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PubMed1993

Oxy-radicals, lipid peroxides and essential fatty acids in patients with glomerular disorders.

It is now believed that free radicals and eicosanoids participate in the pathogenesis of immune mediated mesangial cell injury and renal tissue damage including glomerulonephritis. But relatively little information is available about the role of essential fatty acids, (EFAs), the precursors of eicosanoids, in renal diseases. We studied the levels of superoxide anion, hydrogen peroxide, lipid peroxides and the concentrations of various metabolites of EFAs in the plasma phospholipid fraction of patients with glomerular disorders. A significant increase in the production of superoxide anion and hydrogen peroxide both by unstimulated and phorbol-myristate acetate (PMA)-stimulated leukocytes, increase in the plasma lipid peroxide levels and a marked reduction in the levels of arachidonic acid (AA) and eicosapentaenoic acid, the precursors of 2 and 3 series prostaglandins (PGs) respectively, were observed in these patients. Since eicosapentaenoic acid and prostacyclin, which is derived from AA, are believed to be of benefit in the prevention of progression of renal disease, and as free radicals can cause renal dysfunction, our results suggest that free radicals and the metabolites of EFAs play a significant role in the pathogenesis of glomerular disorders.

Adolescent↗
PubMed1992

Lipid peroxidation capacities in the myocardium of endurance-trained rats and mice in vitro.

The endurance-training programme in Experiment 1 (Exp. 1) consisted of a total swimming time of 149-159 h per male Han Wistar rat and in Experiment 2 (Exp. 2) the male NMRI-mice run on a treadmill at a speed of 25 m min-1 1 h per day, 5 days a week for 3 weeks. One group of the rat hearts was perfused with 0.3 mM cumene hydroperoxide (CumOOH) while the others were fractioned (mitochondria, sarcolemma and sarcoplasmic reticulum) and these cell fractions and homogenates were used to determine the total concentration of peroxidative lipids and the susceptibility to lipid peroxidation. The perfusion with CumOOH caused the release of thiobarbituric acid reactive substances (TBARS) into the perfusate. The release of TBARS from the trained hearts was smaller than that of the control hearts (P < 0.01). The concentration of TBARS was also smaller in the myocardium of the right ventricle of the trained rats (P < 0.01). The concentration of reduced GSH remained at a higher level after the CumOOH perfusion suggesting a better redox state in the hearts of trained animals. The concentration of the lipids susceptible to lipid peroxidation was lower in the homogenates of the trained rat hearts (P < 0.05). However, this decrease could not be explained by any of the tissue fractions used when studied in rat hearts. In Exp. 2 the total concentration of lipids susceptible to peroxidation remained unchanged in the mice hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of fig latex on lipid peroxidation and CCl4-induced lipid peroxidation in rat liver.

The oral and intraperitoneal effects of fig milk latex on lipid peroxidation and CCl4-induced lipid peroxidation in liver homogenates of female rats were investigated. Oral treatment had no effect, while i.p. administration produced a significant increase in hepatic lipid peroxidation. When the latex was given before CCl4 treatment; it produced no protective effect against CCL4-induced hepatotoxicity. Addition of the latex to the incubation mixture produced a dose-dependent increase in lipid autoxidation, while the chloroform and ether extracts of the latex, as well as heated latex, had no effect on hepatic lipid autoxidation.

Administration, Oral↗
PubMed2000

Interactions of nitric oxide with lipid peroxidation products under aerobic conditions: inhibitory effects on the formation of malondialdehyde and related thiobarbituric acid-reactive substances.

Under aerobic conditions, exposure of peroxidized lipids to nitric oxide (NO) was found to result in a rapid decrease in the levels of thiobarbituric acid-reactive substances (TBARS). Addition of 10-100 microM NO to rat brain homogenates preincubated for 2 h at 37 degrees C caused up to a 20% decrease in the levels of TBARS compared to controls. A similar inhibitory effect was observed on TBARS produced by Fe(2+)-induced decomposition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE), due apparently to NO-induced decomposition of the hydroperoxide (ferrous oxidation/xylenol orange assay). Prostaglandin G(2) (PGG(2), 35 microM), as a model bicyclic endoperoxide, and malondialdehyde (MDA, 20 microM), the main component of TBARS, proved also susceptible to degradation by NO or NO donors (diethylamine NONOate, DEA/NO) at concentrations of 100 microM or higher in 0.05 M phosphate buffer, pH 7.4, and at 37 degrees C, as indicated by the reduced response to the TBA assay. No significant effect on TBARS determination was caused by nitrite ions. These and other data indicate that NO can inhibit TBARS formation by decomposing primary lipid peroxidation products, chiefly 15-HPETE and related hydroperoxides, and, to a lesser extent, later stage TBARS precursors, including bicyclic endoperoxides and MDA, via nitrosation and other oxidative routes, without however affecting chromogenic reactions during the assay.

