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PubMed1992

Interpretation of the thiobarbituric acid reactivity of rat liver and brain homogenates in the presence of ferric ion and ethylenediaminetetraacetic acid.

The thiobarbituric acid (TBA) reactivity of rat liver and brain homogenates was characterized to elucidate what kinds of aldehyde species contributed to the reactivity. Characteristic pH dependence of the reactivity with a maximum at around pH 3 and marked enhancement of the reactivity by t-butyl hydroperoxide (t-BuOOH) and ferric ion were similar to those of alkadienals. The amounts of aldehyde species, including alkadienals determined as 2,4-dinitrophenylhydrazones, were high enough to account for the enhanced reactivity. The reactivity was inhibited by ethylenediaminetetraacetic acid (EDTA) but not completely, suggesting the presence of malonaldehyde whose reactivity was not affected by EDTA. The amounts of malonaldehyde determined as 1-(2,4-dinitrophenyl)pyrazole could account for a part of the reactivity in the presence of EDTA. Hence, the TBA reactivity of liver and brain homogenates at around pH 3 in the presence of t-BuOOH and ferric ion may be accounted for by alkadienals and malonaldehyde and that in the presence of EDTA by malonaldehyde.

Animals↗
PubMed1989

Thiobarbituric acid-reactive substance formation of rat kidney brush border membrane vesicles induced by ferric nitrilotriacetate.

An iron chelate, ferric nitrilotriacetate (Fe3+-NTA), is nephrotoxic and also carcinogenic to the kidney in experimental animals. Iron-promoted lipid peroxidation in the proximal tubules is thought to be responsible for the pathologic process. In the present study, iron-promoted lipid peroxidation, with thiobarbituric acid (TBA) formation as an indication, in the tubular surface was simulated in vitro using rat kidney brush border membrane vesicles and the results were compared with those using linoleate micelles and rat liver microsomal lipid liposomes. Addition of ascorbate, cysteine, or dithiothreitol to the Fe3+-NTA solution resulted in consumption of dissolved oxygen and promoted the lipid peroxidation in the micelles and in the liposomes. In contrast, addition of glutathione to the Fe3+-NTA solution caused only sluggish oxygen consumption and far less peroxidation in these lipid systems. When the brush border membrane vesicles were used for the peroxidation substrate, Fe3+-NTA and glutathione could promote TBA formation at a rate comparable to that elicited by Fe3+-NTA with cysteine or dithiothreitol. Acivicin, a gamma-glutamyl transpeptidase inhibitor, suppressed the peroxidation of the brush border membrane vesicles promoted by Fe3+-NTA and glutathione. These results suggest the following mechanism of proximal tubular cell lipid peroxidation promoted by Fe-NTA: Fe3+-NTA filtered through glomeruli is rapidly reduced by cysteine and Fe2+-NTA starts lipid peroxidation at the site, leading to proximal tubular necrosis. Cysteine is amply supplied by the decomposition of glutathione within the lumen by the action of gamma-glutamyl transpeptidase and dipeptidase situated at the proximal tubular brush border membrane.

Acetates↗
PubMed1990

Polychlorinated biphenyls-induced lipid peroxidation as measured by thiobarbituric acid-reactive substances in liver subcellular fractions of rats.

Rats were given a 0.05% polychlorinated biphenyls (PCB) diet supplemented with adequate nutrients for 10 days and not only PCB-induced lipid peroxidation as measured by thiobarbituric acid (TBA)-reactive substances but also variations of lipid peroxides scavengers in liver and its subcellular fractions (nuclei and cell debris, mitochondrial, microsomal and cytosolic fractions) were investigated. The lipid peroxidation in liver and subcellular fractions in the PCB-treated group increased significantly except in the nuclei and cell debris fraction. The increase in lipid peroxidation in the microsomal fraction appeared to be associated in part with the decrease in vitamin E (alpha-tocopherol) content and induction of drug-metabolizing enzymes. In the cytosolic fraction, the total lipid content increased, glutathione peroxidase (GSHPx) activity decreased and the quantity of free radical-reactive substances suppressing lipid peroxidation was low as measured by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) value. From these results, the increase in lipid peroxidation in the cytosolic fraction in the PCB-treated group was ascribed to the abundance and availability of oxidizable substrate attended with fatty liver, to the decline in GSHPx activity, and to the insufficiency in antioxygenic activity as observed by the decrease in the DPPH value.

