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PubMed2003

Akt-dependent phosphorylation of serine 1179 and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 cooperatively mediate activation of the endothelial nitric-oxide synthase by hydrogen peroxide.

Hydrogen peroxide mediates vasodilation, but the mechanisms responsible for this process remain undefined. We examined the effect of H(2)O(2) on nitric oxide (NO*) production and the signaling events involved. NO* release from bovine aortic endothelial cells was detected with an NO*-specific microelectrode. The addition of H(2)O(2) caused a potent dose-dependent increase in NO* production. This was partially Ca(2+)-dependent because BAPTA/AM reduced NO* production at low (<50 microM) but not high (>100 microM) concentrations of H(2)O(2). Phosphatidylinositol (PI) 3-kinase inhibition [with wortmannin or 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], infection with a dominant-negative mutant of Akt, or mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 (MEK/ERK1/2) inhibition (with PD98059 or U0126) partially attenuated, whereas inhibition of both PI 3-kinase and MEK1/2 abolished H(2)O(2)-dependent NO* production. ERK1/2 seemed necessary for NO* production early (<5 min) after H(2)O(2) addition, whereas PI 3-kinase/Akt was more important at later time points. Phosphorylation of endothelial nitric-oxide synthase (eNOS) at serine 1179 was observed >10 min after the addition of H(2)O(2), and this was prevented by wortmannin but not by PD98059. c-Src family tyrosine kinase(s) was found to be upstream of H(2)O(2)-dependent Akt and eNOS serine 1179 phosphorylation and subsequent NO* production. In summary, H(2)O(2) causes endothelial NO* release mediated by cooperative effects between PI 3-kinase/Akt-dependent eNOS serine 1179 phosphorylation and activation of MEK/ERK1/2. This may represent an acute cellular adaptation to an increase in oxidant stress.

Animals↗
PubMed2002

Mineralization of a sorbed polycyclic aromatic hydrocarbon in two soils using catalyzed hydrogen peroxide.

Hydrogen peroxide (H2O2) catalyzed by soluble iron or naturally occurring soil minerals, (i.e., modified Fenton's reagent) was investigated as a basis for mineralizing sorbed and NAPL-phase benzo[a]pyrene (BaP), a hydrophobic and toxic polycyclic aromatic hydrocarbon, in two soils of different complexity. 14C-Benzo[a]pyrene was added to silica sand and a silt loam soil, and mineralization was investigated using three-level central composite rotatable experimental designs. The effects of H2O2 concentration, slurry volume, and iron(II) amendment were investigated in the silica sand systems. In a Palouse loess silt loam soil, the variables included H2O2 concentration, slurry volume, and pH, with H2O2 catalyzed by naturally occurring iron oxyhydroxides. Regression equations generated from the data were used to develop three-dimensional response surfaces describing BaP mineralization. Based on the recovery of 14C-CO2, 70% BaP mineralization was achieved in the sand within 24 h using 15 M H2O2 and an iron(II) concentration of 6.6 mM with a slurry volume of 0.3 x the field capacity of the sand. For the silt loam soil, 85% mineralization of BaP was observed using 15 M H2O2, no iron amendment, and a slurry volume of 20 x the soil field capacity. The balance of the radiolabeled carbon remained as unreacted BaP in the soil fraction. Gas-purge measurements over 5 d confirmed negligible desorption under nontreatment conditions. However, oxidation reactions were complete within 24 h and promoted up to 85% BaP mineralization, documenting that the natural rate of desorption/dissolution did not control the rate of oxidation and mineralization of the BaP. The results show that catalyzed H2O2 has the ability to rapidly mineralize sorbed/NAPL-phase BaP and that partitioning, which is often the rate-limiting factor in soil remediation, does not appear to limit the rate of vigorous Fenton-like treatment.

Crystallization↗
PubMed1997

Effect of trolox C on cardiac contracture induced by hydrogen peroxide.

