scholarly journals Oxidative interactions between haemoglobin and membrane lipid. A liposome model

1984 ◽  
Vol 220 (3) ◽  
pp. 685-692 ◽  
Author(s):  
J Szebeni ◽  
C C Winterbourn ◽  
R W Carrell
Keyword(s):  
Lipid Peroxidation ◽  
Lipid A ◽  
Cell Model ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Membrane Lipid ◽  
Alpha Tocopherol ◽  
Glutathione Depletion ◽  
Unsaturated Lipid ◽  
Membrane Oxidation

The relationship between haemoglobin and membrane oxidation was studied using liposomes containing haemoglobin (haemosomes) as a red cell model. Rapid oxidation occurred in haemosomes formed from purified haemoglobin and unsaturated lipid (egg phosphatidylcholines). After 3 h at 37 degrees C most of the haemoglobin was oxidized, predominantly to methaemoglobin with some haemichrome formation. The oxidation of haemoglobin was paralleled by membrane lipid peroxidation as measured by thiobarbituric acid reactivity. These changes were largely abolished by using freshly prepared haemolysate instead of purified haemoglobin, or when haemosomes were prepared with saturated phosphatidylcholines. In haemosomes consisting of fresh haemolysate and saturated phosphatidylcholine, the rate of haemoglobin oxidation at 37 degrees C corresponded to that of non-encapsulated haemolysate, and after 4 months storage at 4 degrees C 45% of oxyhaemoglobin was oxidized. In haemosomes prepared from purified haemoglobin and egg lecithin, alpha-tocopherol, catalase and ascorbate each protected against both haemoglobin oxidation and lipid peroxidation. Superoxide dismutase or reduced glutathione had no effect. In unsaturated-lipid haemosomes containing haemolysate, the rate of haemoglobin oxidation increased when catalase was inhibited or reduced glutathione was depleted, but after long term incubation only concurrent catalase-inhibition and glutathione depletion could increase thiobarbituric acid reactivity. These results demonstrate a close interdependence between haemoglobin oxidation and lipid peroxidation, and show that constituents of haemolysate strongly protect against both processes. H2O2 appears to be an important mediator, with its removal by either catalase or the glutathione/glutathione peroxidase system protecting against both oxidative changes.

Skeletal muscle lipid peroxidation in exercised and food-restricted rats during aging

1989 ◽  
Vol 67 (1) ◽  
pp. 69-75 ◽  
Author(s):  
J. W. Starnes ◽  
G. Cantu ◽  
R. P. Farrar ◽  
J. P. Kehrer
Keyword(s):  
Lipid Peroxidation ◽  
Gastrocnemius Muscle ◽  
Thiobarbituric Acid ◽  
Exercise Group ◽  
Alpha Tocopherol ◽  
Treadmill Running ◽  
Control Group ◽  
Muscle Lipid ◽  
Fischer 344 ◽  
Skeletal Muscle Lipid

The effects of chronic endurance exercise and food restriction on nonenzymatic lipid peroxidation (LP) of gastrocnemius muscle during aging were studied in male, Fischer 344 rats. One set of rats aged 6 and 18 mo were assigned to an exercise group (treadmill running) or an age-matched sedentary control group. After 6 mo (at the ages of 12 and 24 mo), LP and levels of alpha-tocopherol and its oxidized form, alpha-tocopheryl quinone, were measured. The extent of LP was determined in homogenates by measuring the content of thiobarbituric acid-reactive substances. After homogenization, the muscles were immediately evaluated for basal LP and also incubated in the presence of oxidant stressors for 2 h to assess antioxidant capacity (AOC) and for 24 h to estimate total peroxidizable lipid (TPL). Basal LP was not affected by age or exercise. AOC was not affected by exercise at either age. However aging significantly decreased AOC and increased alpha-tocopheryl quinone in both sedentary and exercised groups. TPL was not affected by age, but was increased by exercise training (P less than 0.05). Another set of rats was divided into the following three groups at 3 mo of age: sedentary, fed ad libitum (S); sedentary, caloric restricted by alternate day feeding (R); and exercised by forced treadmill running (E). Two years later, when the rats were 27 mo of age, the extent of LP was assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

Bitter Melon Protects Against Lipid Peroxidation Caused by Immobilization Stress in Albino Rats

2009 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Chaturvedi
Keyword(s):  
Lipid Peroxidation ◽  
Immobilization Stress ◽  
Reduced Glutathione ◽  
Cumene Hydroperoxide ◽  
Liver Homogenate ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Bitter Melon ◽  
Protective Effects

In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. After seven days, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substances, reduced glutathione, and catalase. In vitro effects of M. charantia extract on lipid peroxidation in liver homogenate of normal, control, and rats pretreated with extract were carried out against cumene hydroperoxide-induced lipid peroxidation. Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.

scholarly journals Hibiscus sabdariffaAffects Ammonium Chloride-Induced Hyperammonemic Rats

2007 ◽  
Vol 4 (3) ◽  
pp. 321-325 ◽  
Author(s):  
M. Mohamed Essa ◽  
P. Subramanian
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Activity ◽  
Ammonium Chloride ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Alcoholic Extract ◽  
Hibiscus Sabdariffa ◽  
Protein Nitrogen ◽  
Antioxidant Effects ◽  
Brain Tissues

