PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Lipid Peroxidation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2002

Effect of ursodeoxycholic acid on hydrogen peroxide induced lipid peroxidation in sheep liver mitochondria.

The effect of various concentrations of ursodeoxycholic acid (UDCA), a potent hepatoprotective agent on hydrogen peroxide-induced mitochondrial swelling was evaluated in vitro to find out the mechanism of action of the drug. Aliquots of sheep liver mitochondria were pre-incubated with various concentrations of UDCA [0-600 micrograms] and swelling was induced by hydrogen peroxide [1 mM]. Swelling was assessed at various time intervals and lipid peroxide, reduced glutathione status were also evaluated simultaneously. UDCA minimized hydrogen peroxide-induced swelling in a dose-dependent manner. Time-dependent elevation in the level of lipid peroxides was noted in mitochondria treated with hydrogen peroxide and this elevation was minimized in UDCA pre-treatment. UDCA also maintains the reduced glutathione level in mitochondria. UDCA acts against the oxidative stress imposed in liver mitochondria. It reduces lipid peroxidation-induced abnormalities such as swelling and thiol group depletion and the anti lipid peroxidative efficacy of the drug may be related to its hydrophilic nature which might protect the hydrophobic regions of the mitochondrial membranes which are prone for free radical-mediated reactions.

Animals↗
PubMed2000

TNF-alpha and IL-1alpha induce apoptosis in subconfluent rat mesangial cells. Evidence for the involvement of hydrogen peroxide and lipid peroxidation as second messengers.

Apoptosis of mesangial cells (MC) plays a role in glomerulonephritis (GN). In this study we investigated cytokine-induced apoptosis of cultured rat MC by morphological and biochemical features. TNF-alpha and IL-1alpha induced apoptosis in rat MC in a time- and concentration-dependent fashion. RT-PCR experiments revealed that MC express the TNF-receptor 1 (p60) gene constitutively. TNF-alpha as well as IL-1alpha stimulated the production of reactive oxygen species (ROS) and induced lipid peroxidation. Coincubation with catalase inhibited TNF-alpha and IL-1alpha induced apoptosis as well as lipid peroxidation. TNF-alpha, but not IL-1alpha increased the expression of c-jun. These results provide evidence that TNF-alpha and IL-1alpha induce apoptosis in rat MC with hydrogen peroxide and lipid peroxidation as second messengers. Increased c-jun expression may be a downstream intracellular signal of TNF-alpha-, but not IL-1alpha-induced apoptosis.

Animals↗
PubMed1980

Antiinflammatory effects of free radical scavengers and antioxidants: further support for proinflammatory roles of endogenous hydrogen peroxide and lipid peroxides.

Scavengers of reactive oxygen species were tested by local administration during granulomatous inflammation in the rat, induced by the subdermal implantation of carrageenin-soaked sponges. Drugs were administered either in a single dose immediately after sponge implantation, or in daily doses on days 3-6 of inflammation. The effects of the injected drugs were assessed using the day 7 granuloma. When given at the moment of sponge implantation, catalase showed antiinflammatory effects, whereas superoxide dismutase did not. However, the addition of superoxide dismutase to catalase, prior to injection, markedly potentiated the inhibition of granuloma formation by catalase alone. Negative results obtained with scavengers of hydroxyl radicals and singlet molecular oxygen suggest that protection of superoxide dismutase by catalase from inactivation by hydrogen peroxide, is a likely explanation for the observed potentiation. When administered at the moment of the induction of inflammation, alpha-tocopherol and propyl gallate, both antioxidants, also inhibited granuloma formation. All drugs tested were either ineffective or even enhanced granuloma weight following administration into a preformed granuloma. An inhibitor of both pathways of arachidonate metabolism, phenidone, inhibited granuloma formation irrespective of the moment of administration. The results presented in this paper suggest proinflammatory roles for hydrogen peroxide and lipid peroxides and a possible involvement of hydroxyl radicals and singlet oxygen in the breakdown of collagen.

Animals↗
PubMed2001

Influence of rice bran oil on serum lipid peroxides and lipids in human subjects.

