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PubMed1995

Lipid peroxidation and changes in T lymphocyte subsets and lymphocyte proliferative response in experimental iron overload.

This study was undertaken to investigate the hypothesis that lipid peroxidation might be associated with immunological abnormalities in experimental hemosiderosis. The correlation between the degree of plasma and spleen lipid peroxidation with lymphocyte proliferative response and with the proportion of T lymphocyte subsets was studied in normal and iron overloaded male Sprague Dawley rats. The iron-loading protocol consisted of a total dose of iron-dextran (1.5 mg/Kg body weight) divided in daily i.m. injections over twenty consecutive days. Lipid peroxidation was measured by the thiobarbituric acid assay in plasma and in homogenates of spleen. Plasma lipid peroxide level increased rapidly after i.m. administration of iron-dextran and decreased sharply at 48 h after the last injection. Conversely, a progressive increase of lipid peroxidation in homogenates of spleen was observed in the course of the iron overload protocol, remaining high even at 50 days after initiation of iron-dextran injections. The increase of spleen lipid peroxide levels was associated with decreased lymphocyte proliferative response to Con A in iron overloaded rats. The addition of superoxide dismutase and catalase to lymphocyte cultures reversed the inhibition of the proliferative response, implicating reactive species of oxygen as the causative agents of these alterations. These effects may be related with the enhanced membrane and DNA damage occurring during intracellular and extracellular peroxidation. Negative correlations between helper/cytotoxic ratio and malondialdehyde levels were obtained in blood and spleen during iron administration. These results supports the hypothesis that lipid peroxidation plays a role in the immunological abnormalities observed in experimental hemosiderosis.

Animals↗
PubMed1997

Effects of pressor substances on low density lipoprotein peroxidation by Cu++.

To investigate whether pressor substances accelerate low density lipoprotein peroxidation by Cu++, low density lipoprotein was dialysed against physiological saline containing O-5 mumol/l CuCl2 and/or 1 mumol/l of various pressor substances. Lipid peroxide value of low density lipoprotein changed little with the addition of norepinephrine to the saline, but the addition of norepinephrine to 1 mumol/l CuCl2 accelerated the peroxidation. When low density lipoprotein was dialysed against saline with norepinephrine, epinephrine, serotonin or dopamine, there were no significant differences in the lipid peroxide values of low density lipoprotein. Although the addition of serotonin into the dialyzate did not accelerate the peroxidation of low density lipoprotein due to Cu++, the addition of norepinephrine, epinephrine and dopamine accelerated the Cu(++)-peroxidation with a significant increase in the acceleration rate starting at the 36 hour point. Thus, it is speculated that various stresses stimulating the sympathetic nervous system accelerate the peroxidation of low density lipoprotein and produce peroxidized low density lipoprotein in the blood.

Analysis of Variance↗
PubMed1999

AA-2414, an antioxidant and thromboxane receptor blocker, completely inhibits peroxide-induced vasoconstriction in the human placenta.

We hypothesized that AA-2414, a novel thromboxane receptor blocker with antioxidant properties, would inhibit peroxide-induced vasoconstriction in the isolated perfused human placental cotyledon. In study 1, placental cotyledons (n = 5) were perfused serially for 20- min intervals with control KrebsRinger-bicarbonate (KRB) buffer, t-butyl hydroperoxide (Px; 100 microM), KRB buffer, and KRB buffer containing Px to which progressively increasing concentrations of AA-2414 were added (1 x 10(-8) to 1 x 10(-4) mol/l). In study 2, placental cotyledons (n = 6) were perfused with control KRB buffer, Px alone, KRB buffer, 1 x 10(-5) mol/l AA-2414 alone, Px plus AA-2414, and Px alone. Compared with control, perfusion with Px significantly increased perfusion pressure, vascular resistance, and the maternal and fetal secretion rates of lipid peroxides, thromboxane B2 (TXB2) and 6-keto prostaglandin F1alpha. In study 1, AA-2414 + Px produced a dose-response inhibition of Px-induced increases in perfusion pressure, vascular resistance, and maternal secretion of lipid peroxides and TXB2. In study 2, perfusing AA-2414 at a dose of 1 x 10(-5) mol/l completely inhibited Px-induced vasoconstriction and increases in lipid peroxide and TXB2 secretion rates, but only partially inhibited the increase in 6-keto prostaglandin F1alpha secretion. We conclude that AA-2414 inhibited peroxide-induced vasoconstriction in the human placenta, as well as peroxide- induced increases in the placental secretion rates of lipid peroxides and thromboxane, but only partially inhibited peroxide-induced increases in the placental secretion rate of prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Lipid peroxidation and tissue damage.

