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PubMed1989

Prevalence of hydrogen peroxide-producing Lactobacillus species in normal women and women with bacterial vaginosis.

A predominance of Lactobacillus species in the vaginal flora is considered normal. In women with bacterial vaginosis, the prevalence and concentrations of intravaginal Gardnerella vaginalis and anaerobes are increased, whereas the prevalence of intravaginal Lactobacillus species is decreased. Because some lactobacilli are known to produce hydrogen peroxide (H2O2), which can be toxic to organisms that produce little or no H2O2-scavenging enzymes (e.g., catalase), we postulated that an absence of H2O2-producing Lactobacillus species could allow an overgrowth of catalase-negative organisms, such as those found among women with bacterial vaginosis. In this study, H2O2-producing facultative Lactobacillus species were found in the vaginas of 27 (96%) of 28 normal women and 4 (6%) of 67 women with bacterial vaginosis (P less than 0.001). Anaerobic Lactobacillus species (which do not produce hydrogen peroxide) were isolated from 24 (36%) of 67 women with bacterial vaginosis and 1 (4%) of 28 normal women (P less than 0.001). The production of H2O2 by Lactobacillus species may represent a nonspecific antimicrobial defense mechanism of the normal vaginal ecosystem.

Cervix Mucus↗
PubMed1999

DNA damage by hydroquinone in human white blood cells: analysis by alkaline single-cell gel electrophoresis.

The genotoxicity of hydroquinone (HQ) in human white blood cells was investigated by means of alkaline single-cell gel electrophoresis (SCGE). The exposure of purified lymphocytes to HQ (0.5-50 microg/ml) produced significant and dose-related increases in DNA migration; conversely, no induction of DNA damage was observed in leukocytes after in vitro treatment of whole blood samples (100-500 microg/ml). Similar differences in DNA damage between whole blood samples and purified lymphocytes were observed after treatments with hydrogen peroxide (H2O2, 50 microM). The DNA damaging activity of HQ was significantly (p<0.001, U-test) inhibited by exogenous catalase (250 U/ml), indicating the generation of peroxides in the mechanism of genotoxicity of HQ. Parallel experiments using the standard SCGE protocol, and an acellular method entailing the lysis of cells before HQ treatment, provided fairly similar results, indicating that HQ oxidation does not require endogenous metabolism. Experiments to compare the effectiveness of HQ in the induction of single-strand breaks and alkali-labile sites in resting cells and micronuclei in cytokinesis-blocked cells indicate that despite the extensive DNA damage detected by SCGE immediately after treatment, a significant excess of micronuclei is not observed after stimulation and in vitro cultivation. These data explain the apparent discrepancy between the high DNA damaging potential of HQ in human lymphocytes, as revealed by SCGE, and the relatively low activity reported in most cytogenetic assays with HQ on the same cell type.

Adult↗
PubMed1990

Generation of reactive oxygen species and reduction of ferric chelates by microsomes in the presence of a reconstituted system containing ethanol, NAD+ and alcohol dehydrogenase.

Many of the toxic metabolic actions of ethanol on the liver have been ascribed to the enhanced cellular production of NADH, which arises as a consequence of the oxidation of ethanol by alcohol dehydrogenase (ADH). Experiments were conducted to evaluate whether NADH generated from a reconstituted system containing ethanol plus NAD+ plus ADH could interact with ferric chelates to promote microsomal lipid peroxidation and generation of a hydroxyl radical (OH)-like species. In the presence of the reconstituted system and iron, microsomes produced.OH as assessed by the oxidation of .OH scavenging agents. This oxidation was inhibited by catalase and competitive.OH scavengers but not by superoxide dismutase. The ADH-dependent microsomal production of.OH was effectively catalyzed by ferric-EDTA and -diethylenetriamine pentaacetic acid (-DTPA), but not by ferric-ATP or -citrate. However, all these ferric chelates were reduced by the microsomes in the presence of the reconstituted system. Hydrogen peroxide (H2O2) was produced in the presence of ADH and appeared to be a limiting factor for the production of.OH. The reconstituted system also catalyzed microsomal lipid peroxidation, and the pattern of effectiveness of ferric chelates was opposite that of catalysis of.OH production. There was little effect by catalase, superoxide dismutase or dimethyl sulfoxide (DMSO) on the ADH-dependent microsomal lipid peroxidation. The reconstituted system was characterized with respect to dependence on NAD+ and ADH; ethanol could be replaced by other alcohols, which are substrates for ADH. Pyrazole, a potent inhibitor of ADH, blocked the ability of the reconstituted system to interact with iron and microsomes to produce reactive oxygen species.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Dehydrogenase↗
PubMed1993

Peroxide plasma level in patients with coronary heart disease as a possible indicator of ischemia during exercise test.