To study the effect of rice bran oil (RBO) on serum lipids and lipid peroxides in human volunteers. Nine healthy volunteers, aged between 42 to 57 years were given 75 ml of RBO thrice daily as the cooking medium with break fast, lunch and dinner for a period of 50 days. At the beginning and at the end of 50 days, 5 ml of blood were drawn from an ante cubital vein. Serum lipids and lipid peroxides levels were estimated from the blood sample. There was a significant decrease in the levels of lipid peroxides, triglycerides, LDL, VLDL, and total cholesterol in human volunteers who switched over to RBO. RBO has evidently antioxidant and antilipidemic activities in human subjects.

Adult↗
PubMed1984

Superoxide and hydrogen peroxide-dependent lipid peroxidation in intact and triton-dispersed erythrocyte membranes.

Isolated erythrocyte membranes incubated with xanthine, xanthine oxidase, and Fe(III) underwent lipid peroxidation, as indicated by the thiobarbituric acid reaction and iodometric determination of hydroperoxides. In detergent-free medium (phosphate buffered saline) peroxidation was inhibited by superoxide dismutase, catalase, and EDTA; but was promoted by OH. scavangers, eg. mannitol. Generation of OH. in the system via iron-catalyzed reduction of H2O2 by O-2 was demonstrated by EPR spectrometry using spin trapping. In membranes treated with Triton X-100 lipid peroxidation was stimulated by EDTA and suppressed by OH. traps. This and other evidence suggests that OH. in the medium was an effective initiator of lipid peroxidation in detergent-dispersed membranes, but not in intact membranes.

Catalase↗
PubMedDate not supplied

[Effect of L-carnitine on lipid peroxidation and lipid composition in blood serum in hemic hypoxia].

Sodium nitrite has been studied for its effect on lipid metabolism of Wistar line rats. It is shown that a single administration of sodium nitrite in account 5 mg per 100 g of the body weight results in the intensification of lipids peroxidation, hyperbetalipoproteinemia, hypertriglyceridemia, hypercholesterolemia and to the decrease of the coefficient phospholipids/cholesterin/. Prophylactic administration of carnitine chloride in account of 20 mg per 100 g of the body weight stabilizes the level of lipids peroxidation, decreases concentration of total lipids, triglycerides, total cholesterin, phospholipids, lipoproteids of low and very low density, in the rat blood serum, normalizes the coefficient phospholipids/cholesterin.

Acute Disease↗
PubMed1995

[Effect of bushenhuoxue tablet on serum lipid peroxide, blood lipid and blood sugar in type II diabetics].

Sixty-eight patients suffering from diabetes mellitus (DM) type II with Kidney Deficiency and blood stasis were enrolled and divided randomly into treatment group (34 cases) and placebo group (34 healthy subjects). The amount of serum lipid peroxide (LPO), blood lipid and blood sugar was determined. The results showed that the serum LPO in treatment group was higher than that in placebo group. The serum LPO increased significantly in DM patients with vascular disease or with uncontrolled blood sugar. The serum LPO was positively correlated with triglyceride (TG). After using Bushenhuoxue Tablet (BSHX) serum LPO lowered, blood sugar decreased and high density lipoprotein-cholesterol (HDL-C)increased in treatment group, but in placebo group these three parameters were not changed significantly. These results indicated that LPO reaction in type II DM patients increased. The higher the blood sugar and TG or complicated with vascular disease, the LPO reaction enhanced markedly. BSHX tablets have the function of reducing the serum LPO and blood sugar, clearing cholesterol. Therefore, this tablet will have a good prospect in the prevention and treatment for DM patients complicated with vascular disease.

Adult↗
PubMed1982

Effect of carbon tetrachloride on cardiac lipid peroxidation, serum lipids and enzymes of albino rats.

Carbon tetrachloride (CCl4) at the dose of 0.3 ml/100 g body weight i.p. induced changes after 18 h in the cardiac lipid-peroxidation, serum-free fatty acids (FFA), cholesterol, and enzymes in the rats. The cardiac lipid peroxidation and the activity of serum enzymes GOT and GPT were significantly increased. The levels of serum FFA and cholesterol were significantly decreased.