Animals↗
PubMed1984

Phenylhydrazine-induced lipid peroxidation of red blood cells in vitro and in vivo: monitoring by the production of volatile hydrocarbons.

Human red blood cells and male Sprague-Dawley rats were treated in vitro and in vivo, respectively, with phenylhydrazine in order to determine whether the release of volatile hydrocarbons can serve as a suitable index for phenylhydrazine-induced red blood cell peroxidation. Lipid peroxidation following phenylhydrazine administration (in vitro experiments: dosage calculated at 0.5-50 mM; in vivo experiments: intraperitoneal injection of 2.8 mg/100 g body wt) was monitored by the release of ethane and pentane measured by gas chromatography. Further hydrocarbons such as ethylene, propane, n-butane, iso-butane and iso-butene were monitored to form a basis of comparison. In vitro haemolysis was also determined during the course of incubation. Red blood cell suspensions yielded more than 15-fold concentrations of propane and more than 2-fold concentrations of iso-butane compared to pentane and ethane yields. Haemoglobin solutions also produced propane and iso-butane in the presence of phenylhydrazine, whereas pentane and ethane were not detectable. Time-course studies revealed that ethane and pentane reached maximum in vitro levels after red blood cell suspensions had been incubated for 2 hr whereas the maximum degree of haemolysis (approximately 60%) was attained between 60 and 90 min following the beginning of phenylhydrazine treatment. The dosage did not affect the final degree of haemolysis. Rats treated with phenylhydrazine exhaled greater concentrations of ethane (6-fold increase) and pentane (2-fold increase) compared to control animals. Exhaled propane showed a 30-fold increase in concentration following drug treatment. Our results suggest that the release of pentane and ethane may be useful in assessing red blood cell lipid peroxidation in the presence of phenylhydrazine in vitro and in vivo.

Alkanes↗
PubMedDate not supplied

Effect of paraquat intoxication and ambroxol treatment on hydrogen peroxide production and lipid peroxidation in selected organs of rat.

Paraquat (Pq) is a herbicide which is very toxic to all animals and to man. It generates free radicals and leads to acute or chronic lung injury and usually to death. So far, the role of lipid peroxidation of cell membranes in the mechanism of its toxicity has not been proved satisfactorily and therefore in the present study we examined the concentration of hydrogen peroxide (H2O2) and various lipid peroxidation products (LPP) such as conjugated dienes (CD), lipid hydroperoxides (LH), malonyldialdehyde (MDA) and Schiff bases in selected organs of the rat given a single intraperitoneal dose 35 mg kg-1 Pq. We also evaluated the influence of a mucolytic and probably antioxidant drug, ambroxol, on Pq-induced changes in the concentration of H2O2 and LPP. Paraquat increased the hepatic concentration of H2O2, CD, LH and MDA by approximately fourfold. Though the dose of Pq was nearly twice the LD50 dose, we did not notice any changes in the concentration of these substances in the critical organ, lung or heart and kidney. Ambroxol alleviated the increase of H2O2 in the liver but did not reduce the concentration of LPP. Moreover, the drug administered alone induced lipid peroxidation in the liver. Our results indicate that Pq dose not induce H2O2 production and lipid peroxidation in the lung but it increases the concentration of H2O2 and LPP in the liver. Ambroxol inhibits the Pq-induced increase in the concentration of H2O2 in the liver without protecting it against lipid peroxidation. Moreover, the drug alone may act as a pro-oxidant.

Ambroxol↗
PubMed1992

Changes in lipid peroxidation levels and lipid composition in the lungs, livers, kidneys and brains of mice treated with paraquat.