BACKGROUND: This study evaluated the possible changes in production of free oxygen species during myocardial ischemia in the course of exercise testing of ischemic coronary disease. METHODS: Exercise testing was performed on 58 patients with suspected ischemic coronary disease. Plasma hydrogen peroxide (H2O2) level was assayed according to Frew et al. (Anal Chim Acta 1983, 155:139-150) in venous blood samples obtained before the test, at submaximal and maximal work loads, and after 30 minutes of rest. RESULTS: Hydrogen peroxide plasma level significantly increased (P < 0.001) at maximal work load in patients with positive exercise test results. Patients with negative exercise test results initially manifested a higher H2O2 level that dropped during maximal work load. CONCLUSIONS: The rise in plasma H2O2 level during myocardial ischemia indicates that intensification of oxygen free radical production occurs. This may be the result of hypoxanthine conversion by xanthine oxidase, catecholamine auto-oxidation, polymorphonuclear neutrophil activation, and/or derangement within mitochondrial electron transfer. The noticed difference between patients with a positive exercise test and those diagnosed as without ischemia may be of clinical relevance.

Adult↗
PubMed1985

Influence of endogenous catalase activity on the sensitivity of the oral bacterium Actinobacillus actinomycetemcomitans and the oral haemophili to the bactericidal properties of hydrogen peroxide.

Actinobacillus actinomycetemcomitans and the genetically-related oral haemophili (Haemophilus segnis, Haemophilus aprhophilus and Haemophilus paraphrophilus) exhibit a range of sensitivities to the lethal effect of hydrogen peroxide (H2O2), A. actinomycetemcomitans being the most resistant. To extend this information, susceptibility to a range of H2O2 concentrations (10(-6)-10(-3) M) was assessed by incubating bacterial suspensions for 1 h at 37 degrees C in the presence of H2O2 and spreading the suspensions on chocolate agar plates to determine the concentration of H2O2 producing a 50 per cent reduction in colony-forming units (LD50). Catalase activity was quantified with a Clark-type oxygen electrode, which polarographically monitored the formation of dissolved oxygen in bacterial suspensions or sonicates following addition of reagent H2O2. Sensitivity to H2O2 did not correlate with catalase activity, either in intact cells or in bacterial sonicates. Specifically, some bacterial strains with undetectable catalase activity were highly resistant to H2O2. Micromolar concentrations of sodium azide which completely inhibited cell-associated catalase activity did not affect the resistance of A. actinomycetemcomitans to H2O2. Thus, the endogenous catalase activity of A. actinomycetemcomitans and certain oral haemophili is not an important determinant of resistance to the bactericidal effects of H2O2.

Actinobacillus↗
PubMed1995

A peroxidative model of human erythrocyte intracellular Ca2+ changes with in vivo cell aging: measurement by 19F-NMR spectroscopy.

Numerous changes occur with human erythrocyte aging in vivo, including an increase in free ionic intracellular calcium concentration ([Ca2+]i) (N.R. Aiken et al. (1992) Biochim. Biophys. Acta 1136, 155-160). An attractive hypothesis of cell aging suggests that oxidative stress is responsible for many age-related changes. To determine whether oxidative stress leads to increased intracellular Ca2+ concentrations, we used the fluorinated calcium probe 5,5'-difluoroBAPTA and fluorine nuclear magnetic resonance spectroscopy (19F-NMR) to measure [Ca2+]i following mild hydrogen peroxide (H2O2) stress to young red cells. Cells were separated using density centrifugation, exposed to 815 microM H2O2, loaded with the calcium probe, and [Ca2+]i measured. Intracellular [Ca2+] increased from 62 nM (+/- 4, S.E.) in untreated young cells to 173 nM (+/- 11) in peroxide treated cohort young cells. This value approached our previously reported [Ca2+]i of 221 nM (+/- 25) in old human erythrocytes. Pretreatment of young cells with (a) cobalt, which blocks Ca2+ influx through calcium channels, or (b) carbon monoxide, which prevents methemoglobin formation, inhibited the peroxide-induced increase in ionic intracellular calcium. These findings are consistent with the hypothesis that oxidative stress of erythrocytes contributes to the increased [Ca2+]i found in senescent cells, and that this is due to increased membrane Ca2+ leak resulting from oxidatively induced methemoglobin-cytoskeletal protein crosslinking.

