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At least 1,387 records · Page 77Linked to original sources
PubMed2006

Lipid peroxidation and HSP72/73 expression in rat following cadmium chloride administration: interactions of magnesium supplementation.

OBJECTIVE: to determine whether magnesium (Mg) supplementation could have a protective effect against the cadmium (Cd)-induced oxidative stress in liver, kidneys and testes of adult male rats. Stress was evaluated by measuring lipid peroxidation by thiobarbituric acid reactive substances (TBARS) and the heat shock protein (HSP) 72/73 expression. CdCl2 injections (2.5mg/day/kg body weight) for 10 days resulted in a time dependent increase of Cd accumulation in liver, kidney and testes, the highest levels being found in liver (400 microg/g dried tissue). At the same time, an increase of lipid peroxidation was observed. The effect was maximal at day 1 of Cd treatment in liver and testes, and later (day 5) in kidney. Then, Cd-induced lipid peroxidation decreased, suggesting the activation of antioxidant defense mechanisms. Injections of Mg SO4 (300-600 mg/day/kg body weight) reduced in a dose-dependent manner Cd-induced lipid peroxidation in liver and kidney as well as the accumulation of Cd in liver, kidney and testes. In testes, a protective effect of Mg was found only during the early phase of Cd-poisoning. On days 5 and 10, lipid peroxidation was even increased as compared to controls. In liver and testes only the constitutive HSP73 was detected whereas in kidney both HSP73 and the inducible HSP72 were expressed. HSP72/73 expression was not significantly increased by Cd and HSP73 was even lowered in kidney, probably due to the strong dose used. These results were not modified by Mg injections. CONCLUSION: Mg supplementation can reduce Cd accumulation in organs and lipid peroxidation related to Cd administration.

Animals↗
PubMed2006

Interaction of peroxidized cardiolipin with rat-heart mitochondrial membranes: induction of permeability transition and cytochrome c release.

Cardiolipin peroxidation plays a critical role in mitochondrial cytochrome c release and subsequent apoptotic process. Mitochondrial pore transition (MPT) is considered as an important step in this process. In this work, the effect of peroxidized cardiolipin on MPT induction and cytochrome c release in rat heart mitochondria was investigated. Treatment of mitochondria with micromolar concentrations of cardiolipin hydroperoxide (CLOOH) resulted in a dose-dependent matrix swelling, DeltaPsi collapse, release of preaccumulated Ca2+ and release of cytochrome c. All these events were inhibited by cyclosporin A and bongkrekic acid, indicating that peroxidized cardiolipin behaves as an inducer of MPT. Ca2+ accumulation by mitochondria was required for this effect. ANT (ADP/ATP translocator) appears to be involved in the CLOOH-dependent MPT induction, as suggested by the modulation by ligands and inhibitors of adenine nucleotide translocator (ANT). Together, these results indicate that peroxidized cardiolipin lowers the threshold of Ca2+ for MPT induction and cytochrome c release. This synergistic effect of Ca2+ and peroxidized cardiolipin on MPT induction and cytochrome c release in mitochondria, might be important in regulating the initial phase of apoptosis and also may have important implications in those physiopathological situations, characterized by both Ca2+ and peroxidized cardiolipin accumulation in mitochondria, such as aging, ischemia/reperfusion and other degenerative diseases.

Aging↗
PubMed2005

Lipid peroxidation and renal cell carcinoma: further supportive evidence and new mechanistic insights.

We have recently proposed lipid peroxidation as a unifying mechanistic pathway by which several seemingly unrelated risk/protective factors (obesity, hypertension, diabetes, smoking, oophorectomy/hysterectomy, parity, antioxidants) affect renal cell carcinoma development. In experimental studies, increased lipid peroxidation is a principal mechanistic pathway in renal carcinogenesis induced by different chemicals. In this communication, we provide additional lines of evidence that further support a role for lipid peroxidation on renal cell cancer development. (1) Lipid peroxidation may explain the role of other risk (analgesic use, pre-eclampsia) or protective (alcohol intake, oral contraceptives) factors for renal cell carcinoma. (2) Additional experimental evidence supports lipid peroxidation as an important mechanism in renal carcinogenesis, and (3) Existing evidence support a cross-talk between the lipid peroxidation pathway and other pathways that are relevant to renal carcinogenesis, such as apoptosis, VHL, and possibly other pathways.

