Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Thiobarbiturates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 127 records · Page 7Linked to original sources

Release of 2-thiobarbituric acid reactive products from glutamate or deoxyribonucleic acid by 1,2,4-benzenetriol or hydroquinone in the presence of copper ions.

Cytotoxic effects of various quinone compounds are thought to be due to the formation of semiquinone free radicals. Hydroquinone and 1,2,4-benzenetriol in the presence of copper ions release from glutamate or DNA aldehydic products capable of reacting with 2-thiobarbituric acid (TBA). The formation of TBA reactive products (TBAR) was greater in the presence of 1,2,4-benzenetriol in comparison with hydroquinone. Complete inhibition of formation of TBAR from glutamate by 1,2,4-benzenetriol and copper was observed in the presence of catalase, thiourea and mannitol. Albumin and superoxide dismutase offered substantial protection. Complete protection of formation of TBAR from DNA was observed in the presence of catalase and thiourea. Presence of albumin, mannitol and superoxide dismutase caused only partial inhibition. The formation of TBAR from glutamate or DNA is dependent on copper ion concentration. The present data indicate that hydroquinone and 1,2,4-benzenetriol in the presence of copper ions can lead to the formation of reactive hydroxyl radicals which can release TBAR from glutamate or DNA.

Albumins↗

Intracellular content of thiol compounds, thiobarbituric acid reactive substances and gamma-glutamyl transpeptidase in rat brain during anoxia.

Intracellular thiol compounds like glutathione play an important role in scavenging free radicals. Free radical reactions occur in the respiratory chain, and free radicals are known to accumulate in hypoxia and ischaemia. The content of thiobarbituric acid (TBA) reactive substances, thiol and non-protein thiol (reduced glutathione) concentrations along with the activity of gamma-glutamyl transpeptidase (GGTP), a membrane enzyme, were estimated in three regions of the brain in rats exposed to anoxia. It was observed that no change occurred in the content of TBA-reactive substances in any one of the three brain regions, although a significant increase in the non-protein thiol concentration occurred uniformly during anoxia. A significant increase in GGTP occurred in all the three brain regions during anoxia. The increase in the activity of GGTP is suggestive of an alteration in the function of blood-brain barrier during anoxia. These results are suggestive of an absence of lipid peroxidative damage during anoxia.

Animals↗

Different cellular targets for Cu- and Fe-catalyzed oxidation observed using a Cu-compatible thiobarbituric acid assay.

The widely used thiobarbituric acid (TBA) assay for oxidative damage to biomolecules fails in Cu2(+)-containing solutions due to the formation of a cloudy precipitate. The chelation of Cu2+ ions with EDTA or Chelex was investigated. Both prevented precipitate formation, but only Chelex allowed proper color development in the TBA assay. The Chelex modified assay could be adapted to a variety of systems, and was applied to the detection of Cu2+/ascorbate dependent deoxyribose breakdown and oxidative damage in erythrocyte ghosts, lysates and whole cells. Using this method, it was shown that Cu2+/ascorbate caused membrane damage in ghosts but not in whole red blood cells (RBC). Fe3+/ascorbate, on the other hand, caused formation of TBA-reactive products even in whole RBC. When Cu2+ and Fe3+ were presented to isolated hemoglobin as their 1:1 nitrilotriacetate complexes, the protein bound 10-12 cupric ions per molecule, but no ferric ions. It is suggested that oxidative damage catalyzed by copper or iron ions has different cellular targets, determined by the different binding properties of the two metals to various cellular components.

Chelating Agents↗

Dietary restriction decreases thiobarbituric acid-reactive substances generation in the small intestine and in the liver of young rats.

This study investigated the influence of dietary restriction on thiobarbituric acid-reactive substances (TBARS) contents and on the intracellular antioxidant defence system in the small intestine or liver of young rats. Four weeks of diet restriction (-40%) lowered the TBARS level in both organs. No variations were found for the superoxide dismutase and catalase activities; only liver seleno-dependent glutathione peroxidase was enhanced by the restriction. The protection appeared more marked in the intestine than in the liver, and would be dependent on glutathione concentration.

Animals↗

Effect of hyperthyroidism on the biliary release of thiobarbituric acid reactants in the rat.

The influence of daily doses of 0.1 mg 3,3',5-triiodothyronine (T3)/kg for three consecutive days on hepatic lipid peroxidation was assessed by the biliary release of thiobarbituric acid reactants (TBARS) in anesthetized rats. T3 treatment elicited a significant 80% increase in the biliary efflux of TBARS compared to control values, an effect determined by increments in both the TBARS concentration in bile (44%) and in the bile flow (25%). It is concluded that hyperthyroidism-induced oxidative stress stimulates hepatic lipid peroxidation measured in an in situ liver preparation, which significantly correlates with the enhancement in the rate of TBARS production assessed in liver homogenates.

