Lipid peroxidation in rat uterus

Lipid peroxidation in rat uterus has been studied using NADPH- and ascorbate-induced systems. Lipid peroxidation in rat uterus is low as compared to rat liver. Uterus is more sensitive to ascorbate-induced lipid peroxidation than that induced by NADPH. Uterus contains lower amounts of phospholipids and has a lesser degree of unsaturation in lipids. Co-factor studies show that Fe2+ is more important for ascorbate-induced lipid peroxidation. Endometrium is more sensitive to ascorbate-induced lipid peroxidation than myometrium. It also contains more total lipids and phospholipids besides having a higher degree of unsaturation in the lipids as compared to myometrium. Among the subcellular fractions, mitochondria are more prone to ascorbate-induced lipid peroxidation, whereas microsomes are more sensitive to NADPH-induced lipid peroxidation. Uteri from old rats (24 months) and pregnant rats are more resistant to lipid peroxidation than those from 3-month-old control rats. Uterus of pregnant rats contains more factors which inhibit lipid peroxidation and also has a lesser degree of unsaturation in lipids compared with uterus of control rats. The possible consequences of the resistance of uterus to lipid peroxidation, especially during pregnancy and senescence, are discussed.     

Importance of the polyunsaturated fatty acid to vitamin E ratio in the resistance of rat lung microsomes to lipid peroxidation

Rat lung microsomes and liposomes made from isolated lung microsomal lipids were found to be much more resistant to lipid peroxidation than those from liver in both enzymatic and nonenzymatic systems. The polyunsaturated fatty acid (PUFA) content of isolated lung microsomal lipids was 28% of total fatty acids, while liver was 54%. The vitamin E (α-tocopherol) content of isolated lung microsomal lipids was 2.13 nmol/μmol lipid phosphate and that of liver was 0.43. Individually, neither the lower PUFA content nor higher vitamin E levels could account for the resistance of lung microsomal lipids to peroxidation. Distearoyl-L-a-phosphatidylcholine and/or α-tocopherol were added to liver microsomal lipids to achieve different PUFA to vitamin E ratios at PUFA contents of 28% or 54%, and the resulting liposomes were subjected to an NADPH-dependent lipid peroxidation system utilizing cytochrome P450 reductase, EDTA-Fe⁺³, and ADP-Fe⁺³. Liposomes having PUFA to vitamin E ratios less than approximately 250 nmol PUFA/nmol vitamin E were resistant to peroxidation, whereas lipid peroxidation, as evidenced by malondialdehyde production, occurred in liposomes having higher ratios. When lipid peroxidation occurred, 40%–60% of the liposomal vitamin E was irreversibly oxidized. Irreversible oxidation did not occur in the absence of lipid peroxidation. These studies indicated that the low PUFA to vitamin E ratio in lung microsomes and isolated microsomal lipids was sufficient to account for the observed resistance to lipid peroxidation.     

Role of the lipid peroxidation system of Escherichia coli cells in maintaining their viability in air

The study of 6 E. coli strains differing in their capacity for survival in the air has revealed that the physicochemical characteristics of lipids in microbial cells, such as antioxidizing activity, the concentration of peroxidation products, the content of lipids and their capacity for oxidation, are interrelated, which confirms the existence of the system regulating the peroxidation of lipids in prokaryotic cells, similar to the system regulating lipid peroxidation in eukaryotic cells. The capacity of cells for survival in the air has been shown to depend on the physicochemical state of lipids in cellular membranes.     

The role of thylakoid lipids in the photodamage of photosynthetic activity

The effect of excess light at 10 or 30°C under aerobic or low O₂ condition on peroxidation of thylakoid lipids and primary photochemistry of photoinsynthesis was studied in wheat ( Triticum aestivum L. cv. HD 2329). Photoinhibitory damage to photosythesis was directly proportional to the peroxidation of thylakoid lipids. Photoinhibitory treatment given under low O₂ conditions resulted in significantly less peroxidation of the primary photochemistry of photosythesis measured using chlorophyll fluorescence and photosythetic electron trasport. Short term recovery of F_v/F_m ratio was fast while thylakoid lipids did not show much recovry. However, recovery (of F_v/F_m ratio and thylakoid lipids) was almost complete within 12 h after photoinhibition treatment. A possible relationship between peroxidation of thylakoid lipids and photodamage to photosynthesis is discussed.     