Animals↗
PubMed2005

Amperometric biosensor for the detection of hydrogen peroxide using catalase modified electrodes in polyacrylamide.

A simple biosensor for the detection of hydrogen peroxide in organic solvents has been developed and coupled to a flow injection analysis (FIA) system. Catalase was entrapped in polyacrylamide gel and placed on the surface of platinum (working electrode) fixed in a Teflon holder with Ag-wire (auxiliary electrode), followed by addition of filter paper soaked in KCl. The entrapped catalase gel was held on the electrode using membranes. The effects of cellulose and polytetrafluroethylene (PTFE) membranes on the electrode response towards hydrogen peroxide have been studied. The modified electrode has been used to study the detection of hydrogen peroxide in solvents like water, dimethyl sulfoxide (DMSO), and 1,4-dioxane using amperometric techniques like cyclic voltammetry (CV) and FIA. The CV of modified catalase electrode showed a broad oxidation peak at -150 mV and a clear reduction peak at -212 mV in the presence of hydrogen peroxide. Comparison of CV with hydrogen peroxide in various solvents has been carried out. The electrode showed an irreversible kinetics with DMSO as the solvent. A flow cell has been designed in order to carry on FIA studies to obtain calibration plots for hydrogen peroxide with the modified electrode. The calibration plots in several solvents such as water, dimethyl sulfoxide, 1,4-dioxane have been obtained. The throughput of the enzyme electrode was 10 injections per hour. Due to the presence of membrane the response time of the electrode is concentration dependent.

Acrylic Resins↗
PubMed2006

Enhanced stability of hydrogen peroxide in the presence of subsurface solids.

The stabilization of hydrogen peroxide was investigated as a basis for enhancing its downgradient transport and contact with contaminants during catalyzed H(2)O(2) propagations (CHP) in situ chemical oxidation (ISCO). Stabilization of hydrogen peroxide was investigated in slurries containing four characterized subsurface solids using phytate, citrate, and malonate as stabilizing agents after screening ten potential stabilizers. The extent of hydrogen peroxide stabilization and the most effective stabilizer were solid-specific; however, phytate was usually the most effective stabilizer, increasing the hydrogen peroxide half-life to as much as 50 times. The degree of stabilization was nearly as effective at 10 mM concentrations as at 250 mM or 1 M concentrations. The effect of stabilization on relative rates of hydroxyl radical activity varied between the subsurface solids, but citrate and malonate generally had a greater positive effect than phytate. The effect of phytate, citrate, and malonate on the relative rates of superoxide generation was minimal to somewhat negative, depending on the solid. The results of this research demonstrate that the stabilizers phytate, citrate, and malonate can significantly increase the half-life of hydrogen peroxide in the presence of subsurface solids during CHP reactions while maintaining a significant portion of the reactive oxygen species activity. Use of these stabilizers in the field will likely improve the delivery of hydrogen peroxide and downgradient treatment during CHP ISCO.

Citrates↗
PubMed2004

The measurement of degradation and wear of three glass ionomers following peroxide bleaching.

OBJECTIVES: To investigate, for three glass ionomer dental materials, the effects of a hydrogen peroxide solution on the elution of key elements, and the effects of a novel 6% hydrogen peroxide tooth whitening gel on subsequent wear rates with a toothpaste slurry. METHODS: Discs specimens of three glass ionomers (ChemFlex, Fuji II and Ketac-Fil) were prepared. One set of discs was exposed to either 6% hydrogen peroxide in phosphate buffer, phosphate buffer, water, a carbonated beverage or 38% orthophosphoric acid for 60 min. The ions eluted from the discs were determined by inductively coupled plasma-optical emmision spectroscopy. A second set of discs were conditioned with either a 6% hydrogen peroxide gel (30 min), water (30 min), a carbonated beverage (2 min) or 38% orthophosphoric acid gel (2 min) followed by a three-body abrasive wear treatment (2 min) with a toothpaste slurry. Changes in height of the samples were measured with a digital comparitor. The conditioning and abrasive cycles were repeated thirteen times. RESULTS: For the elution study, the solutions gave only minor release of sodium except orthophosphoric acid which showed increased elution levels of aluminium, silicon and sodium ions. For the wear study, the orthophosphoric acid gave the highest level of wear whilst for the other treatments there were no statistical significant differences in the level of wear (one-way ANOVA). CONCLUSIONS: A 6% hydrogen peroxide solution did not cause significant dissolution, and a novel 6% hydrogen peroxide tooth whitening gel did not significantly increase the three-body wear rate of any of the materials tested.

