scholarly journals Antioxidant protection by haemopexin of haem-stimulated lipid peroxidation

1988 ◽  
Vol 256 (3) ◽  
pp. 861-865 ◽  
Author(s):  
J M Gutteridge ◽  
A Smith
Keyword(s):  
Lipid Peroxidation ◽  
Protoporphyrin Ix ◽  
Thiobarbituric Acid ◽  
Iron Chelator ◽  
Oxygen Radical ◽  
Butylated Hydroxytoluene ◽  
Radical Reactions ◽  
Antioxidant Protection ◽  
Reactive Material ◽  
Chain Breaking

Haem (ferrous protoporphyrin IX) is a reactive low-molecular-mass form of iron able to participate in oxygen-radical reactions that can lead to the degradation of proteins, lipids, carbohydrates and DNA. Oxygen-radical reactions are likely to occur upon tissue damage. Extracellular fluids rely on antioxidant mechanisms different from those found inside the cell, and circulating proteins limit radical reactions by converting pro-oxidant forms of iron into less-reactive forms. Of the compounds tested, only apohaemopexin and the chain-breaking antioxidant butylated hydroxytoluene inhibited (by more than 90%) haemin-stimulated peroxidation as measured by formation of conjugated dienes, thiobarbituric acid-reactive material from linolenic acid or peroxidation-induced phospholipid fluorescence. Haptoglobin, the haemoglobin-binding serum protein, was ineffective. Conversely, only haptoglobin significantly inhibited haemoglobin-stimulated lipid peroxidation. Iron-salt-induced lipid peroxidation was inhibited only by apotransferrin and the iron-chelator desferrioxamine. All lipid peroxidations were inhibited by the radical scavengers butylated hydroxytoluene and propyl gallate. These findings support the concept that transport and conservation of body iron stores are closely linked to antioxidant protection.

Lipid peroxidation in rheumatoid arthritis: Thiobarbituric acid-reactive material and catalytic iron salts in synovial fluid from rheumatoid patients

1984 ◽  
Vol 66 (6) ◽  
pp. 691-695 ◽  
Author(s):  
David Rowley ◽  
John M. C. Gutteridge ◽  
David Blake ◽  
Margaret Farrs ◽  
Barry Halliwell
Keyword(s):  
Rheumatoid Arthritis ◽  
Lipid Peroxidation ◽  
Synovial Fluid ◽  
Knee Joint ◽  
Thiobarbituric Acid ◽  
Radical Reactions ◽  
Local Inflammation ◽  
Reactive Material ◽  
Iron Salts

1. Thiobarbituric acid (TBA)-reactive material is present in serum and knee joint synovial fluid from rheumatoid patients, consistent with lipid peroxidation occurring in vivo. 2. The amount of TBA-reactive material in synovial fluid correlates with the concentration of iron salts present as determined by the bleomycin method, presumably because iron is an important catalyst of radical reactions in vivo. 3. There appear to be significant correlations between the contents of TBA-reactive material and bleomycindetectable iron in synovial fluid and the activity of rheumatoid arthritis as assessed with a clinical index of local inflammation and with various laboratory parameters.

293 EFFECT OF GUAIAZULENE ON IN VITRO BOVINE EMBRYO PRODUCTION

2007 ◽  
Vol 19 (1) ◽  
pp. 262 ◽  
Author(s):  
I. Dimitriadis ◽  
E. A. Rekka ◽  
E. Vainas ◽  
G. S. Amiridis ◽  
C. A. Rekkas
Keyword(s):  
Lipid Peroxidation ◽  
Embryo Development ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Early Embryo ◽  
Bovine Embryo ◽  
Embryo Production ◽  
Reactive Material