四种中草药抗白内障形成中晶状体脂类过氧化水平及脂类含量的变化

我们观察了中草药防治大鼠半乳糖性白内障形成中脂类含量的变化及脂类过氧化水平。结果表明,与正常晶状体相比,白内障晶状体中总脂类的含量明显降低,总胆固醇的含量及脂类过氧化水平明显升高,总脂类与总胆固醇之比明显下降。而同时分别用黄苓、石斛、菟丝子及玉蝴蝶四种中草药水煎剂灌胃的大鼠晶状体中,总胆类与总胆固醇的含量基本恢复至正常;脂类过氧化水平虽仍高于正常晶状体,但也明显低于白内障晶状体,表明脂类过氧化参与了白内障的形成,上述四种中草药具有抑制脂类过氧化的作用。     

Lipid metabolite involvement in the activation of the human heme oxygenase-1 gene

Cellular effects of ultraviolet A (UVA) radiation include peroxidation of membrane lipids as well as a decrease in intracellular glutathione. We have investigated whether damage to membrane lipids is involved in the activation of the human heme oxygenase-1 gene by UVA. Irradiation of human skin fibroblasts in the presence of the lipophilic antioxidants, butylated hydroxytoluene and a-tocopherol, enhances the UVA-induced HO-1 mRNA accumulation, suggesting that peroxidation of plasma membrane lipids is not involved. Furthermore, sodium ascorbate, which induces lipid peroxidation mainly in the plasma membrane, induces HO-1 mRNA to low levels only. The decrease in GSH by UVA radiation is not affected by the presence of the lipophilic antioxidants while ascorbate treatment increases the intracellular GSH by twofold above controls. These results indicate that peroxidation of internal membrane lipids, a decrease in the intracellular GSH levels and the integrity of the plasma membrane are all important for the UVA-induction of heme oxygenase-1. Both nonenzymatic as well as enzymatic lipid peroxidation metabolites are inducers of heme oxygenase-1. The nonenzymatic lipid peroxidation product 4-hydroxynonenal induces heme oxygenase-1 mRNA up to 40-fold and the phospholipase metabolites diacylglycerol and arachidonic acid induce this mRNA by three-to sixfold above basal levels. We also demonstrate that the cyclooxygenase metabolites of arachidonic acid are important for the UVA-activation of the heme oxygenase-1 gene.     

Effects of opioid neuropeptides on the prostaglandin system and lipid peroxidation processes in the myocardium during stress-induced damage

The stress was subsequenced by lowering of Thromboxane A2 level and activation of peroxidation of lipids without any changes of prostacyclin content in myocardium. It was found that the pre-increase of the opioid peptides in blood plasma led to the absence of prostacyclin and thromboxane dynamic and myocardial lipids peroxidation inhibition during the subsequent stress.     

Aluminum Tolerance Acquired during Phosphate Starvation in Cultured Tobacco Cells

Al toxicity in cultured tobacco cells (Nicotiana tabacum L. cv Samsun; nonchlorophyllic cell line SL) has been investigated in nutrient medium. In this system, Al and Fe(II) (ferrous ion) in the medium synergistically result in the accumulation of both Al and Fe, the peroxidation of lipids, and eventually death in cells at the logarithmic phase of growth (+P cells). A lipophilic antioxidant, N,N[prime]-diphenyl-p-phenylenediamine, protected +P cells from the peroxidation of lipids and from cell death, suggesting that a relationship exists between the two. Compared with +P cells, cells that had been starved of Pi (-P cells) were more tolerant to Al, accumulated 30 to 40% less Al and 70 to 90% less Fe, and did not show any evidence of the peroxidation of lipids during Al treatment. These results suggest that -P cells exhibit Al tolerance because their plasma membranes are protected from the peroxidation of lipids caused by the combination of Al and Fe(II). It seems likely that the exclusion of Fe from -P cells might suppress directly Fe-mediated peroxidation of lipids. Furthermore, since -P cells accumulated [beta]-carotene, it is proposed that this carotenoid pigment might function as a radical-trapping antioxidant in the plasma membrane of cells starved of Pi.     