Animals↗

Determination of a guanosine-malonaldehyde adduct in urine by high-performance liquid chromatography with a thiobarbituric acid reaction detector.

A new method for the determination of a guanosine-malonaldehyde adduct, beta-D-ribofuranosylpyrimido[1,2-a]purin-10(3H)-one (GMA), in rat and human urine is described. The method involves rapid pretreatment using, in sequence, polyamide, ion-exchange and reversed-phase cartridges; determination is by means of high-performance liquid chromatography with a thiobarbituric acid reactor in series with a fluorescence detector. This device can quantitatively determine the adduct at the sub-picomole level. This rapid, selective and sensitive method is suitable for the determination of guanine-malonaldehyde adducts in biological samples, such as human and rat urine. A semi-preparative method for the extraction and purification of these adducts from rat urine and for their identification by mass spectrometry and high-performance liquid chromatography with ultraviolet detection is also reported.

Animals↗

High-performance liquid chromatographic separation of malondialdehyde-thiobarbituric acid adduct in biological materials (plasma and human cells) using a commercially available reagent.

The assay of malondialdehyde (MDA) is widely used in clinical chemistry laboratories to investigate lipid peroxidation in oxidative pathologies. In the present work, the thiobarbituric acid (TBA) reaction was carried out on plasma, human erythrocytes and fibroblasts. The reagents used were those of the fluorimetry MDA kit manufactured by Sobioda. We have defined the application of this kit to high-performance liquid chromatography. This adaptation satisfied the criteria of good analytical practice. The detection limit was 2.5 pmol per injection. The retention time of the MDA-TBA2 peak (4.96 +/- 0.07 min) led to excellent resolution of the complex. The within-assay (6-12%) and between-assay (11-12%) precisions were satisfactory. The analytical recovery of MDA after spiking samples of human plasma with tetraethoxypropane standards varied from 70 to 100%. The mean lipoperoxide concentration determined in 32 healthy adults (20-40 years) was 1.04 +/- 0.23 mumol l-1 in plasma. Applied to the erythrocytes of fifteen laboratory workers, the method furnished physiological values of 0.59 +/- 0.21 mumol l-1. Concentrations were significantly higher in chronic renal dialysis patients (4.15 +/- 2.35 mumol l-1. The MDA content of fibroblasts cultured in standard medium was 0.38 +/- 0.04 mumol per g of protein and increased (5.78 +/- 1.38 mumol per g of protein) if the cells were grown in an iron-enriched medium. This accurate high-performance liquid chromatographic method for detection of MDA is the first one which can be applied to plasma, red blood cells and cultured cells. This technique will prevent false positives and should make inter-laboratory comparisons possible.

Adult↗

High-performance liquid chromatographic determination of nicotine and its urinary metabolites via their 1,3-diethyl-2-thiobarbituric acid derivatives.

The 1,3-diethyl-2-thiobarbituric acid (DETBA) assay for nicotine metabolites has been improved so that it can be used to determine the concentrations of nicotine and up to 12 metabolites in the urine of humans and laboratory animals, including phase 2 metabolites. The products of beta-glucuronidase cleavage found in human urine were mainly trans-3'-hydroxycotinine, cotinine, and a small amount of nicotine. Following isolation, spectroscopic analyses showed the structure of the nicotine DETBA derivative to be the one-to-one ring-opening product of DEBTA and the cyanopyridinium salt of nicotine.

Animals↗

Effect of aging on lipid peroxide levels induced by L-glutamic acid and estimated by means of a thiobarbituric acid test in rat brain tissue.

Studies of age-related changes based on the thiobarbituric acid (TBA) test appear to be inconsistent and contradictory. In our work, real basal (hypothetical, corrected to the zero concentration of atmospheric oxygen), basal (atmospheric oxygen-stimulated) and stimulated (L-glutamic and hydrochloric acids) levels of TBA-reactive products (TBARP) were estimated in the brain (hippocampus--HPC, cortex--COR, cerebellum--CRB) from young (3 months) and old (28 months) male and female Wistar rats. The values of basal levels of TBARP were different in young (HPC > COR > CRB) as well as in old animals (COR > CRB > HPC). Thus, the process of aging caused a significant decrease in the HPC (to 72%) and no change in the COR and CRB. Levels stimulated by L-glutamic acid were significantly decreased (COR, CRB) and unchanged (HPC) in old compared to young animals. The real basal levels estimated by regression analysis seem to be higher in the brain tissue damaged by aging. We discuss the usefulness of the TBA test applied to aged tissue, the effect of acidosis, the effectivity of L-glutamic acid to generate free radicals and the differences between individual brain areas.