Aluminum↗
PubMed2005

Evaluation of the validity of the UN SADT H.4 test for solid organic peroxides and self-reactive substances.

Many self-accelerating decomposition temperatures (SADTs) of solid organic peroxides and self-reactive substances have been determined with the UN test method H.4, which is a scaled down test in a small Dewar vessel. For solid organic peroxides and solid self-reactive substances Fierz has questioned this procedure in a recent paper. Fierz concluded that the Dewar test results should not be extrapolated to beyond 8l packages, owing to the thermal insulation value of solids. On the other hand, long term experience with the test, with a great variety of solid organic peroxides and self-reactive substances show about equal critical temperatures in the small Dewar vessel and on 50 kg scale. In the present work, we first checked, by numerical simulations, the Dewar scale versus the larger scale, in a way comparable with Fierz' method: both scales are simulated by spheres, consisting of a number of annular layers, for the large scale the usual external heat loss term is used but for the small scale the outside heat transfer is strongly limited. The outcome of these simulations, covering a variety of physical parameters, supports the concerns expressed by Fierz. After this, we performed accurate cooling and heating experiments with solid organic peroxide in the usual Dewar vessel, provided with a large set of thermocouples. The results of these experiments showed that the simulation model for the Dewar vessel has to be changed from a spherical analogue to a short cylinder of solid material with heat exchange mainly via its top (U(top) approximately 3.5 W/(m(2)K), overall heat transfer coefficient) and some heat exchange (U(side) approximately 0.29 W/(m(2)K)) through its cylindrical and bottom part. With this "modified cylinder" model (being neither an infinitely long cylinder nor a slab) of the Dewar vessel, we found that the UN method H.4 enables an accurate prediction of the SADT, with small deviations of 0+/-2.5 degrees C. Further, by performing a truly three-dimensional (3D) finite element calculation in FEMLAB, the new heat characteristics of the Dewar vessel as well as a 50 kg package of dilauroyl peroxide, a solid organic peroxide, were checked. The outcome was compared with the critical ambient temperatures known for various package sizes, which agreed well.

Environmental Monitoring↗
PubMed2005

Rac1 inhibition protects against hypoxia/reoxygenation-induced lipid peroxidation in human vascular endothelial cells.

Both in vivo models of ischemia/reperfusion and in vitro models of hypoxia (H)/reoxygenation (R) have demonstrated the crucial role of the Rac1-regulated NADPH oxidase in the production of injurious reactive oxygen species (ROS) by vascular endothelial cells (ECs). Since membrane lipid peroxidation has been established as one of the mechanisms leading to cell death, we examined lipid peroxidation in H/R-exposed cultured human umbilical vein ECs (HUVECs) and the role of Rac1 in this process. H (24 h at 1% O2)/R (5 min) caused an increase in intracellular ROS production compared to a normoxic control, as measured by dichlorofluorescin fluorescence. Nutrient deprivation (ND; 24 h), a component of H, was sufficient to induce a similar increase in ROS under normoxia. Either H(24 h)/R (2 h) or ND (24 h) induced increases in lipid peroxidation of similar magnitude as measured by flow cytometry of diphenyl-1-pyrenylphosphine-loaded HUVECs and Western blotting analysis of 4-hydroxy-2-nonenal-modified proteins in cell lysates. In cells infected with a control adenovirus, H (24 h)/R (2 h) and ND (24 h) resulted in increases in NADPH-dependent superoxide production by 5- and 9-fold, respectively, as measured by lucigenin chemiluminescence. Infection of HUVECs with an adenovirus that encodes the dominant-negative allele of Rac1 (Rac1N17) abolished these increases. Rac1N17 expression also suppressed the H/R- and ND-induced increases in lipid peroxidation. In conclusion, ROS generated via the Rac1-dependent pathway are major contributors to the H/R-induced lipid peroxidation in HUVECs, and ND is able to induce Rac1-dependent ROS production and lipid peroxidation of at least the same magnitude as H/R.

