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PubMed1997

Increased hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients.

Symptoms of bronchial asthma are a manifestation of airway inflammation. Circulatory leucocytes (predominantly eosinophils, mast cells and neutrophils), release inflammatory mediators, including reactive oxygen species, i.e. superoxide anion which is dismutated to hydrogen peroxide (H2O2). Neutrophils from asthmatics generate greater amounts of these species than those of healthy subjects. Some of the H2O2 and thiobarbituric acid-reactive products (TBARs) can evaporate from alveolar lining fluid, and could be expired from the airways of asthmatics. In this study, therefore, we determined whether asthmatic patients exhale more H2O2 and TBARs than healthy subjects. We examined 10 healthy subjects as a control group and 21 asthmatic subjects. In asthmatic subjects, forced expiratory volume in one second (FEV1), was 68+/-9% of predicted value, peak expiratory flow rate (PEFR) was 65+/-8% pred, and bronchial reversibility was 34+/-5% of prebronchodilated FEV1. The mean H2O2 level measured spectrofluorimetrically in the expired breath condensate of asthmatic subjects was 26 fold higher than that in healthy controls (0.26+/-0.29 vs 0.01+/-0.03 nM; p<0.05). The concentration of TBARs in breath condensate was also higher in asthmatic patients compared with nonasthmatics (0.073+/-0.071 vs 0.004+/-0.009 nM; p<0.05). There was a significant correlation between H2O2 level and concentration of TBARs in asthmatic patients (r=0.74; p<0.01). There was also a strong inverse correlation between H2O2 content of all asthmatics and FEV1% pred (r=-0.63; p<0.005) and PEFR% pred (r=-0.52; p<0.05). We conclude that there are elevated levels of hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients, and that measurement of these substances in the expired breath condensate could be a simple, noninvasive method that could be used as a biochemical marker of airway inflammation.

Adult↗
PubMed1991

Reactive oxygen metabolites cause massive, reversible proteinuria and glomerular sieving defect without apparent ultrastructural abnormality.

To identify the specific in vivo renal effect of reactive oxygen species (ROS), hydrogen peroxide (H2O2) was infused directly into the left renal artery in Munich-Wistar rats. H2O2 (5 to 50 mumol over 1 h) induced a dose-dependent increase in urine protein excretion rate in infused kidneys, reaching a maximum at the dose of 35 mumol (on average, a 60-fold increase from baseline). The H2O2 (35 mumol)-induced proteinuria peaked over 1 h and completely normalized by 24 h after the infusion. Electrophoresis revealed that the urine protein is primarily of glomerular origin. Fractional clearances of graded-size neutral dextran of larger molecular radii, an index of glomerular size selectivity, were significantly and substantially elevated immediately but normalized by 24 h after the infusion. GFR and RPF rate remained unchanged throughout the entire time course examined. The H2O2-induced proteinuria was largely prevented by pretreatment with catalase (20 mg, iv) or deferoxamine (30 mg/100 g body wt, iv). Thus, iron-dependent metabolites of hydrogen peroxide appear to be involved in this proteinuria and glomerular size-selective defect. Light and electron microscopy, including determination of anionic site density at lamina rara externa of glomerular capillary wall by polyethyleneimine staining, did not reveal any appreciable abnormality throughout the study period, including at the peak of proteinuria. Thus, ROS can cause massive, reversible proteinuria by inducing a molecular size-selectivity defect of the glomerular capillary wall without apparent ultrastructural abnormalities. The results raise the possibilities: (1) that persistent proteinuria of a variety of renal diseases may reflect persistence of pathogenic ROS acting on glomeruli because the potent proteinuric effect of ROS can be transient (2) that the light and electron microscopy abnormalities in glomeruli of ROS-induced renal injuries reported thus far may have no direct causal linkage to proteinuria; and, finally, (3) ROS-induced reversible proteinuria may relate to the mechanism of clinical functional proteinuria, which involves increased oxygen and ROS metabolism, e.g., exercise-induced proteinuria.

Animals↗
PubMed1996

Investigation of TL properties of sand collected from sewage sludge as an "in situ" dosimeter in radiation disinfection.