Hydrogen peroxide (H2O2) perfused into the aorta of the isolated rat heart induces a positive inotropic effect, with cardiac arrhythmia such as extrasystolic potentiation or cardiac contractures, depending on the dose. The last effect is similar to the "stone heart" observed in reperfusion injury and may be ascribed to lipoperoxidation (LPO) of the membrane lipids, to protein damage, to reduction of the ATP level, to enzymatic alterations and to cardioactive compounds liberated by LPO. These effects may result in calcium overload of the cardiac fibers and contracture ("stone heart"). Hearts from male Wistar rats (300-350 g) were perfused at 31 degrees C with Tyrode, 0.2 mM trolox C, 256 mM H2O2 or trolox C + H2O2. Cardiac contractures (baseline elevation of the myograms obtained) were observed when hearts were perfused with H2O2 (Tyrode: 5.9 +/- 3.2; H2O2: 60.5 +/- 13.9% of the initial value); perfusion with H2O2 increased the LPO of rat heart homogenates measured by chemiluminescence (Tyrode: 3,199 +/- 259; H2O2: 5,304 +/- 133 cps mg protein-1 60 min-1), oxygen uptake (Tyrode: 0.44 +/- 0.1; H2O2: 3.2 +/- 0.8 nmol min-1 mg protein-1) and malonaldehyde (TBARS) formation (Tyrode: 0.12 +/- 0; H2O2: 0.37 +/- 0.1 nmol/ml). Previous perfusion with 0.2 mM trolox C reduced the LPO (chemiluminescence: 4,098 +/- 531), oxygen uptake (0.51 +/- 0) and TBARS (0.13 +/- 0) but did not prevent the H2O2-induced contractures (33.3 +/- 16%). ATP (Tyrode: 2.84 +/- 0; H2O2: 0.57 +/- 0) and glycogen levels (Tyrode: 0.46 +/- 0; H2O2: 0.26 +/- 0) were reduced by H2O2. Trolox did not prevent these effects (ATP: 0.84 +/- 0 and glycogen: 0.27 +/- 0). Trolox C is known to be more effective than alpha-tocopherol or gamma-tocopherol in reducing LPO though it lacks the phytol portion of vitamin E to be fixed to the cell membranes. Trolox C, unlike vitamin A, did not prevent the glycogen reduction induced by H2O2. Trolox C induced a positive chronotropic effect that resulted in higher energy consumption. The reduction of energy level seemed to be more important than LPO in the mechanism of H2O2-induced contracture.

Animals↗
PubMed1994

Modulation of human colonic T84 cell secretion by hydrogen peroxide.

Hydrogen peroxide (H2O2) is a reactive oxygen species that can be produced in the digestive tract by inflammatory cells or during reperfusion following ischemia. To evaluate a possible direct effect of H2O2 on epithelial secretory cells, well-differentiated colonic T84 cells were grown to confluence on permeable membranes and studied in Ussing chambers. In this model, where the measured short-circuit current (Isc) reflects electrogenic secretion, we observed that H2O2 stimulated a concentration-dependent and transient secretory response: 5.5 mM H2O2 produced a peak Isc of 12.4 microA/cm2 after 4 min, 2.2 mM H2O2 a peak Isc of 7.9 microA/cm2 after 4 min, and 1.1 mM H2O2 a peak Isc of 5.5 microA/cm2 after 16 min (N = 5). When 97 experiments using 5.5 mM H2O2 were reviewed, the mean peak Isc response was 8.9 +/- 0.5 microA/cm2. A similar secretory response was elicited whether H2O2 was added to the serosal, to the mucosal, or simultaneously to both sides of the T84 cell monolayer. This secretory response reflected transcellular chloride secretion because it was inhibited by the depletion of chloride in the medium and by the suppression of the Na+,K+,2Cl- co-transporter activity necessary for the chloride gradient driving chloride secretion. When T84 cell monolayer resistance was studied, 5.5 mM H2O2 produced a transient decrease in resistance, reflecting transcellular chloride secretion, and a gradual decline in resistance (75% of the initial value after 55 min). The secretory response to H2O2 was increased 2-fold in T84 cells maximally stimulated with 10 nM vasoactive intestinal peptide (VIP), a neuropeptide which acts via cAMP, demonstrating synergism between the two agents. In contrast, the secretory responses produced by H2O2 and carbachol, which acts through the Ca2+ pathway, were additive. A late inhibitory effect of H2O2 was also observed: in cells previously treated with 5.5 mM H2O2, the subsequent secretory responses to either VIP or carbachol were partially inhibited. These secretory effects were specific for the oxidant properties of H2O2 because they were inhibited by 450 U/mL catalase and by 5 mM dithiothreitol, but were unaffected by 50 microM deferoxamine B or Fe3+. H2O2 may be a potential modulator of intestinal or colonic secretion in certain pathologic conditions such as inflammation or ischemia-reperfusion.