Adult↗
PubMed1983

The oxidative burst and related phenomena in mouse macrophages elicited by different sterile inflammatory stimuli.

Mouse peritoneal macrophages (MPM) elicited by paraffin oil (PO) or thioglycollate (TG) were compared in their capacity to generate oxidative burst (OB) products such as superoxide ion (O2-) and hydrogen peroxide (H2O2) and lyse target erythrocytes. Strong OB stimulants such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA), opsonized zymosan; and wheat-germ agglutinin (WGA) were found to stimulate O2 and H2O2 production by both PO- and TG-elicited MPM. PO-elicited MPM exhibited a vigorous OB response compared to TG-elicited MPM and showed a higher degree of self iodination in the presence of 125I. Macrophage-mediated cytolysis of 51Cr-labeled red blood cells, following OB stimulation, was revealed by PO-elicited MPM triggered by TPA, opsonized zymosan, WGA, and Concanavalin A. TG-elicited MPM failed to respond to TPA and opsonized zymosan. In the presence of horseradish peroxidase, both PO- and TG-elicited MPM exhibited augmented cytocidal activities upon stimulation with TPA, whereas catalase abrogated the capacity of TPA-stimulated MPM to lyse red blood cells, which may suggest the involvement of H2O2 in the lytic process.

Animals↗
PubMed1998

Different mechanisms of thioredoxin in its reduced and oxidized forms in defense against hydrogen peroxide in Escherichia coli.

The present experiments were done to elucidate the roles of thioredoxin and thioredoxin reductase system in defense against hydrogen peroxide (H2O2) in Escherichia coli. The thioredoxin-deficient mutant (trxA) was more sensitive to H2O2 than was the wild-type strain, when challenged in the stationary and exponentially growing phase. Thioredoxin reductase-deficient mutant (trxB) in the stationary phase also exhibited increased sensitivity, compared with the wild-type strain. These results indicated that reduced form of thioredoxin is required for defense against H2O2, possibly by scavenging radicals generated in the cells. In contrast, the trxB mutant in the growing phase had higher survival after exposure to H2O2 than the wild-type strain. The acquirement of resistance related to increased capacity for removing H2O2 in the trxB mutant and was not observed in a catalase-negative background. Furthermore, enhanced expression of the katG :: lacZ gene occurred in the mutant. Therefore, it was concluded that oxidized form of thioredoxin confers H2O2 resistance on E. coli cells by increasing activity to remove H2O2, which was brought about by enhanced induction of the katG-coded catalase/hydroperoxidase I at the transcriptional level. In addition, this resistance to H2O2 correlated well with reduced amount of DNA damage caused by H2O2, determined by the induction level of the recA :: lacZ fusion gene after treatment with H2O2.

Acatalasia↗
PubMed1978

Synergistic killing of Escherichia coli by near-UV radiation and hydrogen peroxide: distinction between recA-repairable and recA-nonrepairable damage.

Wild-type cells and six DNA repair-deficient mutants (lexA, recA, recB, recA, recB, polA1, and uvrA) of Escherichia coli K-12 were treated with near-ultraviolet radiation plus hydrogen peroxide (H2O2). At low H2O2 concentrations (6 X 10(-6) to 6 X 10(-4) M), synergistic killing occurred in all strains except those containing a mutation in recA. This RecA-repairable damage was absent from stationary-phase cells but increased in logarithmic cells as a function of growth rate. At higher H2O2 concentrations (above 6 X 10(-4) M) plus near-ultraviolet radiation, all strains, including those with a mutation in recA, were synergistically killed; thus, at high H2O2 concentrations, the damage was not RecA repairable.

DNA Repair↗
PubMed1988

Cytolysis mediated by phagocytosing neutrophils. Influence of the presence of an alternative target cell population.

When added to the hypochlorous acid (HOCl)-dependent cytolytic system constituted of opsonized zymosan (OPZ)-triggered neutrophils and chicken erythrocyte (CRBC) targets, human erythrocytes (HRBCs) inhibited the lysis. The replacement of HRBCs with cells pretreated with amino-triazole (AT) to inactivate catalase prevented the HRBC inhibitory effect almost completely. HRBCs, pretreated with carmustine (BCNU) to inhibit glutathione cycle activity, behaved as untreated cells. Thus, HRBCs appear to protect CRBCs via an AT-inhibitable, i.e. catalase-dependent, process. When measured under conditions similar to those used for the lytic assay, both the hydrogen peroxide (H2O2) and the HOCl recovery from the neutrophil-CRBC system was reduced by HRBCs and restored by pulsing HRBCs with AT but not BCNU. The results suggest that HRBC catalase rescues CRBCs from neutrophil-delivered attack by "stealing" H2O2 from the neutrophil HOCl-generating myeloperoxidase (MPO)-H2O2 system.