Thermoluminescence (TL) properties of sand, collected from sewage sludge, were studied after extensive cleaning procedures. In the sand samples treated with either hydrogen peroxide (H2O2) or hydrofluoric acid (HF), there was a prominent TL peak at about 220 degrees C after gamma-irradiation and 120 degrees C, 20 min post-irradiation annealing treatment. The dose vs TL response curves in hydrogen-peroxide-treated and HF-treated sand samples were found to be linear up to 30 and 100 Gy, respectively, beyond which they were supra-linear. The extent of post-irradiation fading in the sand sample, which was treated with H2O2 and post-irradiation annealed at 120 degrees C for 20 min, was observed to be 8% after 21 days, while no detectable fading was observed for the sample which was HF treated and annealed at 120 degrees C for 20 min after gamma-irradiation. Therefore, H2O2- as well as HF-treated sludge sand samples could be considered for use as in situ TL dosimeters for radiation disinfection of sewage sludge.

Cobalt Radioisotopes↗
PubMed1993

A simplified in vitro model of oxidant injury using vascular endothelial cells.

Oxidant injury of the vascular endothelium is considered an early event in the pathogenesis of atherosclerosis. The model of oxidant injury is crucial to the investigation of antioxidants. In the present study, a convenient in vitro model of oxidant injury induced by hydrogen peroxide (H2O2) was developed using bovine pulmonary artery endothelial cells (PAEC). Viability of PAEC grown in 96-well culture plates was determined with methylthiazol tetrazolium (MTT) colorimetric assay. Cell membrane integrity was measured by lactate dehydrogenase (LDH) release from PAEC grown in 24-well plates. Malondialdehyde (MDA, a product of lipid peroxidation) in PAEC grown in 6-well plates was detected by a thiobarbituric acid fluorometric assay. Incubation of H2O2 with PAEC caused a dose-dependent decrease of cell viability, an increase of LDH release, and an elevation of MDA production. MTT assay was convenient, quantitative, non-radioactive, and suitable for testing a large number of samples. The fluorometric assay for measuring MDA production in endothelial cells used 6-well plates instead of 80-cm2 flasks employed by previous investigators. The use of multiwell culture plates in these assays made it possible for more samples to be tested in any single experiment. The three assays are reproducible with low intraplate and interplate coefficients of variation. This in vitro model is suitable for screening antioxidants and for studying pharmacodynamics at the cellular level.

Animals↗
PubMed1987

Spin-trapping of sulfite radical anion, SO3-., by a water-soluble, nitroso-aromatic spin-trap.

Sulfite radical anion, SO3-., which is generated either by non-enzymatic reaction of hydrogen peroxide (H2O2-) with sulfite (SO3(2-)) or by the oxidation of bisulfite (HSO3) with Ce4+ ion, can be trapped with a water-soluble, nitroso-aromatic spin-trap, sodium 3,5-dibromo-4-nitrosobenzenesulfonate (DBNBS, 1), yielding an ESR spectrum with coupling constants [aN (1) = 12.9 G, aH (2) = 0.8 G] and a g-value of 2.0063. The SO3- radical adduct (spin adduct) was observed even in the presence of the very low concentration of H2O2 (1.21 X 10(-2) mumol).

Benzenesulfonates↗
PubMed1991

Comparison of a fluorimetric and a colorimetric method for the determination of hydrogen peroxide production by rat pleural macrophages.

A fluorimetric and a colorimetric method for the determination of hydrogen peroxide (H2O2) production by isolated cells were compared. Despite a higher sensitivity of the fluorimetric assay, using homovanillic acid (HVA) as reagent, a significantly lower H2O2 production by rat pleural macrophages was measured in comparison to the colorimetric phenol red method. A negative influence of HVA on H2O2 production was detected in the colorimetric assay. These results suggest that the fluorimetric assay with HVA is unsuitable for determining H2O2 formation by isolated cells.

Animals↗
PubMed2000

Coffee drinking increases levels of urinary hydrogen peroxide detected in healthy human volunteers.