Aging↗

The reaction of 2-thiobarbituric acid with biologically active alpha,beta-unsaturated aldehydes.

The standard assay for lipid peroxidation is the measurement of the pink, 532 nm absorbing chromogen which is formed upon reaction of 2-thiobarbituric acid (TBA) with the lipid peroxidation product malonaldehyde (MDA). The present studies indicate that the toxic lipid peroxidation product trans-4-hydroxynonenal and its dehydration product trans,trans-nonadienal react with TBA to form chromogens which absorb maximally at 530 and 532 nm, respectively. Other biologically active alpha,beta-unsaturated aldehydes, such as acrolein and crotonaldehyde, short-chain homologs of alkenals formed during lipid peroxidation, and trans,trans-muconaldehyde, a novel diene dialdehyde, react with TBA to form products which absorb maximally at 495 nm. The molar extinction coefficients of the aldehyde:TBA chromogens formed were found to vary widely, suggesting that only small contributions to the 532 nm absorption by TBA adducts of reactive aldehydes other than MDA may be encountered during the use of the TBA assay.

Aldehydes↗

Lipid peroxidation measured as thiobarbituric acid-reactive substances in tissue slices: characterization and comparison with homogenates and microsomes.

Liver slices were used to measure lipid peroxidation induced by bromotrichloromethane, tert-butyl hydroperoxide (t-BOOH), or ferrous iron. The responses of liver homogenates and microsomes to oxidative conditions were compared with the response of tissue slices. Lipid peroxidation was evaluated by the production of thiobarbituric acid-reactive substances (TBARS). As was observed in homogenates and microsomes, TBARS production by liver slices depended upon the amount of tissue, the incubation time, inducer, the amount of inducer, and the presence of antioxidant. Control liver slices incubated at 37 degrees C for 2 h produced 19 nmol of TBARS per g of liver. When slices were incubated in the presence of 1 mM BrCCl3, 1 mM t-BOOH, or 50 microM ferrous iron, TBARS production increased 4.6-, 8.2-, or 6.7-fold over the control value, respectively. Comparable induction of TBARS by liver homogenates and microsomes was observed when these preparations were incubated with the same inducers. Addition of 5 microM butylated hydroxytoluene (BHT) prevented the induction of TBARS by 50 microM ferrous iron by liver slices. The results indicate the usefulness of tissue slices to measure lipid peroxidation. The usefulness of tissue slices is emphasized when a number of compounds or tissues are studied and tissue integrity is desired as in toxicological, pharmacological, and nutritional studies where reduced numbers of experimental animals is a relevant issue.

Animals↗

Potential thiobarbituric acid-reactive substances in peroxidized lipids.

This paper describes what components produce a red pigment in the thiobarbituric acid (TBA) test of peroxidized lipids. Alk-2-enals, alka-2,4-dienals and hydroperoxide functions are potential candidates for the red pigment in the TBA test. The TBA test can be regarded as an excellent method to reflect the combined effect of these components and thus the degree of lipid oxidation.

Aldehydes↗

Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury.

Increasing appreciation of the causative role of oxidative injury in many disease states places great importance on the reliable assessment of lipid peroxidation. Malondialdehyde (MDA) is one of several low-molecular-weight end products formed via the decomposition of certain primary and secondary lipid peroxidation products. At low pH and elevated temperature, MDA readily participates in nucleophilic addition reaction with 2-thiobarbituric acid (TBA), generating a red, fluorescent 1:2 MDA:TBA adduct. These facts, along with the availability of facile and sensitive methods to quantify MDA (as the free aldehyde or its TBA derivative), have led to the routine use of MDA determination and, particularly, the "TBA test" to detect and quantify lipid peroxidation in a wide array of sample types. However, MDA itself participates in reactions with molecules other than TBA and is a catabolic substrate. Only certain lipid peroxidation products generate MDA (invariably with low yields), and MDA is neither the sole end product of fatty peroxide formation and decomposition nor a substance generated exclusively through lipid peroxidation. Many factors (e.g., stimulus for and conditions of peroxidation) modulate MDA formation from lipid. Additional factors (e.g., TBA-test reagents and constituents) have profound effects on test response to fatty peroxide-derived MDA. The TBA test is intrinsically nonspecific for MDA; nonlipid-related materials as well as fatty peroxide-derived decomposition products other than MDA are TBA positive. These and other considerations from the extensive literature on MDA. TBA reactivity, and oxidative lipid degradation support the conclusion that MDA determination and the TBA test can offer, at best, a narrow and somewhat empirical window on the complex process of lipid peroxidation. The MDA content and/or TBA reactivity of a system provides no information on the precise structures of the "MDA precursor(s)," their molecular origins, or the amount of each formed. Consequently, neither MDA determination nor TBA-test response can generally be regarded as a diagnostic index of the occurrence/extent of lipid peroxidation, fatty hydroperoxide formation, or oxidative injury to tissue lipid without independent chemical evidence of the analyte being measured and its source. In some cases, MDA/TBA reactivity is an indicator of lipid peroxidation; in other situations, no qualitative or quantitative relationship exists among sample MDA content, TBA reactivity, and fatty peroxide tone. Utilization of MDA analysis and/or the TBA test and interpretation of sample MDA content and TBA test response in studies of lipid peroxidation require caution, discretion, and (especially in biological systems) correlative data from other indices of fatty peroxide formation and decomposition.