Mechanisms of the initiation of lipid peroxidation in the synaptosomes of marine teleosts

The initial rates of NAD- and NADPH-dependent enzymic and Fe+-ascorbic acid-dependent nonenzymic lipid peroxidation have been measured in synaptosomes from the brain of 4 teleost species. The rates of peroxidation were compared with lipid composition and fatty acid composition of total lipids in order to reveal factors accounting for the intensity of peroxidation in the excitable membranes from the brain of ectotherms. The data obtained indicate that the rates of enzymic lipid peroxidation do not correlate with lipid and fatty acid compositions, depending on the efficiency of production of oxygen in the active form by pyridine nucleotide-dependent enzymic systems. Activation of lipid peroxidation during adaptation of animals to the environment may be considered as one of the mechanisms which account for compensatory changes in fatty acid composition of the membrane lipids.     

Effects of cystamine and cysteamine on the peroxidation of lipids and the release of proteins from mitochondria

1. Cystamine slightly stimulated the peroxidation of lipids in mitochondria. Maximal effects were obtained at low concentrations (0.5mm). 2. Cysteamine, when allowed to autoxidize, had much stronger effects than cystamine. 3. Cysteamine and GSH did not induce peroxidation when their autoxidation was counteracted. 4. When kept reduced, cysteamine prevented the ascorbate-induced peroxidation of lipids. GSH was less efficient. 5. Cystamine as well as cysteamine prevented the loss of proteins from mitochondria induced by ascorbate, whereas cadaverine, GSSG and GSH were inefficient.     

Effect of lecithin on liver microsomal lipid peroxidation]

The effect of exogeneous (egg) lecithin on peroxidation of microsomal lipids was studied with the view of elucidating the role of various components of lipid substrate in the overall oxidation rate of the lipids. The following processes were studied a) NADPH-dependent microsomal lipid peroxidation in the presence of lecithin; b) ascorbate-dependent microsomal lipid peroxidation in the presence of lecithin; c) oxidation of lipid mixture, isolated from the microsomes, and that of lecithin in the presence of the Fe2+ + ascorbate system; 4) oxidation of lecithin induced by the Fe2+ + ascorbate system. It was found that in the presence of exogeneous lecithin the oxidation of microsomal lipids in inhibited, which is probably due to the peculiarities of lecithin oxidation. It was shown that the specific rate of lecithin oxidation is decreased with an increase in lecithin concentration. Possible mechanisms of lecithin effect on microsomal lipid peroxidation are discussed.     