Freshly-voided human urine contains significant concentrations of hydrogen peroxide (H2O2). This H2O2 appears to arise in whole or in part by superoxide-dependent autoxidation of urinary biomolecules. Since instant coffee also contains high levels of H2O2, we examined the effect of coffee drinking on urinary levels of H2O2. Studies on healthy human volunteers showed that coffee drinking is rapidly and reproducibly followed by increased levels of H2O2 detectable in the urine for up to 2 h after drinking the coffee. The levels of H2O2 detected in urine suggest that exposure of human tissues to H2O2 may be greater than is commonly supposed. It is possible that H2O2 in urine could act as an antibacterial agent, and that H2O2 is involved in the regulation of glomerular function.

Adult↗
PubMed1998

Cytotoxic activity of BCG-activated macrophages against L929 tumor cells is nitric oxide-dependent.

The tumoricidal activity of activated macrophages has been attributed largely to the release of tumor necrosis factor (TNF), or to the production of reactive oxygen or nitrogen intermediates. The L929 tumor cell line (a murine fibroblast-like cell) when treated with actinomycin D (ActD) has been used to measure TNF alpha cytotoxicity. In the present study, we determined the cytotoxic activity of BCG-activated peritoneal macrophages against ActD-untreated L929 tumor cells. Furthermore, we measured the production of hydrogen peroxide (H2O2), nitric oxide (NO) and TNF by macrophages cultured in the presence or absence of L929 cells. As expected, BCG-activated macrophages produced significant amounts of H2O2 (16.0 +/- 3.0 microM), TNF (512 U/ml) and NO (71.5 +/- 3.2 microM). TNF (256 U/ml) and NO (78.9 +/- 9.7 microM) production was unchanged in co-cultures of L929 cells with BCG-activated macrophages but H2O2 production was totally inhibited. The cytotoxic activity was dependent on NO release since L-NAME (2.5, 5.0 and 10 mM), which blocks NO synthase, inhibited the killing of L929 cells. Addition of anti-TNF (20 micrograms/ml) antibodies to the cultures did not affect the tumoricidal activity of macrophages. Our results indicate that macrophage-mediated killing of L929 cells is largely dependent on NO production but independent of H2O2 or TNF release.

Animals↗
PubMed1997

Effect of nitric oxide, prostacyclin, and thromboxane on the vasospastic action of hydrogen peroxide on human umbilical artery.

BACKGROUND: The effect of hydrogen peroxide (H2O2) on vascular tone in the human umbilical artery was investigated to determine the mechanism of vasospasm in preeclampsia. METHODS: Helical sections of the umbilical artery were obtained from healthy pregnant women who delivered between the 37th and 39th week of gestation. Changes in the maximal tension induced by prostaglandin F2 alpha (PG F2 alpha) were measured (isometric mechanical activity). Segments were treated with H2O2 alone or H2O2 after pretreatment with a scavenger of hydroxyl radicals (mannitol), an inhibitor of thromboxane synthesis (sodium ozagrel), and an inhibitor of nitric oxide synthesis (L-NG-monomethyl arginine, LNMA), or an inhibitor of prostacyclin synthesis (tranylcypromine, TCP). RESULTS: Vascular tension was potentiated by H2O2 in a concentration-dependent manner. Pretreatment with mannitol significantly suppressed the vasospastic effect of H2O2. Removal of the endothelium decreased the vascular tension induced by H2O2. Treatment with TCP and LNMA potentiated the vascular tension. Pretreatment with TCP and LNMA reduced the vasospastic action of H2O2, whereas pretreatment with sodium ozagrel did not. CONCLUSION: Vascular tension in human umbilical arteries was potentiated by H2O2, and may be mediated by a suppression of the activity of nitric oxide or of prostacyclin. A direct action of H2O2 on vascular smooth muscle may also be involved.

Epoprostenol↗
PubMed1980

Role of hydrogen peroxide in the cytotoxic reaction of T lymphocytes.