Animals↗

Ferrous-iron-induced oxidation in chicken liver slices as measured by hemichrome formation and thiobarbituric acid-reactive substances: effects of dietary vitamin E and beta-carotene.

Hemichrome formation in chicken liver slices was determined by employing a Heme Protein Spectra Analysis Program (HPSAP) on the visible spectrum of the liver tissue. Relative hemichrome formation (RHF) in liver tissue exposed to ferrous iron for 1 h at 37 degrees C could be predicted according to the general catalytic equation RHF = k.[Fe2+]/(Ap + [Fe2+]), with k = 132 +/- 30, where the factor Ap represents the additive antioxidative potential in the liver tissue. RHF in Fe2+ exposed liver slices incubated at 37 degrees C for 1 h correlated significantly with formation of thiobarbituric acid-reactive substances (TBARS) (r = .77, P < .0001). RHF was found to decrease significantly with increasing vitamin E concentration in liver tissue exposed to ferrous iron (1 h, 37 degrees C). However, the influence of beta-carotene on RHF in ferrous-iron exposed liver slices (1 h, 37 degrees C) was less evident, as the concentration of Fe2+ was found to be decisive for whether beta-carotene acted as an antioxidant or a prooxidant under the conditions in question. Results in the liver slice model system regarding the effect of vitamin E and beta-carotene on iron overload were supported in a subsequent in vivo iron injection experiment with chicks. These observations indicate that RHF is a sensitive marker for ferrous-iron-induced oxidative damage in the present tissue slice system.

Animals↗

Probucol scavenged 1,1-diphenyl-2-picrylhydrazyl radicals and inhibited formation of thiobarbituric acid reactive substances.

Probucol is suggested to have antioxidant properties. The direct scavenging action of probucol on hydroxyl radicals, superoxide and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals were examined using electron spin resonance (ESR) spectrometry. Probucol scavenged DPPH radicals dose dependently but showed no effect on hydroxyl radicals and superoxide generated by Fenton reaction and by hypoxanthine-xanthine oxidase system, respectively. It inhibited the formation of thiobarbituric acid reactive substances (TBARS) in rat cortex homogenate induced by ascorbic acid and FeCl2 at low dose, but it increased TBARS formation at high doses. Probucol showed no effect on the carbon centered radicals. Iron injection into the rat cortex, which is an experimental model for traumatic epilepsy, increased TBARS level in the cortex, hippocampus, striatum and cerebellum, but pretreatment with probucol inhibited the increase in these brain parts except for the hippocampus. These results suggest that the antioxidant property of probucol is partly due to its free radical scavenging effect.

Animals↗

Variable effects of exercise intensity on reduced glutathione, thiobarbituric acid reactive substance levels, and glucose concentration.