Animals↗
PubMed1993

A phospholipase A2 inhibitor decreases generation of thiobarbituric acid reactive substance during lung ischemia-reperfusion.

A novel active-site directed specific inhibitor of phospholipase A2 (PLA2), 1-hexadecyl-3-trifluoroethylglycero-sn-2-phosphomethanol (MJ33), administered endotracheally co-dispersed in liposomes, significantly reduced the formation of thiobarbituric acid reactive substances (TBARS) in isolated rat lungs subjected to ischemia-reperfusion. Elevated conjugated dienes were unaffected. This contrasts with the effects of the cyclo-/lipoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA), which decreased formation of both TBARS and conjugated dienes (CD). The effects of MJ33 plus ETYA were additive for TBARS but results for CD were similar to ETYA alone. A similar dissociation of inhibition of TBARS and CD formation by MJ33 was observed with t-butyl hydroperoxide induced lipid peroxidation of isolated lung microsomes. Assay of lung homogenate with phosphatidylcholine as substrate showed that MJ33 selectively inhibited the Ca(2+)-independent acidic PLA2. MJ33 had no effect on thromboxane B2 release by the isolated lung, indicating the effects of acidic PLA2 inhibition do not involve the arachidonate cascade. MJ33 also partially prevented lung edema and lactate dehydrogenase release associated with ischemia-reperfusion. The observations show that this PLA2 inhibitor can be delivered to oxidant-sensitive lung sites by its co-dispersal in liposomes, and that oxidant-induced lipid peroxidation in this model of lung injury occurs in a complex lipid prior to PLA2 activity.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1984

Elevation of thiobarbituric acid values in the rat liver intoxicated by T-2 toxin.

In the present study we first demonstrated that T-2 toxin markedly stimulated lipid peroxidation specifically in the liver of rats. The amount of lipid peroxides in the liver, estimated by the thiobarbituric acid (TBA) method, increased dose dependently, being proportional to the extent of its acute toxicity measured by various parameters in rats fed a commercial diet. Further, to elucidate the mechanism of lipid peroxidation and its role in hepatic injury caused by T-2 toxin, time-course studies on the correlation between lipid peroxide content and some biological and histopathological data were undertaken in rats given 4 mg of the toxin/kg perorally. The TBA reactive substances in the liver began to increase after 6 hr. However, much earlier than this there were some other alterations, which included decreases in the amount of cytochrome P-450 in the liver, of GPT (thereafter an increase) and phospholipids in the plasma, and of basophilic masses in the hepatocytes (arrayed as a rough endoplasmic reticulum in the electron micrograph). The vitamin E-deficient study showed that vitamin E markedly inhibited the stimulative effect of T-2 toxin on lipid peroxidation, but not diminish any other measured parameters of the injury. The toxin-induced stimulation of lipid peroxidation does not appear to be caused by activation of microsomal NADPH-cytochrome c reductase nor by a decrease in the level of cytosolic glutathione peroxidase. These results suggest that T-2 toxin might induce some alteration of the membrane structure and consequently might stimulate lipid peroxidation in situ.

Animals↗
PubMed1979

Catalase, superoxide dismutase, glutathione reductase and thiobarbituric acid-reactive products in normal and dystrophic human muscle.

The level of thiobarbituric acid-reactive products and the specific activities of catalase and glutathione reductase were significantly higher in muscles from patients with major forms of muscular dystrophies over those of control subjects. Superoxide dismutase activity was not altered in dystrophic muscles. These findings indicate the occurrence in human dystrophic muscles of an increased level of lipid peroxidation and the possible activation of certain enzymes that could conceivably inhibit lipid peroxidation in vivo.

Catalase↗
PubMed1981

Superoxide dismutase, glutathione peroxidase and thiobarbituric acid-reactive compounds in erythrocytes in Duchenne muscular dystrophy.

The activities of erythrocyte superoxide dismutase and glutathione peroxidase in patients with Duchenne muscular dystrophy were normal compared with healthy male controls, as were the levels of thiobarbituric acid-reactive compounds produced during incubation of erythrocytes in the presence of 10 mmol.1-1 hydrogen peroxide. These results suggest that the chief mechanisms for protecting the erythrocyte membrane from peroxidative damage are unimpaired and do not support the idea that the reported erythrocyte abnormalities in this disease result from increased susceptibility to lipid peroxidation.