Evidence is presented that T lymphocyte cytotoxicity is mediated by hydrogen peroxide (H2O2). At a concentration of 5 x 10(-4) M H2O2 induced 51Cr release from pre-labelled P815 mastocytoma cells. H2O2 was generated when T lymphocytes from mouse spleen were exposed to P815 cells. The concentration of H2O produced was apparently one thousand times lower than the concentration required to lyse the P815 cells. This suggests that the H2O2 is produced and acts at a highly localized site on the target cell. Sulphydryl groups on the target cell were particularly sensitive both to H2O2 and to spleen cell attack. The activity of the spleen cells was inhibited by cyanide and azide and by reducing agents which protected the target cells. Cytotoxicity was enhanced by agents which prevented H2O2 breakdown.

Animals↗
PubMed1986

Cytoskeletal changes as an early event in hydrogen peroxide-induced cell injury: a study in A549 cells.

Hydrogen peroxide (H2O2) and other oxygen metabolites have been implicated in the pathogenesis of cell and tissue injury. The nature of the injury occurring in cells exposed to oxygen metabolites is unknown. A549 cells, derived from human lung carcinoma, were exposed to glucose-glucose oxidase or hydrogen peroxide in vitro. The distribution of actin and cytokeratin filaments, as well as 51chromium (51Cr) release and trypan blue dye exclusion were assessed. Both glucose-glucose oxidase and H2O2 resulted in changes which were time- and dose-dependent. Alterations in the cytoskeleton were detected by immunofluorescence microscopy at two hours, at which time the cells excluded trypan blue dye, while 51Cr release and trypan blue uptake first occurred at 8 h and required a five-fold greater concentration of glucose oxidase. The addition of catalase to glucose-glucose oxidase or H2O2, or inactivation of glucose oxidase by boiling, abrogated the injury. Therefore, one of the early targets of H2O2-induced cell injury may be the cytoskeleton.

Actins↗
PubMed1987

Hydrogen peroxide in the rabbit anterior chamber: effects on glutathione, and catalase effects on peroxide kinetics.

Intracameral hydrogen peroxide (H2O2) is cleared at a faster rate in young (t1/2, 93 seconds) than in adult (t1/2, 109 seconds) rabbits. Extrapolated zero time concentrations of H2O2 were 3.3 mM in adults and 3.2 mM in young. The more rapid disappearance of H2O2 correlated with greater catalase levels in iris (35%) and corneal endothelium (50%) in young as compared to adult animals. Catalase levels have been found to be reduced in ocular tissues with 3-amino-1H-1,2,4-triazole (3AT) in a dose-related manner up to 6 ml/kg of an intravenous 3M solution. Iris and ciliary processes showed a linear reduction with dose, while corneal endothelium, liver and lung reached near maximal decreases in catalase activity at 2, 4, and 6 ml/kg, respectively. 3AT caused a significant dose-dependent extension of the rate of clearance of H2O2 from the anterior chamber, that was directly related to catalase loss. The t1/2 for H2O2 disappearance in adult animals increased from 109 seconds with no 3AT, to 147 seconds after 2 ml/kg 3M 3AT, to 161 seconds after 4 ml/kg 3M 3AT and 184 seconds after 6 ml/kg 3M 3AT. Corneal endothelial oxidized glutathione levels were transiently increased after intracameral hydrogen peroxide. Considering the sum total of all tissues of the anterior segment, specific incremental decreases of catalase generated by intravenous 3AT caused the t1/2 of H2O2 clearance from the anterior chamber to become longer, while the reducing power of anterior segment tissues excluding lens epithelium is related clearly to the systemic dose of 3AT.(ABSTRACT TRUNCATED AT 250 WORDS)

Amitrole↗
PubMed2026

A CsWRKY46-CsPBL9-CsARI1 tripartite regulatory module coordinates H2O2 production and callose deposition in citrus fruit immunity.