Peroxidation of liposomal lipids

Free radicals, formed via different mechanisms, induce peroxidation of membrane lipids. This process is of great importance because it modifies the physical properties of the membranes, including its permeability to different solutes and the packing of lipids and proteins in the membranes, which in turn, influences the membranes’ function. Accordingly, much research effort has been devoted to the understanding of the factors that govern peroxidation, including the composition and properties of the membranes and the inducer of peroxidation. In view of the complexity of biological membranes, much work was devoted to the latter issues in simplified model systems, mostly lipid vesicles (liposomes). Although peroxidation in model membranes may be very different from peroxidation in biological membranes, the results obtained in model membranes may be used to advance our understanding of issues that cannot be studied in biological membranes. Nonetheless, in spite of the relative simplicity of peroxidation of liposomal lipids, these reactions are still quite complex because they depend in a complex fashion on both the inducer of peroxidation and the composition and physical properties of the liposomes. This complexity is the most likely cause of the apparent contradictions of literature results. The main conclusion of this review is that most, if not all, of the published results (sometimes apparently contradictory) on the peroxidation of liposomal lipids can be understood on the basis of the physico-chemical properties of the liposomes. Specifically: (1) The kinetics of peroxidation induced by an “external” generator of free radicals (e.g. AAPH) is governed by the balance between the effects of membrane properties on the rate constants of propagation (k _p) and termination (k _t) of the free radical peroxidation in the relevant membrane domains, i.e. in those domains in which the oxidizable lipids reside. Both these rate constants depend similarly on the packing of lipids in the bilayer, but influence the overall rate in opposite directions. (2) Peroxidation induced by transition metal ions depends on additional factors, including the binding of metal ions to the lipid–water interface and the formation of a metal ions-hydroperoxide complex at the surface. (3) Reducing agents, commonly regarded as “antioxidants”, may either promote or inhibit peroxidation, depending on the membrane composition, the inducer of oxidation and the membrane/water partitioning. All the published data can be explained in terms of these (quite complex) generalizations. More detailed analysis requires additional experimental investigations. Dedicated to Prof. K. Arnold on the occasion of his 65th birthday.     

Effects of gallic acid on brain lipid peroxide and lipid metabolism in streptozotocin-induced diabetic Wistar rats

This study evaluated the protective effects of gallic acid on brain lipid peroxidation products, antioxidant system, and lipids in streptozotocin-induced type II diabetes mellitus. Streptozotocin-induced diabetic rats showed a significant increase in the levels of blood glucose, brain lipid peroxidation products, and lipids and a significant decrease in the activities of brain enzymic antioxidants. Oral treatment with gallic acid (10 mg and 20 mg/kg) for 21 days significantly decreased the levels of blood glucose, brain lipid peroxidation products, and lipids and significantly increased the activities of brain enzymic antioxidants in diabetic rats. Histopathology of brain confirmed the protective effects of gallic acid. Furthermore, in vitro study revealed the free radical scavenging action of gallic acid. Thus, our study shows the beneficial effects of gallic acid on brain metabolism in streptozotocin-induced type II diabetic rats. A diet containing gallic acid may be beneficial to type II diabetic patients.     

Properties of liposomes adsorbed by montmorillonite

Adsorption of phosphatidylcholine liposomes by montmorillonite was studied for its effect on peroxidation of phospholipids and structure of the bilayer. The UV spectroscopy has shown that adsorption decreases peroxidation of lipids. A parameter is suggested for estimating an oxidation degree of lipids at the stage of the intensive formation of secondary products of their peroxidation. Fluorescent probes (1-anilinonaphthalene-8-sulphonate and pyrene) are used to establish that structural changes of the bilayer take place in adsorbed liposomes being followed by a decrease in the mobility of surface zones of phospholipid "heads" and by an increase in the polarity of hydrophobic parts of the bilayer.     

Ceroid lipofuscinosis in sheep. I. Bis(monoacylglycero)phosphate, dolichol, ubiquinone, phospholipids, fatty acids, and fluorescence in liver lipopigment lipids

The ceroid lipofuscinoses are inherited lysosomal diseases of children characterized by a fluorescent lipopigment stored in a variety of tissues. Defects in lipid metabolism or the control of lipid peroxidation have been postulated to explain their pathogenesis. In the present study, lipopigment was isolated from the liver of sheep affected with ceroid lipofuscinosis. It was 70% protein, the rest being mainly lipids. These were only one-sixth as fluorescent as total liver lipids, but contained a number of fluorophors. None were major components of the lipopigment or the postulated fluorescent product of lipid peroxidation. Lipopigment lipids included the lysosomal marker bis(monoacylglycero)phosphate that contained 42.9% linoleate and 16.5% linolenate. Lipopigment neutral lipids were dolichol, dolichyl esters, ubiquinone, free fatty acids, and cholesterol, indicative of a lysosomal origin of the lipopigment. Phosphatidylcholine, phosphatidylinositol, phosphatidylserine, and phosphatidylethanolamine were present in proportions and with fatty acid profiles typical of lysosomes. No differences were found between the lipids of total control and affected livers, nor the fatty acid profiles of their phosphatidylcholine, phosphatidylethanolamine, or triglycerides. It is concluded that ovine ceroid lipofuscinosis is not a lipidosis, nor does the lipopigment arise from the abnormal peroxidation of lipids. Strong similarities between the lipopigment and the age pigment lipofuscin were noted.     