Adenocarcinoma↗
PubMed2000

Role of peroxiredoxins in regulating intracellular hydrogen peroxide and hydrogen peroxide-induced apoptosis in thyroid cells.

Peroxiredoxins (Prxs) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. One mechanism for this action involves modulation of hydrogen peroxide (H(2)O(2))-mediated cellular responses. This report examines the expression of Prx I and Prx II in thyroid cells and their roles in eliminating H(2)O(2) produced in response to thyrotropin (TSH). Prx I and Prx II are constitutively expressed in FRTL-5 thyroid cells. Prx I expression, but not Prx II expression, is stimulated by exposure to TSH and H(2)O(2). In addition, methimazole induces a high level of Prx I mRNA and protein in these cells. Overexpression of Prx I and Prx II enhances the elimination of H(2)O(2) produced by TSH in FRTL-5 cells. Treatment with 500 micrometer H(2)O(2) causes apoptosis in FRTL-5 cells as evidenced by standard assays of apoptosis (i.e. terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end labeling, BAX expression, and poly(ADP-ribose) polymerase cleavage. Overexpression of Prx I and Prx II reduces the amount of H(2)O(2)-induced apoptosis measured by these assays. These results suggest that Prx I and Prx II are involved in the removal of H(2)O(2) in thyroid cells and can protect these cells from undergoing apoptosis. These proteins are likely to be involved in the normal physiological response to TSH-induced production of H(2)O(2) in thyroid cells.

Animals↗
PubMed1988

Influence of lipid peroxidation and hydrogen peroxide on muscarinic cholinergic receptors and ATP level in rat myocytes and lymphocytes.

Isolated rat neonatal cardiac myocytes and rat lymph-node lymphocytes were treated with Fe2+ cumene hydroperoxide or hydrogen peroxide. The intensity of lipid peroxidation was estimated by measuring production of malondialdehyde (MDA). The level of muscarinic cholinergic receptors was determined by [3H]-QNB binding. Cumene hydroperoxide treatment was found to induce lipid peroxidation in both myocytes and lymphocytes, the process being more pronounced in myocytes. An important decrease of muscarinic cholinergic receptor level and a significant drop of intracellular ATP level in these cells were simultaneously observed. In both cell types, hydrogen peroxide treatment decreased the ATP level while lipid peroxidation and muscarinic cholinergic receptors were unaffected. The different effect of hydrogen peroxide on lipid peroxidation and the level of muscarinic cholinergic receptors on the one hand and the ATP level on the other suggests that this substance acts mainly in the intracellular space.

Adenosine Triphosphate↗
PubMedDate not supplied

Comparison of the clinical efficacy and safety of carbamide peroxide and hydrogen peroxide in at-home bleaching gels.