Plant immunity against pathogens involves multiple immune responses and intricate regulatory networks. However, how immune networks are deployed in fruit remains poorly understood. Here, we show that citrus fruit immune responses, including hydrogen peroxide (H2O2) production and callose deposition, are multiply regulated by transcriptional activation, phosphorylation, and ubiquitination. Citrus sinensis genes encoding nicotinamide adenine dinucleotide phosphate (NADPH) oxidase CsRBOHG and callose synthase CsCalS5, responsible for H2O2 production and callose deposition, respectively, are transcriptionally activated by CsWRKY46. Phosphorylation-enhanced activity of CsRBOHG by CsPBL9 enhances immunity. RING1-IBR-RING2 (RBR)-type E3 ligase CsARI1, acting as an immune brake, ubiquitinates CsRBOHG and CsCalS5 for degradation. Interestingly, CsARI1 also shows a moonlight function wherein it interacts with CsPBL9 in a non-ubiquitination manner, disrupting CsPBL9's interaction with CsRBOHG. This CsARI1-CsPBL9 interaction is stimulated by H2O2 as feedback. Moreover, H2O2 contributes to callose deposition, indicating an interplay between two immune responses. Our study reveals a tripartite regulatory hub orchestrating self-linked immunity in citrus fruit.

CP: plants↗
PubMed1997

High resolution 1H NMR investigations of the reactivities of alpha-keto acid anions with hydrogen peroxide.

The chemical reactivity of various alpha-keto acid anions (beta-hydroxypyruvate, beta-phenylpyruvate, 2-ketobutyrate and 2-ketoglutarate) with hydrogen peroxide (H2O2) was investigated at physiological pH (7.4) and a temperature of 25 degrees C. The initial concentration of the alpha-keto acid anions was kept constant at 1.00 mM whilst that of added H2O2 was varied from 0.25 to 1.00 mM, and the rate and extent of these reactions was evaluated using 1H NMR spectroscopy. At all H2O2 concentrations utilised, the order of reactivity of the alpha-keto acid anions was beta-hydroxypyruvate > beta-phenylpyruvate > 2-ketobutyrate > 2-ketoglutarate. The results obtained are in agreement with a proposed mechanism for these reactions, involving nucleophilic attack of the mono-deprotonated peroxide species (HO2-) at the C-2 carbonyl group carbon centre. The antioxidant capacity of such alpha-keto acids is discussed in terms of their potential use as therapeutic agents in clinical conditions where H2O2 has been shown to play a critical role in the disease process, i.e., those involving 'oxidative stress'.

Butyrates↗
PubMed1994

The inhibitory effects of coffee on radical-mediated oxidation and mutagenicity.

Hydrogen peroxide (H2O2) has been implicated as a major contributor to coffee mutagenicity and genotoxicity in vitro. We have used three assays to show the gradual formation of H2O2 in freshly prepared roasted ground coffee and in instant coffees over time reaching levels of 400-450 microM after a 1-h incubation period. Formation of H2O2 occurs through an auto-oxidation process where polyphenolics, in the presence of transition metals, reduce atmospheric oxygen. However, because of these polyphenolics, coffee also possesses in vitro antioxidant activity as shown by its capacity to inhibit lipid peroxidation in Fenton-catalysed hydroxylation reactions. The pro- and antioxidative effects of coffee are also reflected in its mutagenic and antimutagenic activity in the Ames test. Coffee is directly mutagenic in strains TA100 and TA102 due to H2O2 formation. However, coffee is also an antioxidant and antimutagen. This beverage exerts a strong protective effect against the mutagenicity and cytotoxicity induced by the oxidant t-butylhydroperoxide (t-BOOH). Thus, coffee, like many antioxidants, exhibits dual effects in vitro which are highly dependent upon parameters such as dose, atmospheric oxygen, transition metals as well as the biological and chemical endpoints used for measurement. Consequently, the data obtained on the pro- and antioxidant properties of foods and beverages from in vitro bioassays must be interpreted with caution and the results are not easily extrapolated in vivo to assess the impact on human health.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1991

Hydrogen peroxide modulation of the respiratory burst of human neutrophils.