Adenoviridae↗
PubMed1992

Hydrogen peroxide and reoxygenation cause prostaglandin-mediated contraction of human placental arteries and veins.

OBJECTIVE: Because our previous studies in several vascular preparations suggest that posthypoxic reoxygenation elicits tone responses by generation of hydrogen peroxide we compared the actions of reoxygenation and hydrogen peroxide on isolated human placental arteries and veins. STUDY DESIGN: Endothelium-intact and denuded arteries and veins (1 to 2 mm diameter, from normal term deliveries), incubated under 95% oxygen/5% carbon dioxide or 5% oxygen/5% carbon dioxide (balance nitrogen) and precontracted with 1 to 10 nmol/L U46619, were exposed to hypoxia (95% nitrogen/5% carbon dioxide, PO2 8 to 10 torr) followed by reoxygenation and to 1 to 100 mumol/L hydrogen peroxide in the presence and absence of the inhibitor of prostaglandin biosynthesis, 10 mumol/L indomethacin. RESULTS: In both arteries and veins posthypoxic reoxygenation or exposure to hydrogen peroxide produced vascular contraction that was eliminated or reversed to a modest relaxation by indomethacin, consistent with mediation by prostaglandins. Hypoxia after incubation with 5% oxygen, but not 95% oxygen, caused a modest prostaglandin-independent relaxation. Removal of the endothelium did not alter any of these responses. CONCLUSION: Placental arteries and veins show a similar prostaglandin-mediated contraction to hydrogen peroxide and posthypoxic reoxygenation, consistent with a possible involvement of hydrogen peroxide in the response to reoxygenation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Preeclampsia, lipid peroxidation, and calcium adenosine triphosphatase activity of red blood cell ghosts.

OBJECTIVE: We evaluated the effect of lipid peroxidation on the calcium adenosine triphosphatase activity of red blood cell ghosts from normotensive pregnant women and compared it with the adenosine triphosphatase activity and lipid peroxidation in preeclampsia. STUDY DESIGN: Ten nulliparous normotensive and 10 nulliparous preeclamptic pregnant women (38 to 39 weeks of gestation) were used as blood donors. Preeclampsia was diagnosed on the basis of blood pressure (>140/90 mm Hg) and proteinuria (>0.5 gm of urinary protein per day). Red blood cell ghosts were prepared for both groups and used for calcium adenosine triphosphatase activity and lipid peroxidation determinations. Control ghosts (normotensive) were irradiated with ultraviolet light for different lengths of time. RESULTS: Calcium adenosine triphosphatase activity of red blood cell ghosts from normotensive women is sensitive to lipid peroxidation. The lipid peroxidation of red blood cell ghosts from preeclamptic women is higher than that from normotensive women. CONCLUSION: The diminution of the calcium adenosine triphosphatase activity with preeclampsia could be explained by the sensitivity of this adenosine triphosphatase to lipid peroxidation.

Adult↗
PubMed1990

Ocular injury induced by methyl ethyl ketone peroxide.

Methyl ethyl ketone peroxide is a commonly used catalyst in various industries. We studied 19 eyes with a single exposure to methyl ethyl ketone peroxide that developed clinical patterns of mild injury, moderate injury, severe injury, or delayed keratitis. Delayed methyl ethyl ketone peroxide keratitis may cause exacerbations and remissions of corneal and limbal disease lasting more than 20 years with palpebral and bulbar hyperemia equal to the initial chemical exposure. With repeat exacerbation, further pannus may occur, which can be associated with a poorer outcome. Based on the capability of methyl ethyl ketone peroxide to change DNA to a new weak antigen, we suggest possible methods of therapy to prevent or limit delayed methyl ethyl ketone peroxide keratitis. This proposed type of injury has important implications in studying various limbal and corneal diseases. A major factor in the severity of ocular injury was the length of time from exposure to methyl ethyl ketone peroxide to obtaining a topical ocular local anesthetic to perform adequate lavage.

Adult↗
PubMed2003

Dual method for the determination of peroxidase activity and total peroxides-iodide leads to a significant increase of peroxidase activity in human sera.