OBJECTIVE: The aim of this study was to evaluate the clinical efficacy of home-administered vital bleaching procedures and possible adverse effects derived from their use. One gel containing 3.5% hydrogen peroxide with a 5% potassium nitrate component (FKD, Kin Lab) was compared with a carbamide peroxide-based gel with a concentration of 10% (Opalescence, Ultradent). METHOD AND MATERIALS: Two sample groups were designed, each composed of 8 patients. All patients employed both bleaching products, 1 in the maxillary arch and the other in the mandibular arch on a random basis. The treatment was applied for 3 hours a day for 4 weeks. The degree of bleaching was evaluated using the Vita guide arranged by brightness. Dental sensitivity was measured with a specially designed 4-point scale. Gingival irritation was registered by the presence or absence of lesions in the marginal gingiva related to treatment. RESULTS: The degree of bleaching was similar with both products (4.8 Vita shade tabs). The hydrogen peroxide product with potassium nitrate provoked less dental sensitivity, although the difference between the 2 products was insignificant (P = .063). Gingival irritation appeared in 6 subjects, but was unrelated to the applied product. CONCLUSION: Under the conditions of this study, no statistically significant differences were detected between 3.5% hydrogen peroxide containing 5% potassium nitrate (FKD) and the 10% carbamide peroxide-based product (Opalescence).

Acrylic Resins↗
PubMed1993

Relationship between peroxisome-proliferating sulfur-substituted fatty acid analogs, hepatic lipid peroxidation and hydrogen peroxide metabolism.

The effect of the administration of three peroxisome-proliferating sulfur-substituted fatty acid analogs on hepatic antioxidant status and lipid peroxidation was studied in rats. After 14 days of treatment, the ratio of induction of peroxisomal fatty acyl-CoA oxidase to catalase was 4.2 and 3.5 in rats treated with 1,10 bis-(carboxymethylthio)decane (BCMTD) and 1-mono (carboxymethylthio)tetradecane (CMTTD), respectively, while the corresponding ratio was 1.3 in 1-mono (carboxyethylthio)tetradecane (CETTD)-treated rats. As compared to the controls an increase in hepatic hydrogen peroxide content was noted in BCMTD- and CMTTD-treated rats, but not CETTD-treated rats. Hepatic lipid peroxidation was increased in all the three treatment groups in a manner not related to the potency of the compounds to induce the peroxisomal hydrogen peroxide metabolizing enzymes. Hepatic glutathione content increased while the activities of its associated enzymes such as glutathione transferase, glutathione peroxidase and glutathione reductase decreased in all the treated rats. Taken together, our data show a relationship between the levels of hydrogen peroxide and lipid peroxidation in rat livers treated with BCMTD and CMTTD. However, increased hepatic lipid peroxidation in CETTD-treated rats cannot be accounted for by the changes in the peroxisomal enzymes.

Acyl-CoA Oxidase↗
PubMed2005

Formation of hydroxyl radical from the photolysis of frozen hydrogen peroxide.

Hydrogen peroxide (HOOH) in ice and snow is an important chemical tracer for the oxidative capacities of past atmospheres. However, photolysis in ice and snow will destroy HOOH and form the hydroxyl radical (*OH), which can react with snowpack trace species. Reactions of *OH in snow and ice will affect the composition of both the overlying atmosphere (e.g., by the release of volatile species such as formaldehyde to the boundary layer) and the snow and ice (e.g., by the *OH-mediated destruction of trace organics). To help understand these impacts, we have measured the quantum yield of *OH from the photolysis of HOOH on ice. Our measured quantum yields (Phi(HOOH --> *OH)) are independent of ionic strength, pH, and wavelength, but are dependent upon temperature. This temperature dependence for both solution and ice data is best described by the relationship ln(Phi(HOOH --> *OH)) = -(684 +/- 17)(1/T) + (2.27 +/- 0.064) (where errors represent 1 standard error). The corresponding activation energy (Ea) for HOOH (5.7 kJ mol(-1)) is much smaller than that for nitrate photolysis, indicating that the photochemistry of HOOH is less affected by changes in temperature. Using our measured quantum yields, we calculate that the photolytic lifetimes of HOOH in surface snow grains under midday, summer solstice sunlight are approximately 140 h at representative sites on the Greenland and Antarctic ice sheets. In addition, our calculations reveal that the majority of *OH radicals formed on polar snow grains are from HOOH photolysis, while nitrate photolysis is only a minor contributor. Similarly, HOOH appears to be much more important than nitrate as a photochemical source of *OH on cirrus ice clouds, where reactions of the photochemically formed hydroxyl radical could lead to the release of oxygenated volatile organic compounds to the upper troposphere.