Animals↗
PubMed1997

Pyruvate protects neurons against hydrogen peroxide-induced toxicity.

Hydrogen peroxide (H2O2) is suspected to be involved in numerous brain pathologies such as neurodegenerative diseases or in acute injury such as ischemia or trauma. In this study, we examined the ability of pyruvate to improve the survival of cultured striatal neurons exposed for 30 min to H2O2, as estimated 24 hr later by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide assay. Pyruvate strongly protected neurons against both H2O2 added to the external medium and H2O2 endogenously produced through the redox cycling of the experimental quinone menadione. The neuroprotective effect of pyruvate appeared to result rather from the ability of alpha-ketoacids to undergo nonenzymatic decarboxylation in the presence of H2O2 than from an improvement of energy metabolism. Indeed, several other alpha-ketoacids, including alpha-ketobutyrate, which is not an energy substrate, reproduced the neuroprotective effect of pyruvate. In contrast, lactate, a neuronal energy substrate, did not protect neurons from H2O2. Optimal neuroprotection was achieved with relatively low concentrations of pyruvate (</=1 mM), whereas at high concentration (10 mM) pyruvate was ineffective. This paradox could result from the cytosolic acidification induced by the cotransport of pyruvate and protons into neurons. Indeed, cytosolic acidification both enhanced the H2O2-induced neurotoxicity and decreased the rate of pyruvate decarboxylation by H2O2. Together, these results indicate that pyruvate efficiently protects neurons against both exogenous and endogenous H2O2. Its low toxicity and its capacity to cross the blood-brain barrier open a new therapeutic perspective in brain pathologies in which H2O2 is involved.

Animals↗
PubMed1997

Effect of Maharishi AK-4 on H2O2-induced oxidative stress in isolated rat hearts.

Oxidative damage to crucial biomolecules due to excess generation of reactive oxygen species has been implicated as a major cause of organ damage and hence compounds capable of negating such damage have potential benefits. Using hydrogen peroxide (H2O2) as a model pro-oxidant to induce oxidative stress, we have examined the ability of natural food supplement Maharishi Amrit Kalash (MAK-4) to decrease oxidative damage in potassium-arrested isolated rat hearts. The protocol was that hearts isolated from male Sprague-Dawley rats were retrograde-perfused with Krebs-Henseleit (K-H) solution for 30 min for equilibration. After this period, the hearts were subjected to cardioplegia with high potassium (26-30 mM), followed by reperfusion with K-H solution in the presence or absence of 200 microM H2O2. As expected, H2O2 treatment following cardioplegia induced a high degree of oxidative stress as assessed by release of lactate dehydrogenase (LDH, a marker of plasma membrane damage) and total glutathione (GSH + GSSG). H2O2 also impaired the ability of heart to regain developed tension during the testing period. However, addition of MAK-4 in the perfusate containing H2O2 decreased oxidative stress in terms of release of LDH and glutathione. In parallel with these biochemical studies, in a few experiments the cardiac function was assessed by measuring developed contractile tension. These preliminary studies also showed that in the presence of MAK-4 the H2O2-treated hearts were able to regain better developed tension. Further in vitro studies to examine the possible mechanisms of MAK-4 action reveal that this formulation contains H2O2 binding activity which resulted in the decreased availability of H2O2 itself. Our studies hence reveal that the ayurvedic food supplement MAK-4 may have potential benefits in reducing oxidative stress.

Animals↗
PubMed1996

Capacity of H2O2 release from monocytes in steroid-sensitive nephrotic syndrome.