In recent years it has become apparent that the oxidation of lipids, or lipid peroxidation, is a crucial step in the pathogenesis of several disease states in adult and infant patients. Lipid peroxidation is a process generated naturally in small amounts in the body, mainly by the effect of several reactive oxygen species (hydroxyl radical, hydrogen peroxide etc.). It can also be generated by the action of several phagocytes. These reactive oxygen species readily attack the polyunsaturated fatty acids of the fatty acid membrane, initiating a self-propagating chain reaction. The destruction of membrane lipids and the end-products of such lipid peroxidation reactions are especially dangerous for the viability of cells, even tissues. Enzymatic (catalase, superoxide dismutasse) and nonenzymatic (vitamins A and E) natural antioxidant defence mechanisms exist; however, these mechanisms may be overcome, causing lipid peroxidation to take place. Since lipid peroxidation is a self-propagating chain-reaction, the initial oxidation of only a few lipid molecules can result in significant tissue damage. Despite extensive research in the field of lipid peroxidation it has not yet been precisely determined if it is the cause or an effect of several pathological conditions. Lipid peroxidation has been implicated in disease states such as atherosclerosis, IBD, ROP, BPD, asthma, Parkinson's disease, kidney damage, preeclampsia and others.

Animals↗
PubMed1992

[Production of reactive oxygen species by rat alveolar macrophages. Dissociation between the intracellular and extracellular release of hydrogen peroxide].

In order to clarify the features of reactive oxygen species produced by rat alveolar macrophages (AMs), the concentrations of intracellular and extracellular hydrogen peroxide were measured under various experimental conditions. Intracellular hydrogen peroxide was measured by DCFH method using a flow cytometer, while the extracellularly released fraction was measured by scopoletin method using a spectrophotometer. The concentration of intracellular hydrogen peroxide after stimulation with opsonized zymosan (10 micrograms/ml) was significantly higher than that after stimulation with phorbol myristate acetate (PMA; 100 ng/ml). On the other hand, hydrogen peroxide released extracellularly after stimulation with PMA was significantly greater that that after stimulation with opsonized zymosan. These results indicate that the soluble membrane stimulant and the phagocytic particles have different mechanisms in activating the production of hydrogen peroxide in AMs. That is, hydrogen peroxide induced by PMA was mainly released extracellularly, while that induced by zymosan was mainly released into the intracellular environment. At rest, the concentration of intracellular hydrogen peroxide in rat AMs was high. Potassium cyanate, a known mitochondrial inhibitor, suppressed the intracellular hydrogen peroxide in AMs not only at rest but also after stimulations, indicating that most of the reactive oxygen species released into the intracellular environment in AM are produced by mitochondria. From these results, in order to gain a closer insight into the function of AMs, it is very important to distinguish the oxidative metabolites produced intracellularly which are related to bactericidal function from those of the extracellularly released fraction which give rise to lung damage.

Animals↗
PubMed1992

Lipid peroxide levels in a murine adenocarcinoma exposed to hyperthermia: the role of glutathione depletion.