Journal Article↗
PubMed1985

Effects of formaldehyde, acetaldehyde, benzoyl peroxide, and hydrogen peroxide on cultured normal human bronchial epithelial cells.

The effects of several aldehydes and peroxides on growth and differentiation of normal human bronchial epithelial cells were studied. Cells were exposed to formaldehyde, acetaldehyde, benzoyl peroxide (BPO), or hydrogen peroxide (HPO). The effect of each agent on the following parameters was measured: (a) clonal growth rate; (b) squamous differentiation; (c) DNA damage; (d) ornithine decarboxylase activity; (e) nucleic acid synthesis; (f) aryl hydrocarbon hydroxylase activity; and (g) arachidonic acid and choline release. None of the agents were mitogenic, and their effects were assessed at concentrations which reduced growth rate (population doublings per day) to 50% of control. The 50% of control concentrations for the 6-h exposure were found to be 0.065 mM BPO, 0.21 mM formaldehyde, 1.2 mM HPO, and 30 mM acetaldehyde. BPO-exposed cells were smaller than controls (median cell planar area, 620 sq microns versus 1150 sq microns), and acetaldehyde-exposed cells were larger than controls (median cell planar area, 3200 sq microns). All agents increased the formation of cross-linked envelopes and depressed RNA synthesis more than DNA synthesis. HPO caused DNA single-strand breaks, while formaldehyde and BPO caused detectable amounts of both single-strand breaks and DNA-protein cross-links. Other effects included increased arachidonic acid and choline release due to HPO. The similarities and differences of the effects of these aldehydes and peroxides to those caused by tumor promoters are discussed.

Acetaldehyde↗
PubMed1991

Cytochrome c-catalyzed membrane lipid peroxidation by hydrogen peroxide.

Cytochrome c(3+)-catalyzed peroxidation of phosphatidylcholine liposomes by hydrogen peroxide (H2O2) was indicated by the production of thiobarbituric acid reactive substances, oxygen consumption, and emission of spontaneous chemiluminescence. The iron chelator diethylenetriaminepentaacetic acid (DTPA) only partially inhibited peroxidation when H2O2 concentrations were 200 microM or greater. In contrast, iron compounds such as ferric chloride, potassium ferricyanide, and hemin induced H2O2-dependent lipid peroxidation which was totally inhibitable by DTPA. Cyanide and urate, which react at or near the cytochrome-heme, completely prevented lipid peroxidation, while hydroxyl radical scavengers and superoxide dismutase had very little or no inhibitory effect. Changes in liposome surface charge did not influence cytochrome c3+ plus H2O2-dependent peroxidation, but a net negative charge was critical in favoring cytochrome c(3+)-dependent, H2O2-independent lipid auto-oxidative processes. These results show that reaction of cytochrome c with H2O2 promotes membrane oxidation by more than one chemical mechanism, including formation of high oxidation states of iron at the cytochrome-heme and also by heme iron release at higher H2O2 concentrations. Cytochrome c3+ could react with mitochondrial H2O2 to yield "site-specific" mitochondrial membrane lipid peroxidation during tissue oxidant stress.

Cytochrome c Group↗
PubMed2006

Tooth bleaching by different concentrations of carbamide peroxide and hydrogen peroxide whitening strips: an in vitro study.