Hibiscus sabdariffa(HS) is an edible medicinal plant, indigenous to India, China and Thailand and is used in Ayurveda and traditional medicine. Alcoholic extract of HS leaves (HSEt) was studied for its anti-hyperammonemic and antioxidant effects in brain tissues of ammonium chloride-induced hyperammonemic rats. Oral administration of HSEt (250 mg kg−1body weight) significantly normalizes the levels of ammonia, urea, uric acid, creatinine and non-protein nitrogen in the blood. HSEt significantly reduced brain levels of lipid peroxidation products such as thiobarbituric acid and reactive substances (TBARS) and hydroperoxides (HP). However, the administered extract significantly increased the levels of antioxidants such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) in brain tissues of hyperammonemic rats. This investigation demonstrates significant anti-hyperammonemic and antioxidant activity of HS.

Dehydroepiandrosterone administration prevents the oxidative damage induced by acute hyperglycemia in rats

1997 ◽  
Vol 155 (2) ◽  
pp. 233-240 ◽  
Author(s):  
M Aragno ◽  
E Brignardello ◽  
E Tamagno ◽  
V Gatto ◽  
O Danni ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acute Hyperglycemia ◽  
Tissue Resistance ◽  
In Vivo Administration ◽  
Different Doses

Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.

scholarly journals Antioxidant and Ethylene-related Changes in `Chandler' Strawberry Fruit as Influenced by Maturity

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 807A-807
Author(s):  
Floyd M. Woods* ◽  
William A. Dozier ◽  
Robert C. Ebel ◽  
David G. Himelrick ◽  
Cecilia Mosjidis ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Activity ◽  
Enzyme Activity ◽  
Antioxidant Activities ◽  
Thiobarbituric Acid ◽  
Membrane Lipid ◽  
Strawberry Fruit ◽  
Signal Molecule ◽  
Stage Of Development ◽  
Fruit Pericarp

The relationship between fruit maturation and accumulation of hydrogen peroxide (H2 O2), lipid peroxidation, ethylene (C2 H4) production, antioxidant activity (hydrophilic, lipophilic and total) and the antioxidant enzyme ascorbate peroxidase (APX, EC 1.11.1.11) in fruit pericarp tissue of `Chandler' (Fragaria × ananassa Duch.) strawberry were measured. `Chandler' fruit pericarp maturation and ripening were accompanied by a decline in H2 O2 content early in fruit development followed by a rapid accumulation. An increase in membrane lipid peroxidation (thiobarbituric acid reactive substances, TBARS) coincided with accumulation of H2 O2, which preceded a rise in C2 H4 production. In general, antioxidant activity declined as fruit matured and ripened. APX enzyme activity increased by 2-fold and peaked at the pink stage of development and then gradually declined with ripening. H2 O2 may serve as a signal molecule to initiate the cascade of oxidative processes during maturation and ripening. APX enzyme activity during maturation and ripening was not substantial and thus, may not have a role in alleviating accumulation of H2 O2 and subsequent events related to oxidative senescence in fruit pericarp. To our knowledge, this is the first study to present fractionated antioxidant activities (HAA, LAA and TAA) from strawberry pericarp as assessed by the ABTS∼+ radical cation assay. A fundamental understanding of the mechanisms involved in the senescent related-oxidative changes during strawberry fruit ontogeny in relation to quality and nutrition is discussed.

Role of lipid peroxidation in H2O2-induced renal epithelial (LLC-PK1) cell injury

1995 ◽  
Vol 268 (1) ◽  
pp. F30-F38 ◽  
Author(s):  
A. K. Salahudeen
Keyword(s):  
Lipid Peroxidation ◽  
Renal Cell ◽  
Time Course ◽  
Cell Injury ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
In Vivo Studies ◽  
Sequence Of Events

The exact sequence of events or mechanisms by which H2O2 induces renal cell injury remains undetermined. Specifically, whether the attendant lipid peroxidation is a cause or an effect remains unclear. Employing H2O2 and LLC-PK1 cells, we tested the hypothesis that lipid peroxidation is a seminal event and that its inhibition is cytoprotective. In a time course study, lipid peroxidation (thiobarbituric acid reaction) and degradation (release of [3H]arachidonic acid) preceded H2O2-induced cytolysis (51Cr and lactate dehydrogenase release). The role of preceding lipid peroxidation in cytolysis was examined with lipid radical scavengers. alpha-Tocopherol and lazaroid compound 2-methyl aminochroman dose-dependently inhibited H2O2-induced lipid peroxidation and prevented cytolysis. 2-Methyl aminochroman cytoprotection was associated with blockade of lipid degradation. 21-Aminosteroid, another lazaroid, also inhibited lipid peroxidation and prevented cytolysis. These findings provide evidence that lipid alterations contribute to H2O2-mediated LLC-PK1 injury and, for the first time, demonstrate the potency of lazaroids in a renal cell line. In vivo studies with lazaroids may define the role of lipid peroxidation in acute renal injury models.

