scholarly journals Carnosine, homocarnosine and anserine: could they act as antioxidants in vivo?

1989 ◽  
Vol 264 (3) ◽  
pp. 863-869 ◽  
Author(s):  
O I Aruoma ◽  
M J Laughton ◽  
B Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Hypochlorous Acid ◽  
Thiobarbituric Acid ◽  
Structural Similarity ◽  
Iron Ion ◽  
Inhibitory Effects ◽  
Inhibit Lipid Peroxidation ◽  
High Concentrations ◽  
Radical Damage

Carnosine, homocarnosine and anserine have been proposed to act as antioxidants in vivo. Our studies show that all three compounds are good scavengers of the hydroxyl radical (.OH) but that none of them can react with superoxide radical, hydrogen peroxide or hypochlorous acid at biologically significant rates. None of them can bind iron ions in ways that interfere with ‘site-specific’ iron-dependent radical damage to the sugar deoxyribose, nor can they restrict the availability of Cu2+ to phenanthroline. Homocarnosine has no effect on iron ion-dependent lipid peroxidation; carnosine and anserine have weak inhibitory effects when used at high concentrations in some (but not all) assay systems. However, the ability of these compounds to interfere with a commonly used version of the thiobarbituric acid (TBA) test may have led to an overestimate of their ability to inhibit lipid peroxidation in some previous studies. By contrast, histidine stimulated iron ion-dependent lipid peroxidation. It is concluded that, because of the high concentrations present in vivo, carnosine and anserine could conceivably act as physiological antioxidants by scavenging .OH, but that they do not have a broad spectrum of antioxidant activity, and their ability to inhibit lipid peroxidation is not well established. It may be that they have a function other than antioxidant protection (e.g. buffering), but that they are safer to accumulate than histidine, which has a marked pro-oxidant action upon iron ion-dependent lipid peroxidation. The inability of homocarnosine to react with HOCl, interfere with the TBA test or affect lipid peroxidation systems in the same way as carnosine is surprising in view of the apparent structural similarity between these two molecules.

Antioxidant and Antifungal Properties of Benzimidazole Derivatives

2010 ◽  
Vol 65 (9-10) ◽  
pp. 537-542 ◽  
Author(s):  
Canan Kuş ◽  
Fatma Sözüdönmez ◽  
Benay Can-Eke ◽  
Tülay Çoban
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Radical Scavenging ◽  
Liver Microsomes ◽  
Thiobarbituric Acid ◽  
Benzimidazole Derivatives ◽  
Rat Liver Microsomes ◽  
Inhibitory Effects ◽  
Stable Free Radical ◽  
Radical Scavenging Properties

Antioxidant and radical scavenging properties of a series of 2-[4-(substituted piperazin-/ piperidin-1-ylcarbonyl)phenyl]-1H-benzimidazole derivatives were examined. Free radical scavenging properties of compounds 11-30 and 33 were evaluated for the stable free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide anion radical. In addition the inhibitory effects on the NADPH-dependent lipid peroxidation levels were determined by measuring the formation of 2-thiobarbituric acid reactive substances (TBARS) using rat liver microsomes. Compound 33 which has a p-fluorobenzyl substitutent at position 1 exhibited the strongest inhibition (83%) of lipid peroxidation at a concentration of 10-3 M, while the nonsubstituted analogue 13 caused 57% inhibition. This result is fairly consistent with the antimicrobial activity results against both Staphylococcus aureus and Candida albicans.

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.

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 Sensitivity of plant mitochondrial terminal oxidases to the lipid peroxidation product 4-hydroxy-2-nonenal (HNE)

2005 ◽  
Vol 387 (3) ◽  
pp. 865-870 ◽  
Author(s):  
Alison M. WINGER ◽  
A. Harvey MILLAR ◽  
David A. DAY
Keyword(s):  
Lipid Peroxidation ◽  
Cytochrome C ◽  
Cell Cultures ◽  
Cysteine Residue ◽  
Lipid Peroxidation Product ◽  
Amino Acid Residues ◽  
Peroxidation Product ◽  
High Concentrations ◽  
Transport In Mitochondria