OBJECTIVE: To investigate the tooth whitening effects of various concentrations of carbamide peroxide (CP) gels and 6% hydrogen peroxide (HP) whitening strips used on an intrinsic, in vitro stain model in a simulated home-applied bleaching protocol. METHOD: Extracted third molars were sectioned and stained to Vita shade C4 using a standardized tea solution. Stained specimens were then bleached with 10, 15, 20, 22, and 30% CP gels applied in custom-made trays for 8-hour sessions for 14 days. A 6% HP whitening strip product was also tested in a regimen of twice-daily 30-minute treatments for 14 days. Shades were assessed at baseline and at 2, 5, 7, 10, and 14 days of treatment using a shade guide (SG) and a shade vision system (SVS), recorded as shade guide unit (SGU) changes from baseline, and CIE L*a*b* recordings using a chromometer. RESULTS: By day 14, all CP treatments resulted in at least 12 SGU improvements by SG and SVS methods: the HP treatment mean was just less than 12 SGU. With the chromometer, the CP improvements ranged from approximately 19 to 28 units and 16 units for the HP whitening strips. Observationally, by SG and SVS, CP treatments achieved the maximum improvement (12-13 SGU) at different time points: day 5 for 30% CP, day 10 for 22% CP, and day 14 for the other three treatments. SG and SVS data were virtually binary, switching from 0 to scores of 9 or above as bleaching progressed. The differences between the six treatments in the mean day to achieve a positive SG or SVS score (9 or more units) approached significance. For each of the SG, SVS, and L*a*b* scores, the dose-response correlation with CP concentration was significant at one or more assessment times. SG and SVS showed extremely strong agreement in detecting change and substantial agreement with L*a*b*. CONCLUSION: This in vitro study supports the limited data available from the very few available randomized controlled clinical trials indicating that CP and HP home-use bleaching systems can achieve considerable tooth whitening outcomes, albeit at different rates, which appear to be concentration dependent. CLINICAL SIGNIFICANCE: There is a clear significant relationship for both concentration and duration of exposure for CP bleaching agents. The final shade change is independent of the concentration of bleaching agent, with time as the dominant variable. Higher concentrations of CP that have not been investigated previously may be a treatment option for esthetic improvement of shade where time is at a premium, but caution must be exercised in view of the possible increased incidence of sensitivity.

Carbamide Peroxide↗
PubMed2000

A clinical evaluation of carbamide peroxide and hydrogen peroxide whitening agents during daytime use.

BACKGROUND: Vital tooth bleaching for esthetic reasons has gained in popularity during the last few years. However, few studies have investigated the efficacy of daytime bleaching products. The purpose of this double-blind in vivo study was to evaluate the efficacy of 20 percent carbamide peroxide, or CP, and 7.5 percent hydrogen peroxide, or HP, during daytime use. The degree of color change, any color relapse, and tooth or gingival sensitivity were evaluated. METHODS: Twenty-four patients participated in this study. The bleaching gels were randomly applied to the right and left maxillary anterior teeth. Patients were shown how to place the two bleaching agents in a custom tray for one hour, twice a day for two weeks. Patients returned in one, two, three, six and 12 weeks for color evaluation with the colorimeter and shade guides as well as to have color slide photographs taken. The authors evaluated sensitivity by asking the patients to record daily for 21 days any tooth or gingival sensitivity they experienced. RESULTS: Use of the 20 percent CP resulted in significantly more lightness than the 7.5 percent HP during the first 14 days of the study, but at the end of the study, there was no significant difference between products with regard to tooth lightness. In addition, the authors found no statistically significant difference between products with regard to gingival or tooth sensitivity. CONCLUSIONS: Both CP and HP are effective at-home bleaching agents when daytime bleaching is preferred. CLINICAL IMPLICATIONS: Dentists who choose to use daytime bleaching can select either CP or HP.

Adult↗
PubMed1992

Influence of bile acids on stimulated lipid peroxidation and hydrogen peroxide production in rat liver microsomes.