Alanine Transaminase↗
PubMed2003

Effect of DL-alpha-lipoic acid on the status of lipid peroxidation and lipids in aged rats.

The effect of dextro and levo (DL)-alpha-lipoic acid on lipid peroxidation and lipids has been evaluated in plasma, liver, and kidney of young and aged rats. The levels of thiobarbituric acid reactive substances (TBARS) and lipids were considerably higher in aged rats compared with younger controls. DL-alpha-lipoic acid (100 mg/kg body wt/day) was administered intraperitoneally for 7 and 14 days. Supplementation of lipoic acid in aged rats prevents the elevated levels of TBARS and lipids. From our observations, we conclude that lipoic acid is very effective in normalizing age-related alterations in lipids, and it can be implemented in the aged to minimize age-associated disorders where free radicals are the major cause.

Age Factors↗
PubMed1992

Red blood cell susceptibility to lipid peroxidation, membrane lipid composition, and antioxidant enzymes in continuous ambulatory peritoneal dialysis patients.

OBJECTIVE: To investigate the overall susceptibility of red blood cells (RBC) to lipid peroxidation from patients on continuous ambulatory peritoneal dialysis (CAPD). METHODS: The following parameters were measured: RBC malondialdehyde (MDA) production after oxidative stress with H2O2, RBC antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and RBC membrane lipid composition. The levels of plasma vitamin E and serum selenium were also assayed. PATIENTS: Eleven patients on continuous ambulatory peritoneal dialysis. Twenty-one healthy blood donors of similar age were used as normal controls. RESULTS: The MDA formation after H2O2 stimulation was normal in CAPD patients (0.79 +/- 0.1 mumol/gHb versus 0.78 +/- 0.1 in the control group). RBC from CAPD patients also showed a normal SOD activity, a more than adequate vitamin E status, and a peculiar pattern of membrane lipids, with reduced polyunsaturated fatty acids (p less than 0.001) and increased monounsaturated fatty acids (p less than 0.001). Both RBC GSH-Px activity, a selenium-dependent enzyme, and serum selenium levels were significantly lower in CAPD patients, and a significant positive correlation (r = 0.68; p less than 0.02) between the two parameters was found. CONCLUSIONS: This study found a normal sensitivity to oxidant stress in RBC from a group of CAPD patients, despite an impaired GSH-Px activity. The peculiar lipid pattern of RBC membrane, characterized by reduced PUFA and increased MUFA content, may contribute, in addition to adequate SOD activity and vitamin E status, to normal RBC lipid peroxidation.

Aged↗
PubMed1988

Increased lipid peroxidation after lipid infusion as measured by breath pentane output.

We studied the effect of intravenous lipid infusion on lipid peroxidation as measured by breath pentane. Pentane, plasma alpha-tocopherol (alpha-tox) and plasma gamma-tocopherol (gamma-toc), selenium, and Se-dependent glutathione peroxidase (Se-GSHPx) were measured in 10 normal control subjects and in 10 home parenteral nutrition (HPN) patients before and after infusion of 100 mL Nutralipid 10% over 30 min. Before infusion, breath pentane was significantly higher and alpha-toc was significantly lower in the HPN group than in the control subjects. These two measurements were significantly negatively correlated (r = -0.54, p less than 0.05). Pentane, alpha-toc, and Se-GSHPx were significantly increased in both groups after lipid was infused but were still significantly higher in HPN patients than in control subjects. Thus, infusion of a small amount of lipid rich in linoleic acid induced a significant increase in breath pentane, reflective of increased lipid peroxidation.

Adult↗
PubMed1997

Inhibition of lipid peroxidation.

Lipid peroxy radicals (ROO.) were detected by electron spin resonance (ESR) at low temperature after formation by addition of H2O2 into a suspension of mice lymphocytes. If lymphocytes were treated with selenomethionine (Se-Met) prior to addition of H2O2, ROO. formation was inhibited in a fashion that was dependent on Se-Met concentration. Formation of ROO. in the spleen of mice was induced by 60Co irradiation. Animals that were supplemented with Na2SeO3 prior to irradiation exhibited a lower ROO. concentration than that of nontreated animals. Based on our experiments, we have concluded that Se has an oxygen-free radical scavenging effect. This should be a protective effect against lipid peroxy radical cellular attack.