We examined lipid peroxide levels and the lipid composition of homogenates prepared from the lungs, livers, kidneys and brains of 48 male ICR mice treated with 30 mg kg-1 paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride). The mice were divided into eight groups, in which they were killed 0, 1.5, 3, 6, 12, 24, 48 and 120 h after the administration of paraquat. A significant increase in the lipid peroxide level was identified only in the liver. Change in lipid composition was identified in all the examined organs. However, the change was not a characteristic one in which there is a selective decrease of polyunsaturated fatty acids which become degraded in a lipid peroxidation reaction. It is possible that the mechanism of paraquat toxicity may differ in different organs.

Animals↗
PubMed1998

Oral reduced B-nicotinamide adenine dinucleotide (NADH) affects blood pressure, lipid peroxidation, and lipid profile in hypertensive rats (SHR).

A gradual increase in blood pressure (BP), often attaining hypertensive levels, is common during aging--"age-related hypertension." Therefore, means to prevent or ameliorate this elevated BP safely are important. Although oral B-nicotinamide adenine dinucleotide (NADH), a natural coenzyme, is used principally to treat various neurologic disorders, we wished to investigate whether this agent had the same potential to lower BP and benefit the cardiovascular system as does coenzyme Q10, a similar-type agent. As a first approximation, spontaneously hypertensive rats (SHR) were used to determine effects of oral NADH. In a blinded, placebo-controlled study, ten rats received placebo; and ten, NADH for ten weeks. Systolic BP was measured by tail plethysmography. Blood was collected terminally, and chemistries were performed by routine methodologies. Thiobarbituric acid reactive species (TBARS) (an estimate of lipid peroxidation/free radical formation) was measured in renal and hepatic tissues. The following was noted: water and food intake were comparable, and the steady weight gain of young SHR were similar in the placebo and NADH groups. Although systolic BP did not differ between the two groups over the first month, it decreased and stayed markedly lower for the remainder of study in SHR receiving oral NADH. At the end of 60 days, SBP in NADH-treated SHR was 184 mm Hg +/- 2.8 (SEM) compared to 201 mm Hg +/- 2.1 (SEM) in control SHR (p < 0.001). No significant differences were seen in blood levels of glucose, insulin, triglyceride, and HDL levels but NADH intake lowered total cholesterol (p < 0.002) and LDL (p < 0.02). Renal TBARS were also significantly lower in SHR receiving NADH (P < 0.001). Accordingly, supplementation with the natural coenzyme NADH theoretically could prove to be useful in preventing age-related increases in BP and, thus, various cardiovascular maladies.

Administration, Oral↗
PubMed1988

The effect of zinc on iron-induced lipid peroxidation in different lipid systems including liposomes and micelles.

The effect of zinc on FeSO4/ascorbic acid-induced lipid peroxidation was measured by the thiobarbituric acid assay in various lipid systems including small unilamellar liposomes prepared from egg phosphatidylcholine (EPC), ionic micelles prepared from arachidonic acid (C20:4), non-ionic monocomponent micelles prepared from EPC-derived, methylated fatty acids, and an eicosatetrene emulsion. With the exception of C20:4 micelles, zinc inhibited lipid peroxidation in each of the above systems in a similar dose-related fashion, with 0.5 mM zinc having maximal effect. Gas-chromatographic fatty acid analysis too indicated a protective effect of zinc against FeCl3-induced lipid peroxidation in soybean PC vesicles, which do not contain C20:4 moieties. These findings, in particular the inhibition of lipid peroxidation in eicosatetrene emulsion, suggest that the presence of uncharged polar head groups, or packing of lipid molecules into ordered self-assemblages (membranes and micelles) have no critical influence on the antioxidant effect of zinc. The results with Fe2+ are compatible with the concept that zinc interferes with the formation of Fe2+-oxygen-enoic complexes. This mechanism, however, cannot account for the inhibition by zinc of the Fe#+-induced lipid peroxidation, suggesting the involvement of other types of zinc effects in these systems.

Ascorbic Acid↗
PubMed2002

Placental and decidual lipid peroxidation and antioxidant defenses in preeclampsia. Lipid peroxidation in preeclampsia.

