during lipid peroxidation, mainly alpha, beta-unsaturated aldehydes. These compounds yield a number of adducts with DNA. Among them, propeno and substituted propano adducts of deoxyguanosine with malondialdehyde (MDA), acrolein, crotonaldehyde and etheno adducts, resulting from the reactions of DNA bases with epoxy aldehydes, are a very important group of adducts. The epoxy aldehydes are more reactive towards DNA than the parent unsaturated aldehydes. The compounds resulting from lipid peroxidation mostly react with DNA showing both genotoxic and mutagenic action; among them, 4-hydroxynonenal is the most genotoxic, while MDA is the most mutagenic. DNA damage caused by the adducts of lipid peroxidation products with DNA can be removed by the repairing action of glycosylases. The formed adducts have been hitherto analyzed using the IPPA (Imunopurification-(32)P-postlabelling assay) method and via gas chromatography/electron capture negtive chemical ionization/mass spectrometry (GC/EC NCI/MS). A combination of liquid chromatography with electrospray tandem mass spectrometry (LC/ES-MSMS) with labelled inner standard has mainly been used in recent years.

Acrolein↗
PubMed1983

[Modification of an enzymic system of Ca2+ transport in sarcoplasmic reticulum membranes during lipid peroxidation. Induction and regulation systems of lipid peroxidation in skeletal and heart muscles].

The enzymic and non-enzymic systems which induce and control lipid peroxidation (LPO) in muscle cells were studied. The maximal activity of enzymic NADH- and NADPH-dependent LPO was observed in sarcoplasmic reticulum (SR) membranes. It was found that an essential role in enzymic LPO induction belongs to superoxide radical anions and to hydroxyl radicals. The maximal concentration of the natural LPO inhibitor, alpha-tocopherol, was detected in SR membranes. The glutathione peroxidase and superoxide dismutase activities were determined in the cytosol fraction of myocytes. The role of compartmentation of enzymic and non-enzymic systems of LPO induction in muscle cells is discussed.

Animals↗
PubMed2000

Inhibition of glucose-induced insulin secretion by 4-hydroxy-2-nonenal and other lipid peroxidation products.

Lipid peroxidation due to oxidative stress is accelerated under hyperglycemic conditions such as diabetes mellitus. The effect of 4-hydroxy-2-nonenal (HNE) and other lipid peroxidation products on the ability of isolated rat pancreatic islets to secrete insulin was examined in this study. HNE concentration- and time-dependently deteriorated glucose-induced insulin secretion: insulin secretion was decreased by 50% when measured after incubation of islets with 100 microM HNE for 1 h. Other lipid peroxidation products, e.g. 2-hexenal and 2-butenal, also inhibited glucose-induced insulin secretion. HNE at 100 microM lowered alpha-ketoisocaproate-induced insulin secretion, whereas leucine-induced insulin secretion was stimulated. Insulin secretion induced by 10 mM glyceraldehyde was slightly decreased by HNE. On the other hand, HNE severely decreased insulin secretion induced by 10 mM glyceraldehyde and 2.8 mM glucose. Glucose utilization and glucose oxidation were significantly lowered in islets treated with HNE. The amounts of fructose 1,6-bisphosphate and dihydroxyacetone phosphate in islets were decreased by treatment with HNE, whereas the amount of fructose 6-phosphate was increased. Our study indicates that HNE and other lipid peroxidation products impair insulin secretion induced by glucose probably through affecting both the glycolytic pathway and the citric acid cycle.

Aldehydes↗
PubMed1994

Inhibition of S-(1,2-dichlorovinyl)-L-cysteine-induced lipid peroxidation by antioxidants in rabbit renal cortical slices: dissociation of lipid peroxidation and toxicity.

Precision-cut, rabbit renal slices were used to examine the effects of three novel antioxidants (U-74006, U-74500, and U-78517) on S-(1,2-dichlorovinyl)-L-cysteine (DCVC)-induced lipid peroxidation and toxicity. Slices exposed to DCVC showed a dose- and time-dependent increase in lipid peroxidation (TBARS) and a decrease in cellular viability, as evidenced by the loss of intracellular potassium, during the course of a 3 hour incubation. Subsequent studies employed DCVC concentrations of 100 microM. Microemulsion formulations of U-78517, U-74500, and U-74006 (100 microM) inhibited DCVC-induced lipid peroxidation by 100 +/-, 50 +/-, and < 5% (not significant), respectively. However, none of these antioxidants had a significant effect on DCVC-dependent cytotoxicity, as indicated by intracellular potassium release. The effects of U-78517, the most potent of the three antioxidants, were similar to those observed with two model antioxidants, diphenyl-p-phenylenediamine (DPPD) and the iron chelator, deferoxamine. Aminooxyacetic (AOAA), an inhibitor of renal cysteine conjugate beta-lyase, had only a minimal effect on DCVC-induced lipid peroxidation, and no effect on toxicity. These data represent the first report of DCVC-induced lipid peroxidation in rabbit renal cortical slices, a system which has been widely used to investigate mechanisms of nephrotoxicity, including that induced by DCVC. Our results demonstrate that DCVC-induced lipid peroxidation in renal slices can be inhibited by a variety of antioxidant compounds operating by different mechanisms. Because inhibition of lipid peroxidation had minimal effect on DCVC-dependent cytotoxicity, the data suggest that DCVC-induced lipid peroxidation is not a major mechanism in the cytotoxicity induced by this compound.

Aminooxyacetic Acid↗
PubMed1981

Lipid peroxide levels and lipids content of serum lipoprotein fractions of pregnant subjects with or without pre-eclampsia.

Total serum lipids in normal pregnant subjects were significantly higher than those in non-pregnant subjects. This was due to an increase in the lipid content in all of the lipoprotein fractions, especially in VLDL. Serum lipids in pre-eclamptic subjects were higher than those in normal pregnant subjects. This was due to the increase in both VLDL and LDL. Serum lipid peroxide levels in pregnant subjects were significantly higher than those in non-pregnant subjects and further elevation of the levels was observed in pre-eclamptic subjects. The elevation of the peroxide levels in normal pregnant subjects was due to changes in all of the fractions of serum lipoproteins, especially in VLDL. The further elevation of peroxide in pre-eclamptic subjects resulted from an increase in HDL fraction.

Female↗