Increased lipid peroxide levels were obtained 1 h after a 60-min 43 degrees C hyperthermia treatment of a solid murine C3H mammary adenocarcinoma, grown subcutaneously in the hind paws of mice. Previous work from our group revealed that this heat treatment depletes the intracellular glutathione (GSH) content in this tumor. To investigate GSH depletion as one tentative mechanism behind the increased lipid peroxide levels obtained, we also measured the formation of lipid peroxidation products after extensive DL-buthionine-S,R-sulfoximine (BSO)-induced GSH depletion. The lipid peroxide effect provoked by BSO was less than that of the 60-min hyperthermia treatment. We therefore propose that the increased lipid peroxide levels induced by heat treatment do not correlate primarily with the observed decrease in GSH levels. Furthermore, in thermotolerance-induced tumors, lipid peroxide levels after a second heat treatment were observed to increase concomitantly with the cessation of thermotolerance. Lipid peroxide levels were also studied in liver, lung, and heart. Following BSO treatments, and up to 2-fold increase was observed in these organs in non-tumor-bearing mice. It was also observed that the intrinsic lipid peroxide levels in these organs from tumor-bearing mice were approximately 1.5- to 4-fold higher in comparison with non-tumor-bearing mice, thus indicating a systemic effect of the tumor implant.

Adenocarcinoma↗
PubMed2003

Peroxide degradation kinetics of a direct application percarbonate bleaching film.

PURPOSE: To evaluate the hydrogen peroxide (HP) degradation kinetics of a 19% sodium percarbonate (5.3% HP released) direct application bleaching gel on the tooth surface and in saliva during use. METHODS: This was a single center, 14 subject trial, where both maxillary and mandibular teeth were treated. Peroxide concentrations in the tooth scraping sample were determined at 10 minutes, 30 minutes, 1 hour, 2 hours, and 4 hours. Peroxide concentrations in the saliva were determined at 5, 10, 20, 30, and 60 minutes after test product application. RESULTS: The median peroxide concentrations on the teeth at 10 minutes, 30 minutes, 1 hour, 2 hours, and 4 hours of daytime wear were 4.7, 3.5, 1.5, 0.3 and 0.1% respectively, demonstrating significant substantivity of peroxide on the tooth surface. In contrast, the median peroxide concentrations in the saliva at 5, 10, and 20 minutes of daytime wear were very low; 0.001, 0.0001 and 0.0001% respectively. By 30 minutes, median salivary concentrations of peroxide were below the limit of detection (0.00007%). A comparison was made to previously reported data from other peroxide degradation studies with strips, trays and a paint-on tooth bleaching product.

Adult↗
PubMed2004

Reactive oxygen species-producing site in radiation and hydrogen peroxide-induced apoptosis of human peripheral T cells: Involvement of lysosomal membrane destabilization.

In our previous studies, we showed that the apoptotic resistance of the human osteosarcoma cell line HS-Os-1 against irradiation was easily converted to a state of apoptotic-susceptibility by the addition of a relatively low concentration of hydrogen peroxide to the culture medium just prior to irradiation. When we consider the combined use of radiotherapy and hydrogen peroxide in a clinical setting for patients with radioresistant neoplasms, we need to be careful of the possible augmentation of the radiation effect to normal tissues of patients who undergo radiation therapy for their tumor in the presence of a low concentration of hydrogen peroxide in their topical tumor tissue. Therefore, we examined the combined effect of irradiation and hydrogen peroxide compared to that of irradiation alone for human peripheral T cells which were considered to be representative of normal tissue susceptible to apoptosis induced by irradiation. In this study, we compared the morphological changes in human peripheral T cells between both groups by utilizing MitoCapture, H2DCFDA (succinimidyl ester of dichloro-dihydrofluorescein diacetate), DAPI (4',6-diamidino-2-phenylindole), and LysoSensor. Our results showed that ROS formation was apparently augmented in the mitochondria and/or lysosomes instead of in the nuclei of irradiated T cells in the presence of a low concentration of hydrogen peroxide compared to those treated with irradiation alone. Moreover, dysfunction of mitochondrial membrane potential was also more evidently shown in human peripheral T cells irradiated under existence of a low concentration of hydrogen peroxide compared to T cells treated with 5 Gy irradiation alone. Based on these results, we concluded the possible existence of an augmentation effect of irradiation by the existence of a low concentration of hydrogen peroxide for human peripheral T cells. Therefore, we should be alert for the combined effects of radiation therapy and hydrogen peroxide on normal tissues in possible clinical situations when this combination is used for treatment of patients having radioresistant neoplasms such as osteosarcoma, malignant melanoma, and glioblastoma multiforme.