We evaluated lipid peroxidation in serum, placenta and decidua basalis and antioxidant defenses in preeclampsia and normal pregnancy. The study group consisted of 70 women with preeclampsia and 72 healthy pregnant women. Lipid peroxides in serum, placenta and decidua basalis, and serum vitamin E and total carotene were measured by spectrophotometric methods. Unpaired Student's t-test, chi(2)-test and Pearson correlation test were used for the statistical analyses. Levels of lipid peroxides in serum, placenta and decidua basalis were markedly higher; and serum vitamin E, total carotene, bilirubin, albumin levels were markedly lower in preeclamptic pregnants compared with healthy pregnant women. Our findings demonstrated that both placenta and decidua basalis tissues may be a source of lipid peroxides in preeclamptic pregnancies. Prophylactic antioxidant therapy may abate the disease process. Further studies are needed to clarify the pathophysiology of preeclampsia and effectiveness of prophylactic antioxidant therapy in preeclampsia.

Journal Article↗
PubMed2003

The evaluation of lipid peroxidation and acute effect of octreotide on lipid peroxidation in patients with active acromegaly.

BACKGROUND: Although lipid peroxidation has been suggested to play a role in the etiology of many diseases, there is no report about its role in acromegaly in the literature. In the present study, we analyzed the basal levels of lipid peroxides (LPO) in newly diagnosed acromegalic patients, and to evaluate whether octreotide (OCT) has any effect on lipid peroxidation in these patients. METHODS: Plasma lipid peroxide levels before and after acute OCT administration were measured in 12 newly diagnosed acromegalic patients. Blood samples were drawn at basal and 4, 8, and 24 h after octreotide injection (100 microg s.c.). Plasma concentrations of lipid peroxides were estimated from measurement of thiobarbituric acid reactive substance (TBARS), using 1,1,3,3-tetra-ethoxypropane as a standard. RESULTS: This study shows that acromegalic patients have significantly higher basal plasma lipid peroxides levels compared to hours after OCT injection (p<0.001). Although a significant decrease was observed after 8 and 24 h in comparison to basal level (p<0.001), the lipid peroxide levels tended to increase at 24 h though still low when compared to basal level. CONCLUSION: Acromegalic patients have high basal lipid peroxide levels, which was significantly decreased after OCT administration.

Acromegaly↗
PubMed1996

Effects of alpha-tocopherol and beta-carotene on hepatic lipid peroxidation and blood lipids in rats with dietary iron overload.

The ability of dietary antioxidants to reduce lipid peroxidation induced by iron overload was examined in weanling male Sprague-Dawley rats. Animals were fed ad libitum a modified AIN-76A diet (control) or control diet with 0.5% alpha-tocopherol acid succinate, 0.5% crystalline trans-beta-carotene, or 0.5% alpha-tocopherol acid succinate + 0.5% trans-beta-carotene for four weeks. In the following four-week period, the animals received the above diets with 10,000 micrograms Fe/g; a control group continued to receive 35 micrograms Fe/g, and a high-iron group received 10,000 micrograms Fe/g with no antioxidants. After four weeks of dietary supplementation with alpha-tocopherol. Beta-carotene or alpha-tocopherol + beta-carotene, liver concentrations of alpha-tocopherol and beta-carotene increased significantly (p < 0.001). Liver lipid peroxidation, measured by the lipid-conjugated diene assay, increased significantly from 0.012 mumol/mg of lipid in the controls to 0.021 mumol/mg of lipid in animals receiving the high-iron diet. However, lipid peroxidation was significantly reduced in all animals fed the antioxidants, with the group fed alpha-tocopherol + beta-carotene having a lower level than the high-iron group. Total serum cholesterol was elevated in animals fed a high-iron diet and in animals fed the high-iron diet with alpha-tocopherol. In contrast, total serum cholesterol levels in the two groups of animals receiving the diets containing high iron with beta-carotene alone or high iron with beta-carotene + alpha-tocopherol were significantly reduced to the level of the control group. High-density lipoprotein cholesterol also decreased to baseline in the animals receiving beta-carotene alone. Modulation of lipid peroxidation by alpha-tocopherol or beta-carotene may be an important mechanism for reducing oxidative stress.

Animals↗