The substrates used in in vitro embryo production (IVP) mimic the in vivo fluids in which oocytes mature, oocytes are fertilized, and the early embryos develop (follicular and oviductal fluid). It is well established that oxidative stress negatively affects in vitro culture (IVC) outcomes. Guaiazulene (G) is a component of chamomile species oil with known antioxidant properties. In the present study, all IVP media were modified by the addition of G solutions so that the former exhibited a total protection against induced lipid peroxidation (TPaLP) similar to that of the respective in vivo environment. The IVP outcomes were then compared between G-processed and control oocytes. Bovine preovulatory follicular (BF) and oviductal (BO) fluid samples were collected from 10 Holstein 4- to 5-year-old cows in estrus. TPaLP was assessed according to the samples' ability to inhibit rat hepatic microsomal lipid peroxidation, by determination of the 2-thiobarbituric acid reactive material. TPaLP (mean % � SEM) of the BF and BO were 70.63 � 10.03 and 16.33 � 4.33, respectively, whereas those of the IVP [in vitro-matured (IVM), in vitro-fertilized (IVF), and IVC] media were lower (17.94 � 1.66, -1.82 � 0.78, and 14.57 � 1.26, respectively). TPaLP of the 0.1 mM G-modified IVP medium increased to 67.2 � 5.85, 19.98 � 2.49, and 69.19 � 6.22, respectively. A total of 2041 class A oocytes were used. The proportion of cleavage, early embryo development (embryos with more than 4 cells), or both after IVP (18 h IVM–5% CO2 in air, and 18 h IVF, 48 h IVC–5% CO2, 10% O2, 85% N) in the presence of G (n = 1237) during each of the IVP phases or any possible combination of IVP phases was compared with the respective control (C, n = 804). Statistical analysis was performed by a chi-squared test; P < 0.05 was considered significant. G improved cleavage and embryo development rates when present during IVM (79.4 and 57.8% vs. 64.5 and 38.2% for C) or both IVM and IVC (78.0 and 60.7% vs. 57.8 and 36.5%, respectively). When present only during 18 h of IVF, G had no effect on embryo production. However, an increased embryo development rate resulted from the combined exposure to G during IVF and IVM (56.4 vs. 29.6%), during IVF and IVC (55.3 vs. 35.5%), or at all IVP phases (56.6 vs. 34.9%). The latter effect resembled the one obtained after G addition only to the IVC medium (62.5 vs. 39.7%, respectively). We concluded that the addition of G to IVP substrates, at concentrations that mimic the in vivo TPaLP conditions, could promote bovine IVP efficiency.

Influence of hypothyroidism on lipid peroxidation, erythrocyte resistance and antioxidant plasma properties in rabbits

2003 ◽  
Vol 51 (3) ◽  
pp. 343-351 ◽  
Author(s):  
Ewa Brzezińska-Ślebodzińska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Organic Radicals ◽  
Plasma Properties ◽  
Phospholipid Liposomes ◽  
Chain Breaking ◽  
Erythrocyte Resistance ◽  
Radical Damage

The effect of hypothyroidism on some oxidative stress parameters is reported. Moderate hypothyroid state was induced in two groups of female rabbits (3 and 12 months old) by giving 50 mg/kg body weight (BW) of propylthiouracil (PTU) per os for 6 days and 20 mg/kg BW of methimazole (MMI) for further 14 days. Serum T4 and T3 concentrations decreased by about 38-40 and 32-36%, respectively. The induced hypothyroidism resulted in a significant decrease in the serum concentration of the lipid peroxidation end-product malondialdehyde, as measured by the thiobarbituric-acid assay. Erythrocytes of hypothyroid animals exhibited higher resistance to oxidative stress, while submitted to free radicals generator 2,2'-azo-bis(2-amidinopropane) hydrochloride (AAPH) in vitro. Using two detector systems (phospholipid liposomes and deoxyribose), sensitive to either organic or inorganic oxygen radical damage, the ability of euthyroid and hypothyroid rabbit plasma to protect against oxygen radicals was evaluated. The plasma of hypothyroid animals showed about 20% higher ability to protect against iron-binding organic radicals, but about 50% lower chain-breaking antioxidant activity. The antioxidant capacity of plasma against inorganic radicals was not affected by hypothyroidism. In conclusion, the results show that thyroid hormones modulate the free-radical-induced oxidative damage of lipids and that hypothyroidism offers some protection against lipid peroxidation.

scholarly journals Damage to DNA concurrent with lipid peroxidation in rat liver slices

1988 ◽  
Vol 252 (3) ◽  
pp. 893-896 ◽  
Author(s):  
C G Fraga ◽  
A L Tappel
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Rat Liver ◽  
Incubation Time ◽  
Ferrous Iron ◽  
Thiobarbituric Acid ◽  
Butylated Hydroxytoluene ◽  
Thiobarbituric Acid Reactive Substances ◽  
Butyl Hydroperoxide ◽  
Liver Slices

Lipid peroxidation and DNA damage were evaluated in liver slices incubated for 2 h at 37 degrees C with 1 mM-t-butyl hydroperoxide (t-BOOH), 1 mM-BrCCl3 or 50 microM-ferrous iron. t-BOOH induced the greatest amount of damage to DNA and increased the production of thiobarbituric acid-reactive substances (TBARS). Both phenomena depended on the incubation time. Ferrous iron induced both DNA damage and TBARS production, and BrCCl3 did not induce significant DNA damage and was the weakest TBARS inducer. Butylated hydroxytoluene at 1 mM inhibited both DNA damage and TBARS production. DNA damage and lipid peroxidation in liver slices were correlated, indicating that these events were concurrent.