Colorimetry↗
PubMed1981

Improvement of the thiobarbituric acid assay for serum glycosylprotein determination.

This study shows that the thiobarbituric acid (TBA) reaction as applied to the measurement of non-enzymatically glycosylated serum proteins(s) [1], yields erroneous results unless strictly standardized conditions are followed. Critical points are in particular (a) the concentrations of NaBH4 required for the preparation of the blanks by reduction of the ketoamine linkages; (b) the amounts of protein which should be identical in all serum samples to be compared; (c) dialysis for removal of glucose and NaBH4 prior to hydrolysis; (d) increase in the yield of 5-hydroxymethylfurfural (HMF) by appropriate conditions of hydrolysis. From our data obtained with an improved TBA-assay it appears that about 90% of total glycosylated serum protein is accounted for by glycosylated albumin. Thus changes in the latter used for diagnostic purposes in diabetes, may well be reflected by total serum glycosylprotein measurement.

Blood Glucose↗
PubMed1983

Measurement of nonenzymatically glucosylated serum protein by an improved thiobarbituric acid assay.

We describe here some useful modifications of the thiobarbituric acid (TBA) assay for measurement of nonenzymatic glucosylation of serum protein. The modified assay minimizes interference by glucose without a lengthy dialysis step, and does not require an independent blank determination. These modifications should make the TBA assay more convenient for evaluating glycemic control in diabetes. Serum protein is first precipitated with cold ethanol to remove endogenous glucose. The protein is then hydrolyzed in an oxalic acid solution to release glucose as hydroxymethylfurfural (HMF). The HMF is reacted with TBA to form a chromophore which is extracted into isobutanol for spectrophotometric analysis (lambda max = 435 nm). The absorbance at 435 nm is corrected by subtracting a blank reading at 500 nm, and the nmol HMF released is determined using a standard curve prepared with pure HMF. Normal values of this assay for both adults and children are 0.38 +/- 0.10 nmol HMF/mg serum protein (means +/- 2 SD). When the assay was applied to serum samples from a group of 39 Type I diabetic children more than 90% of the children exceeded the normal range of the assay.

Adolescent↗
PubMed1992

Optimized determination of malondialdehyde in plasma lipid extracts using 1,3-diethyl-2-thiobarbituric acid: influence of detection method and relations with lipids and fatty acids in plasma from healthy adults.

We investigated the influence of different concentrations of Fe3+, phosphoric acid, butylated hydroxytoluene and glutathione on the production of the malondialdehyde-1,3-diethyl-2-thiobarbituric acid adduct in plasma lipid extracts. Following organic solvent extraction the stable product was analyzed by spectrophotometry (537 nm), fluorometry (547 nm) and high-performance liquid chromatography with fluorometric detection. Using optimized reaction conditions there was good agreement between the three methods, with slightly higher values for the spectrophotometric method. Plasma total lipid malondialdehyde reference values for 24 healthy adults amounted to 1.30 +/- 0.23 mumol/l (spectrophotometric method) and 1.11 +/- 0.31 mumol/l (fluorometric method). Plasma lipid malondialdehyde concentrations correlated significantly with plasma triglycerides (r = 0.527), total cholesterol (r = 0.612) and total fatty acids (r = 0.810) and with the total number of double bonds present in plasma fatty acids with three or more double bonds (r = 0.923).

Adult↗
PubMed1995

Measurement of serum lipid peroxidation during exercise using three different methods: diene conjugation, thiobarbituric acid reactive material and fluorescent chromolipids.

Serum lipid peroxidation was measured by three different methods (diene conjugation, DC; thiobarbituric acid reactive material, TBARM; and fluorescent chromolipids, FC) during physical exercise of different duration. The aim of the study was to investigate which of the three methods is the most representative in measuring oxidative stress after physiological stimulus (physical exercise) in man. In general, diene conjugation is a measure of early events of lipid peroxidation reactions, TBARM measures end products of lipid peroxidation and FC are products formed by reaction of end products of lipid peroxidation with the amino groups. In trial I, 8 subjects ran 1 km with maximal speed; in trial II, 7 subjects ran 10 km with maximal speed; in trial III, 9 subjects ran 27 km with maximal speed, and in trial IV, 5 subjects cycled 8 days in competition, altogether 1061 km biking. In each trial venous blood samples were taken before and immediately after the exercise. In trials II, III, and IV serum DC concentration increased by 14% (P < 0.05), 11% (P < 0.01), and 25% (P < 0.05), respectively, during the exercise. FC or TBARM did not change in the trials. We conclude that DC as a measure of the early phase of lipid peroxidation may be less affected by protective antioxidant functions than FC and TBARM methods, which both measure end products of lipid peroxidation. Therefore, DC may be the most sensitive of the three methods to estimate serum lipid peroxidation induced by exercise in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Factors affecting the thiobarbituric acid test as index of red blood cell susceptibility to lipid peroxidation: a multivariate analysis.