BACKGROUND: Physical exercise may be associated with a 10- to 20-fold increase in whole body oxygen uptake. Generation of free oxygen radicals (FORs) is elevated to a level that overwhelms tissue antioxidant defense systems in exercise. One of the most reliable indices of exercise-induced oxidant production is tissue glutathione oxidation. METHODS: In this study three different volunteer groups carried out various sports disciplines and worked at least as amateurs for 6-7 years before and after aerobic (Aer)-, anaerobic (Anae)-, or aerobic + anaerobic (Aer-Anae)-dominant exercises. Thiobarbituric acid reactive substances (TBARS) reduced glutathione (GSH) levels, glucose concentration was measured, and we investigated their relationships with different types of exercise. From all groups (n=60, each group comprising 10 females and 10 males), we collected blood samples at the following five different times: before exercise; immediately after exercise, and 4, 24, and 48 h after completion of exercise. These samples were assayed for whole blood GSH, plasma TBARS levels, and glucose concentration. RESULTS: Significant increase in Aer-Anae was noted in levels of TBARS while decrease was observed in glutathione levels in exercise group as compared with prior levels in all groups. However, no statistical difference was observed in total group levels before and after exercise and in male and female groups compared before and after exercise. When gender differences were taken into account, females generally had higher levels of GSH, whereas TBARS levels were higher in males. When compared either before or after exercise, levels of glucose concentration--especially immediately after exercise period in all groups--were higher. In addition, in Anae groups glucose concentrations were higher at 4 and 24 h in females than in males. Aer exercise caused oxidative stress to a lesser degree, whereas Aer-Anae exercise caused oxidative stress of higher degree that was statistically significant. CONCLUSIONS: According to our findings, exercise increased TBARS level significantly in all groups, especially more so in Aer-Anae groups. In addition, GSH was increased more in females than in males, while concentration of glucose did not change remarkably. Additionally, it can be stated that women are more resistant to oxidative stress.

Adult↗

Oxalate modulates thiobarbituric acid reactive species (TBARS) production in supernatants of homogenates from rat brain, liver and kidney: effect of diphenyl diselenide and diphenyl ditelluride.

The aim of this paper was to investigate the mechanism(s) involved in the sodium oxalate pro-oxidative activity in vitro and the potential protection by diphenyl diselenide ((PhSe)(2)) and diphenyl ditelluride ((PhTe)(2)) using supernatants of homogenates from brain, liver and kidney. Oxalate causes a significant increase in the TBARS (thiobarbituric acid reactive species) production up to 4mmol/l and it had antioxidant activity from 8 to 16mmol/l in the brain and liver. Oxalate had no effect in kidney homogenates. The difference among tissues may be related to the formation of insoluble crystal of oxalate in kidney, but not in liver and brain homogenates. (PhSe)(2) and (PhTe)(2) reduced both basal and oxalate-induced TBARS in rat brain homogenates, whereas in liver homogenates they were antioxidant only on oxalate-induced TBARS production. (PhSe)(2) showed a modest effect on renal TBARS production, whereas (PhTe)(2) did not modulate TBARS in kidney preparations. Oxalate at 2mmol/l did not change deoxyribose degradation induced by Fe(2+) plus H(2)O(2), whereas at 20mmol/l it significantly prevents its degradation. Oxalate (up to 4mmol/l) did not alter iron (10micromol/l)-induced TBARS production in the brain preparations, whereas at 8mmol/l onwards it prevents iron effect. In liver preparations, oxalate amplifies iron pro-oxidant activity up to 4mmol/l, preventing iron-induced TBARS production at 16mmol/l onwards. These results support the antioxidant effect of organochalcogens against oxalate-induced TBARS production. In addition, our results suggest that oxalate pro- and antioxidant activity in vitro could be related to its interactions with iron ions.

Animals↗

A novel HPLC method for the measurement of thiobarbituric acid reactive substances (TBARS). A comparison with a commercially available kit.

OBJECTIVES: Malondialdehyde (MDA) as a part of thiobarbituric acid reacting substances (TBARS) is frequently used as an indicator of lipid peroxidation. Most methods for the measurement of TBARS require long derivatization time and addition of antioxidants in the samples. Furthermore, comparison of these methods with commercially available HPLC kits is lacking. DESIGN AND METHODS: We investigated column performance of five different columns, tested eight different acids for the hydrolysis of the samples, and estimated stability of derivatized plasma samples with different anticoagulants. The samples were derivatized with TBA. The peak for the TBA(2)-MDA adduct was separated and detected by HPLC. RESULTS: Performance of the Phenomenex Gemini column was best. PCA at the concentration of 0.1125 N was used in this method. Coefficient of variation (CV %) within the run and between the run was 4.1% and 6.7%, and analytical recovery was 90-94%. The retention time of the TBA(2)-MDA peak was 1.8 min. Reference intervals for TBARS in serum from 250 individuals were 0.53 and 2.1 micromol/l using our HPLC method and 0.07 and 0.24 micromol/l using the Chromsystems assay. Linear regression with log converted values revealed weak relationship between the two methods (r(2) = 0.064). CONCLUSIONS: Our HPLC method for the analysis of TBARS in serum and plasma is fast and accurate and therefore can be used in clinical studies.

Adolescent↗