Mechanisms of t-butyl hydroperoxide-induced toxicity to rabbit renal proximal tubules

1988 ◽  
Vol 255 (1) ◽  
pp. C28-C33 ◽  
Author(s):  
R. G. Schnellmann
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Iron Chelator ◽  
Proximal Tubules ◽  
Butylated Hydroxytoluene ◽  
Specific Sequence ◽  
Lactate Dehydrogenase Activity ◽  
Renal Proximal Tubules ◽  
Butyl Hydroperoxide

This study examined the mechanisms of t-butyl hydroperoxide (TBHP)-induced oxidative injury to a suspension of rabbit renal proximal tubules. TBHP (0.25-1 mM) produced a specific sequence of intracellular events in the tubules. Initially, TBHP increased tubular glutathione disulfide content and lipid peroxidation. Subsequently, there was an increase in ouabain-sensitive oxygen consumption (indicative of an increase in intracellular sodium concentrations), mitochondrial dysfunction, and a decrease in glutathione content. Finally, cell death, as measured by a decrease in tubular retention of lactate dehydrogenase activity, began between 30 and 60 min. The toxicity was dependent on iron-mediated free radical formation, since the iron chelator, deferoxamine, and the antioxidants, promethazine, butylated hydroxytoluene, and dithiotreitol, prevented the lipid peroxidation, the mitochondrial dysfunction, and cell death. Further studies with the antioxidants provided evidence that lipid peroxidation plays an important role in TBHP toxicity in proximal tubules.

Preventing in vitro lipoperoxidation in the malondialdehyde-thiobarbituric assay

2004 ◽  
Vol 42 (8) ◽  
Author(s):  
Ricardo Gonzalo ◽  
Cristofol Vives-Bauza ◽  
Antonio L. Andreu ◽  
Elena García-Arumí
Keyword(s):  
Lipid Peroxidation ◽  
Cultured Cells ◽  
Thiobarbituric Acid ◽  
Reversed Phase ◽  
Butylated Hydroxytoluene ◽  
Reversed Phase Chromatography ◽  
Thiobarbituric Acid Assay ◽  
Acid Reaction

AbstractThe malondialdehyde-thiobarbituric acid assay is widely used to study lipid peroxidation. Among the various methods used to perform the assay, the most widely accepted is the quantification of malondialdehyde using the thiobarbituric acid reaction, followed by reversed-phase chromatography. However, unacceptable results may be obtained as malondialdehyde can be produced in vitro. To study the conditions that inhibit in vitro lipid peroxidation, malondialdehyde levels were measured in cultured cells using different concentrations of butylated hydroxytoluene, EDTA or a combination of both. Butylated hydroxytoluene alone inhibits in vitro lipid peroxidation effectively. EDTA reduces artificially produced malondialdehyde, but not totally. Finally, the combination of EDTA and butylated hydroxytoluene does not improve the results obtained using butylated hydroxytoluene alone. The conclusion is that in the malondialdehyde-thiobarbituric acid assay it is necessary to add an inhibitor of the in vitro lipid peroxidation and assay the necessary concentration depending on the specimen used.

scholarly journals Copper-phenanthroline-induced site-specific oxygen-radical damage to DNA. Detection of loosely bound trace copper in biological fluids

1984 ◽  
Vol 218 (3) ◽  
pp. 983-985 ◽  
Author(s):  
J M C Gutteridge
Keyword(s):  
Oxygen Radicals ◽  
Biological Fluids ◽  
Thiobarbituric Acid ◽  
Oxygen Radical ◽  
Body Fluids ◽  
Reducing Agent ◽  
Reactive Material ◽  
Site Specific ◽  
Radical Damage ◽  
Micromolar Range

Copper(II) ions, in the presence of 1,10-phenanthroline, O2 and a reducing agent, degrade DNA with the release of thiobarbituric-acid-reactive material. This reaction, dependent on the formation of oxygen radicals, was made the basis of a sensitive and specific assay for loosely bound copper in body fluids. When applied to certain extracellular fluids, trace amounts of copper could be detected in the lower micromolar range.