Peroxidation of lipids in the brain of active and passive rats during development of poststress depressions

Peroxidation of lipids in a cortex of the large hemispheres, striatum, hippocampus and hypothalamus of rats of the lina KHA and KLA (Koltushi High and Low Avoidance) during development of poststress depressions was studied. After emotional painful act in initial terms of change, peroxidation of lipids had phasic character and differed in precise structural specificity. During maximal development of depression, the most expressed infringements of lipids peroxidation occurred in KHA rats in striatum and hippocampus, and at KLA rats--in the striatum and hypothalamus. The data confirm the important role of initial strategy of behavioral in mechanisms of pathogenesis of poststress psychopathology.     

Lipid peroxidation in hypertrophic rat kidney

During compensatory growth of kidney, microsomal lipid peroxidation is unchanged in the hypertrophy phase and is doubled in a period of hyperplasia. The maximum lipid peroxidation is preceded by a 2-fold increase in the content of cytochrome P-450. Both in microsomes and cytosol, intense peroxidation of lipids is accompanied by a decrease in glutathione content.     

Postradiation changes in Ca2+-ATPase and Mg2+-ATPase in thymocyte plasma membranes]

The rats were irradiated in the doses 1, 5, 4, 7 and 10 Gr and on the 1, 8, 15, 22 and 30 day after the irradiation activity of Ca(2+)-ATPase and Mg(2+)-ATPase and peroxidation lipids in the thymocytes was determined. It was found that postradiation changes in activity of Mg(2+)-ATPase were characterized by a higher sensitivity to the processes of lipids peroxidation as compared to Ca(2+)-ATPase.     

Dietary supplementation with soybean lecithin increases pulmonary PAF bioactivity in asthmatic rats

The prevalence of asthma has risen over the last few decades, and some studies correlate this with the greater consumption of polyunsaturated fatty acids (PUFAs). Dietary PUFAs are known to increase the susceptibility of biological structures to lipid peroxidation, a process by which platelet-activating factor (PAF)-like lipids can be generated. These lipids functionally mimic the bioactivity of PAF, a potent proinflammatory mediator that exerts several deleterious effects on asthma. Thus, this work aimed to investigate if dietary supplementation with soybean lecithin (SL), a source of PUFAs, increases lipid peroxidation and PAF bioactivity in lungs of asthmatic Wistar rats. Animals were separated into groups: control, supplemented, asthmatic, asthmatic supplemented with SL (2 g/kg body weight), asthmatic supplemented with SL (2 g/kg body weight) and dl-α-tocopheryl acetate (100 mg/kg body weight). Asthmatic inflammation increased pulmonary lipid peroxidation, PAF bioactivity, alveolar–capillary barrier permeability and production of nitric oxide. In asthmatics, dietary supplementation with SL promoted an increase in pulmonary lipid peroxidation and PAF bioactivity, and an increase in the permeability of the alveolar–capillary barrier. Moreover, the treatment of asthmatic rats with dl-α-tocopheryl acetate inhibited the lipid peroxidation and decreased the PAF bioactivity. Therefore, the increase in pulmonary PAF bioactivity in asthmatic individuals elicited by the dietary supplementation with SL probably involves the generation of PAF-like lipids. This finding suggests that PAF-like lipids may account for the deleterious effects of dietary PUFAs on asthma.