scholarly journals Effects of alpha-tocopherol on bacterial translocation and lipid peroxidation in rats with intestinal obstruction

2003 ◽  
Vol 18 (4) ◽  
pp. 283-288 ◽  
Author(s):  
Alberto Schanaider ◽  
Leonaldson dos Santos Castro ◽  
Kalil Madi
Keyword(s):  
Lipid Peroxidation ◽  
Intestinal Obstruction ◽  
Bacterial Translocation ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
Control Group ◽  
Intestinal Epithelial ◽  
Group A ◽  
Mucosal Necrosis ◽  
Control Sham

PURPOSE: Investigate if alpha-tocopherol has a protective effect on intestinal mucosa after obstruction and to evaluate the potential relations between lipid peroxidation and bacterial translocation. METHODS: Ten rats were submitted to a sham laparotomy and six served as control group. A small bowel obstruction was done in sixteen animals and among them eight were pretreated with alpha-tocopherol. Forty-eight hours later, mesenteric lymph node, spleen, liver and blood cultures and also samples from ileal mucosal were obtained, Thiobarbituric acid reactive substances (TBARS) levels were determined and intestinal histological assessment was performed. RESULTS: Bacterial translocation was significantly increased in the obstructed rats compared with the control, sham and antioxidant pretreated groups (p< 0,05). TBARS (nmol/100mg) in untreated obstructed rats increased from 49,0 ± 13,3 in control group to 128,8 ± 40 after 48 hours of intestinal obstruction and achieved 72,3 ± 24,6 in alpha-tocopherol group (p< 0,05). Bacterial adherence to the intestinal epithelial cells surface and mucosal necrosis were significantly increased in the obstructed compared with nonobstructed rats. CONCLUSION: Alpha-tocopherol reduce the deleterious effects of the TBARS over the intestinal mucosal suggesting that in such circumstances there might be an association between bacterial translocation and lipid peroxidation after an intestinal occlusion.

Increased erythrocyte antioxidant status protects against smoking induced hemolysis in moderate smokers

2011 ◽  
Vol 30 (10) ◽  
pp. 1475-1481 ◽  
Author(s):  
Padmavathi Pannuru ◽  
Damodara Reddy Vaddi ◽  
Rameswara Reddy Kindinti ◽  
Nallanchakravarthula Varadacharyulu
Keyword(s):  
Lipid Peroxidation ◽  
Erythrocyte Membrane ◽  
Antioxidant Status ◽  
Reduced Glutathione ◽  
Membrane Lipid ◽  
Red Cell ◽  
Membrane Lipid Peroxidation ◽  
Free Radical Damage ◽  
Human Red Blood Cells ◽  
Nitrite Nitrate

Cigarette smoking is common in societies worldwide and has been identified as injurious to human health. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. In the present study, the possible role of antioxidant status on smoking-induced erythrocyte hemolysis of smokers was studied. Erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, reduced glutathione (GSH) level, erythrocyte membrane lipid peroxidation, total cholesterol and phospholipids were determined. Further, nitrite/nitrate levels (NO2/NO3) in both plasma and erythrocyte lysate were measured. Results showed increased plasma and erythrocyte membrane lipid peroxidation and nitrite/nitrate levels in smokers. The activities of SOD, CAT and GPx were also increased with reduced glutathione (GSH) level in smokers. No significant change was observed in smokers red cell hemolysis and cholesterol/phospholipid (C/P) ratio compared to controls. Erythrocyte membrane lipid peroxidation was positively correlated with SOD ( r = 0.482, p < 0.01) and GPx ( r = 0.368, p < 0.018) in smokers. Increased levels of nitrite/nitrate and antioxidant status of erythrocytes might be playing a crucial role in protecting red cell from free radical damage induced by cigarette smoke.

scholarly journals The flavonoids, quercetin and isorhamnetin 3-O-acylglucosides diminish neutrophil oxidative metabolism and lipid peroxidation.

2001 ◽  
Vol 48 (1) ◽  
pp. 183-189 ◽  
Author(s):  
M Zielińska ◽  
A Kostrzewa ◽  
E Ignatowicz ◽  
J Budzianowski
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Metabolism ◽  
Hypochlorous Acid ◽  
Thiobarbituric Acid ◽  
Membrane Lipid ◽  
Polymorphonuclear Neutrophils ◽  
Inhibitory Influence ◽  
Dependent Manner ◽  
In Vitro Production

Two natural flavonoids, quercetin and isorhamnetin 3-O-acylglucosides, were examined for their inhibitory influence on the in vitro production and release of reactive oxygen species in polymorphonuclear neutrophils (PMNs). The generation of superoxide radical, hydrogen peroxide and hypochlorous acid were measured by, respectively, cytochrome c reduction, dichlorofluorescin oxidation and taurine chlorination. Membrane lipid oxidation was studied by the thiobarbituric acid method in mouse spleen microsomes. The addition of flavonoids at the concentration range 1-100 microM inhibited PMNs oxidative metabolism and lipid peroxidation in a dose-dependent manner. The results suggest that these flavonoids suppress the oxidative burst of PMNs and protect membranes against lipid peroxidation.

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