Simultaneous production of carbon monoxide and thiobarbituric acid reactive substances in rat tissue preparations by an iron-ascorbate system

1998 ◽  
Vol 76 (12) ◽  
pp. 1057-1065 ◽  
Author(s):  
Hendrik J Vreman ◽  
Ronald J Wong ◽  
Catherine A Sanesi ◽  
Phyllis A Dennery ◽  
David K Stevenson
Keyword(s):  
Lipid Peroxidation ◽  
Carbon Monoxide ◽  
Thiobarbituric Acid ◽  
Product Formation ◽  
Conjugated Dienes ◽  
Butylated Hydroxytoluene ◽  
Lipid Hydroperoxides ◽  
Cell Fractionation ◽  
Thiobarbituric Acid Reactive Substances ◽  
Tbars Formation

Most of the carbon monoxide (CO) produced by mammals is a product of the heme oxygenase (HO) reaction, the rate-limiting step in the heme degradation pathway leading to the generation of bilirubin in man. However, some CO is derived from other sources. We studied the association of CO production with lipid peroxidation in tissue preparations from adult male Wistar rats. Supernatants, from 20% tissue homogenates in potassium phosphate buffer, centrifuged for 1 min at 13 000 × g, were incubated for 30 min at 37°C in septum-sealed vials in the dark with ascorbate (100 µM) and Fe(II) (6 µM) and (or) Fe(III) (60 µM). Butylated hydroxytoluene (BHT, 100 µM) was added for the blank reaction. CO produced into the headspace was quantitated by gas chromatography. Thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD), and lipid hydroperoxides (LOOH) in the reaction medium were quantitated by spectrophotometry. Of the tissues studied, CO and TBARS formation was greatest for brain, followed by kidney, lung, spleen, and blood, but no CO or TBARS formation was detected for testes, intestine, liver, and heart. Cell fractionation studies indicated that these differences might be due to the presence of endogenous soluble antioxidants in the latter tissues. Furthermore, these studies demonstrated that CO was exclusively generated by subcellular fractions that contained membranes. The magnitude of the rate of product formation in brain supernatants depended on the concentration of Fe(II) and (or) Fe(III). The formation of CO, TBARS, CD, and LOOH increased linearly with time for up to 30 min, but the rates of product formation were different. Product formation was completely inhibited by BHT (100 µM), biliverdin (50 µM), bilirubin (50 µM), citrate (100 µM), and the Fe(II) chelators, desferrioxamine mesylate (100 µM) and diethylenetriaminepentaacetate, but not by 10 µM of the HO inhibitor, zinc deuteroporphyrin bis glycol. We conclude that CO generation is associated with the process of in vitro lipid peroxidation in tissues with limited antioxidant reserves.Key words: brain, carbon monoxide, conjugated dienes, lipid peroxidation, thiobarbituric acid reactive substances (TBARS).

Lipid peroxidation and altered vascular function in vitamin E-deficient rats

1989 ◽  
Vol 256 (6) ◽  
pp. H1539-H1545 ◽  
Author(s):  
C. A. Hubel ◽  
K. C. Griggs ◽  
M. K. McLaughlin
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Vascular Function ◽  
Pressor Response ◽  
Lipid Hydroperoxide ◽  
Thiobarbituric Acid ◽  
Female Rats ◽  
Dietary Vitamin ◽  
Reactive Material ◽  
Relaxation Responses

Female rats deprived of dietary vitamin E for 35 wk postweaning were analyzed for changes in vascular function. A functional state of vitamin E deficiency was indicated by a marked increase in spontaneous hemolysis of washed red cells by 22 wk of feeding. Elevated thiobarbituric acid-reactive material in aorta, liver, and plasma samples from vitamin-E deficient rats indicated increased lipid hydroperoxide formation. Systolic blood pressures and heart rates measured biweekly were unaltered by diet. Before being killed, the rats were catheterized and allowed to recover from anesthesia (methohexital sodium ip). The pressor response to graded doses of angiotensin II was significantly increased in the vitamin E-deficient group relative to its control. Isolated superior mesenteric artery segments from vitamin E-deficient rats demonstrated significantly decreased relaxation responses to acetylcholine. In contrast, artery contractile responses to 50 mM potassium and to graded doses of extracellular calcium did not differ, indicating that contractile capability was maintained. Surface blebbing of the femoral artery endothelium was observed by scanning electron microscopy. These data support a proposed link between lipid peroxidation and development of altered vascular function.

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