The relationship between formation of thiobarbituric acid reactive substances (TBARS) in red blood cells (RBC) after exposure to H2O2 and factors potentially able to modulate it was investigated by a multivariate analysis in 92 healthy volunteers. The independent covariates considered were: RBC membrane fatty acids and cholesterol, RBC antioxidant enzymes and zinc, plasma vitamins A and E and serum selenium, zinc and copper. The stepwise multiple-linear-regression analysis revealed RBC membrane fatty acids and cholesterol as predictors of a consistent proportion of the RBC-TBARS variability whereas none of the antioxidants entered the equation. The unsaturation index was the most important individual predictor; RBC-TBARS increased with increasing concentrations of total omega-3 polyunsaturated fatty acids, C 20:5 omega-3 and cholesterol, whereas they decreased with increasing concentrations of total monounsaturated fatty acids, saturated fatty acids, C 16:0 and C 18:0. It is suggested that formation of TBARS, at least in currently used conditions, reflects mainly the lipid composition of the tissue under investigation, without giving sufficient information about the status of the antioxidant defences.

Adult↗
PubMed1982

Free-radical damage to lipids, amino acids, carbohydrates and nucleic acids determined by thiobarbituric acid reactivity.

1. The thiobarbituric acid (TBA) reaction, widely applied to the detection of autoxidation in polyunsaturated fatty acids, can be used to measure free-radical damage to amino acids, carbohydrates and nucleic acids. 2. In all of these systems malondialdehyde (MDA) is predominately formed from intermediate precursor molecules which break down during the acid-heating stage of the TBA test. 3. The acid reagent used to bring about these decompositions appears to be critical.

Amino Acids↗
PubMed1996

Automated high-performance liquid chromatographic separation with spectrofluorometric detection of a malondialdehyde-thiobarbituric acid adduct in plasma.

An automated HPLC separation method for the detection of malondialdehyde (MDA) in plasma samples of a healthy population is described. The procedure involves a first step of acidic hydrolysis and complex formation with thiobarbituric acid (TBA), then a protein precipitation step, and finally the separation of TBA-MDA adducts through a complete HPLC apparatus with spectrofluorometric quantification. This procedure is very useful for a routine laboratory because of its rapidity (tR = 1.7 min), simplicity and applicability, and the method gives very good results with respect to linearity (0.1-12 mumol/l), precision (within-assay C.V.%: 8, between-assay C.V.%: 10) and accuracy (recovery average: 91.66%).

Adolescent↗
PubMed1988

Plasma thiobarbituric acid reactivity: reaction conditions and the role of iron, antioxidants and lipid peroxy radicals on the quantitation of plasma lipid peroxides.

The effects of Fe3+, lipid peroxy radicals and the antioxidant butylated hydroxytoluene on the 2-thiobarbituric (TBA) acid quantitation of plasma lipid peroxides were investigated. Whole plasma and plasma fractions prepared by trichloroacetic acid (TCA) protein precipitation and lipid extraction, demonstrated markedly differing TBA reactivities in the presence or absence of added Fe3+. Examination of the spectral profiles of the TBA reacted whole plasma and TCA precipitated fractions demonstrated the presence of interfering compounds which gave rise to an artifactual increase in lipid peroxide concentrations. In contrast the TBA reacted lipid extracts had low levels of interfering compounds that could be removed by our previously described high pressure liquid chromatographic method (Wade, Jackson and van Rij (1985) Biochem. Med. 33, 291-296). Further characterization of the TBA reactivity of the lipid extract showed that Fe3+ at an optimal concentration of 0.5 mM was necessary for the quantitative decomposition of the lipid peroxides to the TBA reactive product malondialdehyde (MDA). However the presence of Fe3+ resulted in further peroxidation of any unsaturated lipids present. Butylated hydroxytoluene (BHT) at an optimal concentration of 1.4 mM inhibited Fe3+ stimulated peroxidation without affecting the formation of the MDA-TBA chromogen. Using a standardized TBA test with plasma lipid extracts and the addition of optimal concentrations of Fe3+ and BHT, we have determined the mean concentration of lipid peroxides in 30 healthy human subjects to be 102.7 +/- 20.0 ngm/ml.