We have investigated the effect of the lipid peroxidation product, HNE (4-hydroxy-2-nonenal), on plant mitochondrial electron transport. In mitochondria isolated from Arabidopsis thaliana cell cultures, HNE inhibited succinate-dependent oxygen consumption via the Aox (alternative oxidase), but had minimal effect on respiration via Cox (cytochrome c oxidase). Maximal Cox activity, measured with reduced cytochrome c as substrate, was only slightly inhibited by high concentrations of HNE, at which Aox was completely inhibited. Incubation with HNE prevented dimerization of the Aox protein, suggesting that one site of modification was the conserved cysteine residue involved in dimerization and activation of this enzyme (CysI). However, a naturally occurring isoform of Aox lacking CysI and unable to be dimerized, LeAox1b from tomato (Lycopersicon esculentum), was equally sensitive to HNE inhibition, showing that other amino acid residues in Aox also interact with HNE. The presence of HNE in vivo in Arabidopsis cell cultures was also investigated. Induction of oxidative stress in the cell cultures by the addition of hydrogen peroxide, antimycin A or menadione, caused a significant increase in hydroxyalkenals (of which HNE is the most prominent). Western blotting of mitochondrial proteins with antibodies against HNE adducts, demonstrated significant modification of proteins during these treatments. The implications of these results for the response of plants to reactive oxygen species are discussed.

scholarly journals Peroxidase activity of hemoglobin and heme destruction in the presence of hydrogen peroxide and CT-DNA

2020 ◽  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Peroxidase Activity ◽  
Hypochlorous Acid ◽  
Iron Ion ◽  
Acid Effect ◽  
High Concentrations ◽  
Ct Dna ◽  
Heme Destruction ◽  
Protein Environment

The aim of this study was to investigate the peroxidase activity of Hb with different concentrations of hydrogen peroxide and compare it with hypochlorous acid effect on Hb. Hypochlorous acid at higher concentrations decomposed Hb and heme, releasing fee iron ion from the metal center. High concentrations of hydrogen peroxide switched the peroxidase activity of Hb towards the partial Hb and heme destruction. Heme alone was degraded showing that the Hb conformation and protein environment protects Hb from the distraction in the presence of highly increased hydrogen peroxide concentration that occurs as a result of oxidative stress. In the presence of CT-DNA acted inhibition of the peroxidase activity of Hb was observed signaling inhibited hydrogen peroxide consumption.

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 The antioxidant action of taurine, hypotaurine and their metabolic precursors

1988 ◽  
Vol 256 (1) ◽  
pp. 251-255 ◽  
Author(s):  
O I Aruoma ◽  
B Halliwell ◽  
B M Hoey ◽  
J Butler
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Radical ◽  
Hypochlorous Acid ◽  
Cysteic Acid ◽  
Iron Ions ◽  
Antioxidant Action ◽  
Iron Ion ◽  
Metabolic Precursors ◽  
Sufficient Concentration

It has been suggested that taurine, hypotaurine and their metabolic precursors (cysteic acid, cysteamine and cysteinesulphinic acid) might act as antioxidants in vivo. The rates of their reactions with the biologically important oxidants hydroxyl radical (.OH), superoxide radical (O2.-), hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) were studied. Their ability to inhibit iron-ion-dependent formation of .OH from H2O2 by chelating iron ions was also tested. Taurine does not react rapidly with O2.-, H2O2 or .OH, and the product of its reaction with HOCl is still sufficiently oxidizing to inactivate alpha 1-antiproteinase. Thus it seems unlikely that taurine functions as an antioxidant in vivo. Cysteic acid is also poorly reactive to the above oxidizing species. By contrast, hypotaurine is an excellent scavenger of .OH and HOCl and can interfere with iron-ion-dependent formation of .OH, although no reaction with O2.- or H2O2 could be detected within the limits of our assay techniques. Cysteamine is an excellent scavenger of .OH and HOCl; it also reacts with H2O2, but no reaction with O2.- could be measured within the limits of our assay techniques. It is concluded that cysteamine and hypotaurine are far more likely to act as antioxidants in vivo than is taurine, provided that they are present in sufficient concentration at sites of oxidant generation.

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