Peroxidases are very important enzymes, e.g., as preventive antioxidants by removing noxious peroxides from the blood. For this reason we evaluated a colorimetric method which detects the activity of endogenous peroxidases by their reaction with hydrogen peroxide, using tetramethylbenzidine as the chromogenic substrate. This assay design can be easily reversed by change of the variable compound to measure also total peroxides in plasma or serum. An increased total antioxidant status was reported previously by the addition of iodide to human serum. In this study iodide activated the endogenous peroxidases significantly in comparison to control sera and isomolar NaCl as well as horseradish peroxidase. Corresponding to the increased peroxidase activity a concomitant decrease of total peroxides occurred in the same samples. This exchangeable assay design is a beneficial opportunity to screen total peroxide levels as well as peroxidase activity in human sera without time-consuming preparations. The method proved to be simple and is favorable due to its specificity, reproducibility, and low costs. Moreover, we were able to find an explanation for the increased total antioxidant status in the presence of iodide, which is presumably an indirect protective effect via an enhanced activity of enzymatic antioxidants, thereby reducing endogenous peroxides.

Adult↗
PubMed1988

Stimulation and inhibition of iron-dependent lipid peroxidation by desferrioxamine.

Peroxidation of rat brain synaptosomes was assessed by the formation of thiobarbituric acid reactive products in either 50 mM potassium phosphate buffer (pH 7.4) or pH adjusted saline. In phosphate, addition of Fe2+ resulted in a dose-related increase in lipid peroxidation. In saline, stimulation of lipid peroxidation by Fe2+ was maximal at 30 uM, and was less at concentrations of 100 uM and above. Whereas desferrioxamine caused a dose-related inhibition of iron-dependent lipid peroxidation in phosphate, it stimulated lipid peroxidation with Fe2+ by as much as 7-fold in saline. The effects of desferrioxamine depended upon the oxidation state of iron, and the concentration of desferrioxamine and lipid. The results suggest that lipid and desferrioxamine compete for available iron. The data are consistent with the hypothesis that either phosphate or desferrioxamine may stimulate iron-dependent lipid peroxidation under certain circumstances by favoring formation of Fe2+/Fe3+ ratios.

Animals↗
PubMed1998

U-101033E (2,4-diaminopyrrolopyrimidine), a potent inhibitor of membrane lipid peroxidation as assessed by the production of 4-hydroxynonenal, malondialdehyde, and 4-hydroxynonenal--protein adducts.

4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) are major lipid peroxidation products generated by free radical attack on membranes and appear to contribute to the cytotoxic effects of oxidative stress by a mechanism involving adduct formation with cellular proteins. In the present studies, we investigated the relationship between lipid peroxidation and eventual inactivation of plasma membrane proteins using a model system consisting of purified red blood cell membranes and Fe2+/EDTA. Using this system, we also analyzed the ability of a novel antioxidant, U-101033E (2,4-diaminopyrrolopyrimidine), to inhibit lipid peroxidation and associated protein damage. Our results demonstrated that significant levels of MDA and 4-HNE are generated in this model system, and that both aldehydes are capable of cross-linking membrane proteins. In addition, we used a monoclonal antibody to demonstrate the presence of 4-HNE-protein adducts in this system. The generation of 4-HNE-protein adducts closely paralleled the time course of lipid peroxidation and membrane protein cross-linking, suggesting that 4-HNE may contribute to membrane protein cross-linking. Analysis of U-101033E in this system showed that this antioxidant inhibited lipid peroxidation, prevented the appearance of 4-HNE-protein adducts, and strongly reduced membrane protein cross-linking, with an EC50 of 0.5 microM. We also show that these antioxidant effects were not due to the scavenging of superoxide anion. Thus, these studies demonstrate the potential usefulness of U-101033E for treating certain disease processes where lipid peroxidation plays a role in disease pathogenesis.

Aldehydes↗
PubMed1999

Antioxidative and prooxidative effects of coumarin derivatives on free radical initiated and photosensitized peroxidation of human low-density lipoprotein.