Butylated Hydroxytoluene↗
PubMed1991

Intestinal, hepatic and renal production of thiobarbituric acid reactive substances and myeloperoxidase activity after temporary aortic occlusion and reperfusion.

Ischemia induced oxygen free radical damage was formerly attributed only to xanthine oxidase in intestine, liver, kidney and heart. A reevaluation indicated neutrophils as one of the major sources of postischemic oxidative tissue damage, chiefly in the intestine. Our data, obtained from the same occlusion time period for intestine, liver and kidney, showed a certain oxidative damage in intestine and kidney already during ischemia, expressed by an increase of thiobarbituric acid reactive substances (TBARS), whereas the liver sustained damage of this kind only during reperfusion. Oxidative stress was expressed by a comparison of the increase of TBARS, though this test is not a measure of a specific product of lipid peroxidation, but rather comprises several breakdown products of free radical damage. Myeloperoxidase as measure of neutrophil stimulation increased in the intestine and liver. The kidney sustained damage without an increase of myeloperoxidase activity, but showed a similar pattern of increase of TBARS as in the intestine. Our data suggest a major role of neutrophils in intestinal ischemia induced damage, where neutrophils can effect initiation and propagation. In the liver neutrophils may play a minor role concerning propagation, but they may act as an important initiating mechanism. Hepatic tissue shows a high ischemic tolerance, which is demonstrated by a missing increase of TBARS in spite of a certain increase of myeloperoxidase activity during ischemia. This can be interpreted by the high capacity of antioxidative mechanisms of liver tissue and the ability of a higher oxygen extraction ratio under nearly ischemic conditions. In the kidney there appears a smaller contribution of neutrophils. The similar pattern of increase of TBARS in kidney and intestine demonstrates a comparable low ischemic tolerance of these two tissues, whereas different initiating and propagating systems may occur.

Animals↗
PubMed1993

Age-associated changes in superoxide dismutase activity, thiobarbituric acid reactivity and reduced glutathione level in the brain and liver in senescence accelerated mice (SAM): a comparison with ddY mice.

The antioxidant defense alteration in young and old senescence accelerated mice (SAM) was studied by examining superoxide dismutase (SOD) activity, thiobarbituric acid (TBA) reactivity, and reduced glutathione (GSH) level in brain and liver tissues. The changes were compared with those in age-paired ddY mice, a strain exhibiting normal aging. SAM mice showed an age-dependent increase in SOD activity in liver, and an age-dependent increase in TBA reactivity in both the brain and the liver; they also showed an age-dependent decrease in the GSH level in the brain and the liver. When compared with ddY mice, SAM mice showed a higher SOD activity in the brain (at both 3 and 11 months old), a lower GSH level in the liver (at 3 months old), and a higher TBA reactivity in the liver (at 3 months old). These findings suggest that the mechanism of senescence acceleration in SAM mice is to some extent related to free radical damage.

Aging↗
PubMed1982

Thiobarbituric acid reactive substances and vitamin E in serum and cerebrospinal fluid from patients with cerebral apoplexy.

Thiobarbituric acid (TBA) reactive substances in serum and cerebrospinal fluid from patients with cerebral apoplexy were determined and their relationship to this disease was studied. TBA reactants in serum were elevated in patients with cerebral apoplexy, but there was no difference between patients with brain tumor or other neurological disease and healthy persons. TBA reactants in cerebrospinal fluid in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma, and its levels in patients with cerebral infarction or brain tumor were also higher than in healthy persons. Serum alpha-tocopherol levels were elevated in patients with cerebral infarction, but were relatively low in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma. The reverse was the case with cerebrospinal fluid levels of alpha-tocopherol. That is, the sequence of decreasing level of alpha-tocopherol in cerebrospinal fluid was intracerebral hematoma, cerebral aneurysm, cerebral arterial and venous anomalies, and cerebral infarction. The levels of TBA reactive substances in patients with cerebral apoplexy showed a positive correlation between serum and cerebrospinal fluid, and the levels of alpha-tocopherol showed a similar correlation.

Aged↗