Addition of micromolar concentrations of hydrogen peroxide (H2O2) to human neutrophils resulted in a dose-dependent luminol-enhanced chemiluminescent response. Pretreatment of neutrophils with micromolar concentrations of H2O2 altered their response to the surface acting stimulants serum-treated zymosan (STZ) and formyl-methionyl-leucyl-phenylalanine (fMLP), but not to the intracellular stimulant phorbol myristate acetate (PMA). The alterations were partially reversible by catalase, but exacerbated by superoxide dismutase. These results suggest a modulatory role for H2O2 in the respiratory burst of neutrophils.

Catalase↗
PubMed1986

The biological activity of hydrogen peroxide. I. Induction of chromosome-type aberrations susceptible to inhibition by scavengers of hydroxyl radicals in human embryonic fibroblasts.

The cytogenetic effect of hydrogen peroxide (H2O2) was investigated in human embryonic fibroblasts. Chromosome-type aberrations were found together with chromatid-type aberrations in metaphase cells harvested 24 h after a single 10-min treatment with 10(-5)-10(-3) M H2O2 in 0.9% NaCl solution. The chromosome-type aberrations were observed to be predominantly dicentrics and deletions. Both types of aberration showed a dose-response relationship to the dose of H2O2 over the range of 10(-5)-1.5 X 10(-4) M H2O2. The intercellular distribution of dicentrics showed a Poisson distribution. Centric and acentric rings and abnormal monocentrics were a minor fraction of the chromosome-type aberrations. The chromatid-type aberrations observed, such as breaks, exchanges and gaps, showed no dose-response relationship. The frequency of isochromatid breaks was higher than that of chromatid breaks and approximately 70% of the isochromatid breaks were found in the centromeric or pericentromeric region. The intercellular distribution of chromatid exchanges showed an over-dispersed distribution. The generation of aberrations by H2O2 was effectively suppressed by catalase and several scavengers of hydroxyl radicals (.OH) such as ethanol, dimethyl sulfoxide (DMSO) and mannitol. This result suggest that .OH plays an essential role in the generation of the chromosome aberrations by H2O2.

Antioxidants↗
PubMed1999

The influence of liposome-encapsulated prostaglandin E1 on hydrogen peroxide concentrations in the exhaled breath of patients with the acute respiratory distress syndrome.

UNLABELLED: Hydrogen peroxide (H2O2) levels are increased in the exhaled breath of patients with the acute respiratory distress syndrome (ARDS). Because liposome-encapsulated prostaglandin E1 (PGE1) downregulates the CD11/CD18 receptor of the neutrophil, thereby limiting endothelial adhesion, the use of this drug should decrease the excretion of H2O2 in the expiratory condensate of patients with ARDS. Patients > 11 yr of age with ARDS (diffuse, patchy infiltrates by chest radiograph; Pao2/fraction of inspired oxygen [P/F] ratio < or = 200 mm Hg; pulmonary capillary wedge pressure < or = 18 mm Hg; and the requirement for mechanical ventilation) were randomized to receive placebo (n = 14) or escalating doses (0.15-3.6 micrograms/kg) of liposomal PGE1 (n = 14) every 6 h for up to 7 days. Condensate was collected every morning from the expiratory tubing that was submerged in an ice saltwater bath (-5 degrees C). H2O2 levels were measured by using a horseradish peroxidase assay. Other data collected included white blood cell count and P/F ratios. There was no significant difference in the concentration of H2O2 in the expiratory condensate between the liposomal PGE1 group and the control group either before (0.99 +/- 0.52 vs 0.93 +/- 0.48 mumol/L) or during treatment (1.04 +/- 0.45 vs 0.76 +/- 0.25 mumol/L). Liposomal PGE1 treatment improved the P/F ratio and decreased the white blood cell count over time. Despite its ability to downregulate the CD11/CD18 neutrophil receptor, liposomal PGE1 did not reduce exhaled H2O2 excretion. IMPLICATIONS: White blood cells (WBC) are thought to be part of the cause of the acute respiratory distress syndrome, a lung disease. WBC in the lung produce hydrogen peroxide, which is exhaled. Liposomal PGE1 inhibits WBC function but was found to have no effect in decreasing exhaled hydrogen peroxide in patients with the acute respiratory distress syndrome.

Adult↗