The pathogenesis of steroid-sensitive nephrotic syndrome (SSNS) is poorly defined. We previously demonstrated that monocytes from SSNS patients with proteinuria were activated to display exaggerated phagocytosis of opsonized particles and paradoxically reduced chemotaxis. In this study, we evaluated the capacity of hydrogen peroxide (H2O2) release from monocytes in 19 patients with SSNS and 13 healthy controls, by exposure to phorbol myristate acetate (PMA), using scopoletin method. Of 19 patients of SSNS, 7 were proteinuric and 12 in remission. The H2O2 release was significantly higher in SSNS patients with proteinuria than those in remission or normal controls [177.49 +/- 94.75 (mean +/- S.D.) vs. 60.67 +/- 58.89 (p < 0.02) or 85.02 +/- 48.62 nmol/90 min/mg cell protein (p < 0.05)]. Follow-up measurements in two SSNS patients showed that H2O2 release was reduced when proteinuric condition was improved to be in remission. Our data suggest that monocytes in SSNS with proteinuria were activated and were prepared to receive some extracellular signaling leading to protein kinase-C activation for releasing H2O2.

Adult↗
PubMed1996

Role of protein tyrosine phosphorylation in H2O2-induced activation of endothelial cell phospholipase D.

Oxidant-induced activation of phospholipase D (PLD) in bovine pulmonary artery endothelial cells (BPAEC) is independent of protein kinase C and calcium. In the present study, the effects of tyrosine kinase and protein tyrosine phosphatase (PTPase) inhibitors on hydrogen peroxide (H2O2)-induced PLD activation and protein tyrosine phosphorylation were examined in BPAEC. Pretreatment of BPAEC with putative tyrosine kinase inhibitors genistein, tyrphostin, and herbimycin attenuated H2O2 (1 mM)-induced PLD activation. The inhibitory effect of the tyrosine kinase inhibitors was highly specific for H2O2-induced modulation and showed no effect on PLD activation mediated by 12-O-tetradecanoylphorbol 13-acetate or bradykinin. Furthermore, addition of H2O2 increased in a time-dependent manner tyrosine phosphorylation of several proteins (17-200 kDa), as determined by immunoblot analysis with antiphosphotyrosine antibodies. H2O2-mediated protein tyrosine phosphorylation preceded PLD activation, and a good correlation was observed on the effect of genistein in H2O2-induced PLD activation and protein tyrosine phosphorylation. Addition of vanadate, a phosphotyrosine phosphatase inhibitor, synergistically increased both PLD activation and protein tyrosine phosphorylation mediated by H2O2. Moreover, vanadate by itself had minimal effect on basal PLD activity in BPAEC; however, at 10 microM vanadate, an increase in protein tyrosine phosphorylation was observed. In addition to vanadate, phenylarsine oxide and diamide potentiated H2O2-induced PLD activation. These results suggest that tyrosine kinase activation may be involved in H2O2-induced PLD activation in vascular endothelial cells.

Animals↗
PubMed1991

Roles of catalase and the glutathione redox cycle in the regulation of anterior-chamber hydrogen peroxide.

The effects of inhibition of both glutathione synthesis and of glutathione reductase and catalase activities have been determined in the regulation of hydrogen peroxide (H2O2) in the anterior chamber of pigmented rabbits. Glutathione reductase inhibition using intravitreal 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) did not significantly alter either total glutathione or the percent oxidized glutathione fraction in the iris-ciliary body. Intravitreal buthionine sulfoximine (BSO) significantly reduced the total glutathione content of iris-ciliary body and corneal endothelium, while not altering the oxidized fraction. BCNU increased the oxidized fraction of glutathione in the aqueous humor from 22 to 63% without significantly altering total glutathione levels. BSO, however, reduced total glutathione by 70% in the aqueous humor, and the oxidized fraction doubled. Decreases in the reduced glutathione concentration caused by BSO correlate with increases in the normally stable ratio of H2O2 to ascorbate concentrations in the aqueous humor, strongly suggesting that glutathione metabolism is correlated with H2O2 regulation at endogenous levels of this oxidant. Both BSO and 3-aminotriazole (3AT) separately increased the half-time for the loss of exogenously added H2O2 from the anterior chamber. BSO increased the half-time by 77% after 10 microliters of 10 mM H2O2 was injected intracamerally, while suppression of catalase activity with 3AT increased it by only 40%. With intracameral injections of 10 microliters of either 25 or 50 mM H2O2, however, 3AT had a greater effect than BSO. The half-time values after 3AT pretreatment were 61 and 135% greater than control values at the concentrations of 25 and 50 mM H2O2, respectively; those after BSO pretreatment were at 14 and 78%. From these data we conclude that the glutathione redox system protects the anterior segment tissues from hydrogen peroxide at low concentrations of this oxidant, while catalase assumes a greater role at higher concentrations of hydrogen peroxide.

Amitrole↗
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↗