The antioxidative and/or prooxidative activity of 4-methylcoumanrin (MC), 7-hydroxy-4-methylcoumarin (HMC) and 7,8-dihydroxy-4-methylcoumarin (DHMC), respectively, in the peroxidation of human low-density lipoprotein (LDL) has been studied. The peroxidation was initiated either thermally by water-soluble initiator 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH), or photochemically by a triplet sensitizer benzophenone (BP) or its water-soluble analogue disodium 3,3'-disulfobenzophenonate (DSBP). The reaction kinetics were monitored by the uptake of oxygen and the depletion of alpha-tocopherol (TOH) present in the native LDL. Kinetic analysis of the peroxidation process demonstrated that DHMC is a good antioxidant for both the AAPH-initiated and BP- and DSBP-photosensitized peroxidation; HMC is a prooxidant for the AAPH-initiated and DSBP-photosensitized peroxidation, but an antioxidant for the BP-sensitized peroxidation; MC is a prooxidant in all of these initiation conditions. The antioxidative action of the coumarin derivatives may include trapping the initiating radicals, trapping the propagating lipid peroxyl radicals, recycling alpha-tocopherol and/or deactivating the excited photosensitizer.

Amidines↗
PubMed2000

Free radicals antioxidant enzymes and lipid peroxidation in different types of leukemias.

Free radicals are highly reactive species that have been implicated in the pathogenesis of many diseases. Reactive oxygen species can initiate lipid peroxidation and DNA damage leading to mutagenesis, carcinogenesis and cell death, if the antioxidant system is impaired. This study was undertaken to examine the prevalence of oxidative stress and the role of antioxidant defence in untreated leukemia patients. The generation of superoxide anion and hydrogen peroxide by leukocytes, plasma malondialdehyde levels, red cell copper zinc superoxide dismutase (Cu-Zn SOD) and glutathione peroxidase (GSH-PX) activities were determined in 30 patients with different types of leukemias prior to therapy. The superoxide anion generation by polymorphonuclear leukocytes was found to be significantly increased in leukemia patients especially those with acute lymphocytic and nonlymphocytic leukemias, while the hydrogen peroxide levels were comparable to the control values. Plasma lipid peroxidation products in untreated leukemia patients were in the normal range. Red cell Cu-Zn SOD and GSH-PX activities were significantly increased and showed no correlation with the hemoglobin content. Although superoxide generation was high, lipid peroxide levels were normal in these patients. This might be due to the increased activities of the antioxidant enzymes (SOD, GSH-PX) which counteract lipid peroxidation. Increased free radical generation, especially superoxide anion in leukemia patients and increased antioxidant defence enzymes, which is an adaptive protective response, are indicative of mild oxidative stress. There were no significant differences for the parameters cited above between different types of leukemias, suggesting that the changes are not specific to the type of leukemia.

Adult↗
PubMed1996

Impact of in vitro fertilization culture media on peroxidative damage to human spermatozoa.

OBJECTIVE: To compare different culture media for their effects on sperm motility and lipid peroxidation. DESIGN: The ability of four different culture media to sustain the motility of human spermatozoa during an overnight incubation was examined in relation to the induction of lipid peroxidation. The role of transition metals in the genesis of peroxidative damage was investigated in experiments involving the addition of iron or the chelating reagent ethylenediamine tetra acetic acid (EDTA). SETTING: Academic research institute. MAIN OUTCOME MEASURES: The generation of malondialdehyde and 4-hydroxyalkenals after the addition of a ferrous ion promoter and the measurement of sperm motility. RESULTS: Spermatozoa incubated in Ham's F-10 medium (GIBCO, Paisley, Scotland) exhibited a marked loss of motility in association with a significant increase in peroxidative damage. Addition of EDTA to Ham's F-10 medium significantly reduced the degree of lipid peroxidation and induced a simultaneous increase in sperm motility. CONCLUSIONS: Ham's F-10 medium is a suboptimal medium for the long-term culture of human spermatozoa because it induces peroxidative damage and a concomitant decline of sperm motility.

Chelating Agents↗
PubMedDate not supplied

Hydrogen peroxide enteritis: the "snow white" sign.

Hydrogen peroxide is a useful disinfectant that has achieved widespread utility in varied clinical settings. We report an epidemic of hydrogen peroxide enteritis that developed in seven patients in our gastrointestinal endoscopy unit during a 2-week period in early 1988. During endoscopy, using recently sterilized endoscopes that were flushed with 3% hydrogen peroxide after the glutaraldehyde cycle, instantaneous blanching (the "snow white" sign) and effervescence were noted on the mucosal surfaces when the water button was depressed. No patient subsequently suffered morbidity or mortality associated with this peroxide enteritis, and the biopsy specimens revealed nonspecific inflammation. The toxicity of hydrogen peroxide when used in enema form is reviewed, as well as the pathogenesis of peroxide enteritis.

Aged↗