Bile acids were found to be effective antioxidants in bile and intestine. The influence of different bile acids on the NADPH-Fe(++)-stimulated lipid peroxidation (LPO) and cytochrome P-450 dependent hydrogen peroxide production (H2O2) in rat liver microsomes was investigated in vitro. LPO was determined as production of thiobarbituric acid reactants (TBAR). Different tri-, di- and monohydroxylated bile acids and cholesterol were given to the incubation mixture in concentrations ranging from 10(-5) to 10(-3) M. Sodium salts of cholic, tauroglycocholic and deoxycholic acids as well as cheno-deoxycholic, ursodeoxycholic, lithocholic acids and cholesterol did not alter the microsomal production of TBAR. H2O2 formation was significantly decreased by sodium deoxycholate whereas cholesterol increased H2O2 production up to 4 times. These results show that bile acids were not able to protect microsomal membrane lipids against peroxidative damage. Cholesterol mediated H2O2 formation as a source of hydroxyl radicals had no toxic effect concerning LPO, TBAR were not enhanced significantly.

Animals↗
PubMed1989

Injurious effect of the eosinophil peroxide-hydrogen peroxide-halide system and major basic protein on human nasal epithelium in vitro.

Tissue injury is observed in allergic and nonallergic eosinophilic rhinitis, but the mechanism of this injury is unclear. Because eosinophils are prominent in biopsy specimens in these conditions, we hypothesized that they may participate in the injury process. Initially, we developed techniques to isolate and purify human nasal epithelial cells from turbinate biopsies to use as target cells for eosinophil granule products. Primary cultures from explants were characterized by electron microscopy and indirect immunofluorescence with a panel of primary monoclonal and polyclonal antibodies. These studies revealed the homogeneity of the cells and confirmed their epithelial nature. Cultured nasal epithelial cells were then exposed to either purified human eosinophil peroxidase, bromide, and glucose plus glucose oxidase, as a continuous source of hydrogen peroxide, or eosinophil major basic protein. Neither eosinophil peroxidase alone nor glucose plus glucose oxidase in the absence of eosinophil peroxidase were injurious, but the combined addition of eosinophil peroxidase, glucose/glucose oxidase, and bromide produced marked target cell lysis. This effect was time- and eosinophil peroxidase dose-dependent. Catalase and azide significantly inhibited the lysis of these cells, suggesting the eosinophil peroxidase-catalyzed products of halide oxidation mediated this form of injury. The addition of purified human eosinophil major basic protein also caused dose- and time-dependent lysis of the nasal epithelial cells but required longer incubation periods to effect injury. We hypothesize that the eosinophil peroxidase-hydrogen peroxide-halide system and major basic protein may injure the nasal epithelium in inflammatory conditions such as allergic and nonallergic eosinophilic rhinitis.

Blood Proteins↗
PubMed1984

Embryotoxic effects of eight organic peroxides and hydrogen peroxide on three-day chicken embryos.

Nine peroxides were tested for embryotoxicity in 3-day chicken embryos using the air-chamber method. The potencies were expressed by the ED50 for the total embryotoxic effect of the chemicals, including deaths and malformations, up to Day 14 of the incubation. The range of the ED50's was from 0.13 to 2.7 mumoles per egg and the order of the potencies was as follows: cyclohexanoneperoxide greater than cumolhydroperoxide greater than ethylmethylketoneperoxide greater than dibenzoylperoxide greater than acetylacetoneperoxide greater than perbenzoic acid-tert-butylester greater than dicumylperoxide greater than dilauroylperoxide greater than hydrogen peroxide. All nine peroxides caused malformations at a moderate frequency. The maximum percentage of malformed embryos of the treated varied from the 16% of perbenzoic acid-tert-butylester to the 56% of dicumylperoxide. The high percentage caused by the latter could, however, result from slow diffusion of high lethal doses from the air chamber to the embryo.

Abnormalities, Drug-Induced↗