Animals↗
PubMed2006

[Assessment of malonyldialdehyde concentration as a product of lipid peroxidation and lipid metabolism in patients on chronic dialysis].

UNLABELLED: Chronic hemodialysis in patients with renal insufficiency is a factor significantly intensifying oxidative stress, resulting in increased lipid and lipoprotein peroxidation. It intensifies atherosclerotic activity. Malonyldialdehyde (MDA) concentration in serum, and isolated fraction of low density lipoprotein is indicators of lipid peroxidation intensification and therefore arteriosclerosis development. THE AIM OF THE STUDY: Assessment of MDA concentration as a product of lipid peroxidation and lipid metabolism in patients on chronic dialysis. MATERIALS AND METHODS: The study included 48 dialyzed patients, age 22-68 undergoing chronic dialysis for, on average, 56 months. On account of dialysis period the patients were included into 3 subgroups: group 1 (n = 17) dialysis period 2 years, group 2 (n = 13) dialysis period 2-5 years and group 3 (n = 18) dialysis period longer than 5 years. Control group consisted of 30 healthy subjects. We assessed: malonyldialdehyde in serum and isolated fraction of low density lipids (LDL) and high density lipid (HDL) and cholesterol (CH) and triglycerides (TG), phospholipids (PL) in serum and isolated lipoprotein fractions. RESULTS: Significantly decreased levels of HDL, LDL fractions and increased triglicerides and elevated levels of MDA in serum and isolated LDL fraction were found in patients on chronic dialysis in comparison to control group (p < 0.05). CONCLUSION: Our results indicate apparent normalization of lipid metabolism in patients on chronic dialysis and suggest that MDA assessment is better marker for arteriosclerosis risk estimation in long-term dialyzed patients.

Adult↗
PubMed1989

Possible generation of hydrogen peroxide and lipid peroxidation of erythrocyte membrane by asbestos: cytotoxic mechanism of asbestos.

We studied a mechanism of hemolysis induced by asbestos particles or silicic acid. This hemolysis was instantly initiated by mixing red blood cells with asbestos particles or silicic acid, and reached a plateau within 10 min. The hemolysis was suppressed by catalase, radical quenchers, deoxygenation, or phospholipids. The degree of the hemolysis was proportional to either the amount of asbestos added into red blood cell suspension or the amount of thiobarbituric acid-reacting substances formed. These findings suggest that in vitro hemolysis induced by asbestos particles (or silicic acid) is ascribed to membrane lipid peroxidation initiated by hydrogen peroxide which was generated by the interaction of the mineral particles with biological membranes.

Asbestos↗
PubMed1989

[The interrelationship of the processes of lipid peroxidation and lipid phospholipase hydrolysis in the synaptosomes].

The influence of Fe2+, alpha-tocopherol, phospholipase A2 and mepacrine on the activity of lipid peroxidation (LPO) and phospholipid hydrolysis (PLH) was studied in synaptosomes. It was established that there is the tight direct interconnection between LPO and PLH in synaptosomes. It is assumed that activation of endogenous phospholipases in neurons is one of the causes of uncompensated LPO-activation during epileptogenesis.

Animals↗
PubMed1997

[Effects of essential oil on lipid peroxidation and lipid metabolism in patients with chronic bronchitis].

Natural concentrations of some essential oils were examined for effects on the system lipid peroxidation-antioxidant defense and lipid metabolism in 150 patients with chronic bronchitis. Lowering of plasm levels of dienic conjugates and ketons, activation of catalase in red cells characteristic of antioxidant effect were observed in exposure to essential oils of rosemary, basil, fir, eucalyptus. Lavender essential oil promotes normalization of the level of total lipids, ratio of total cholesterol to its alpha-fraction.

Adult↗
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↗