Apoptosis↗
PubMed2003

In vitro effects of metal ions on lipid peroxidation induced by alcohol in mice liver homogenate.

The study is aimed to estimate the effect of different heavy metals such as Hg2+, Cd2+, Mn2+, Cr3+, Ni2+, Se2O3(2-), As2O3 water solution and combined effects of Hg2+, Mn2+, Cr3+ on lipid peroxidation in mice liver homogenate in vitro. Lipid peroxidation was determined as thiobarbituric acid-reacting materials (TBA). We select five different concentrations of selected ions for experiments. Correlations used to identify the concentration of ions associated with lipid peroxidation. The rate of lipid peroxide formation in mice liver homogenate increased with the gradual addition of alcohol. When alcohol dose was up to 0.5 ml, the rate of lipid peroxide formation was greatest. At tested concentrations, the effects of metal ions on lipid peroxidation induced by alcohol were classified into three groups, and are as follows: (1) simulative, Hg2+. (2) inhibitory, Mn2+, Cr3+, Ni2+, Se2O3(2-). (3) ambiguous, Cd2+, As2O3 water solution. When Hg2+, Mn2+ and Cr3+ were added to the mice liver homogenate with alcohol at the same time, Hg2+, Mn2+ were the main agents for the rate of alcohol induced lipid peroxidation. The simulative effect of Hg2+ on lipid peroxidation induced by alcohol indicate that alcohol-drinkers will have further health risk when they are exposed in polluted regions than others, and Mn2+, Cr3+, Ni2+, Se2O3(2-) may act as free radical scavengers and preventive remedy for alcoholism in part. Furthermore, analysis of combined effect of Hg2+Mn2+ and Cr3+ provide us a new way to estimate the combined effect of multi-materials.

Analysis of Variance↗
PubMed2005

Protective effects of hydroxyethylpuerarin on cultured bovine cerebral microvascular endothelial cells damaged by hydrogen peroxide.

AIM: To observe the damages induced by hydrogen peroxide in cultured bovine cerebral microvascular endothelial cells (BCMEC) and evaluate the protective effects of hydroxyethylpuerarin on hydrogen peroxide-injured BCMEC. METHODS: BCMEC were cultured and transferred into modified Eagle medium (MEM). The viability of cells was detected by MTT assay. Cell injury was determined by lactate dehydrogenase (LDH) activity in the extracellular medium. Flow cytometry was employed to observe the occurrence of apoptosis. Morphologic changes of cells were visualized under phase contrast and electron microscopes. RESULTS: Hydrogen peroxide (200 micromol x L(-1) for 4 hours) inhibited the viability of cultured BCMEC and stimulated LDH release. Hydrogen peroxide (100 micromol x L(-1) for 4 hours) induced the occurrence of apoptosis. Hydroxyethylpuerarin was shown to increase the survival rate and decrease the activity of LDH of BCMEC damaged by hydrogen peroxide. Hydroxyethylpuerarin was also found to protect BCMEC against apoptosis induced by hydrogen peroxide. CONCLUSION: Hydrogen peroxide induces BCMEC injury either by apoptosis or through necrosis. Hydroxyethylpuerarin protects BCMEC against hydrogen peroxide-induced injury in a concentration-dependent manner. Its antioxidant effects might be involved as the mechanism protection.

Animals↗
PubMedDate not supplied

Evidence for increased lipid peroxidative damage and loss of superoxide dismutase activity as a mode of sublethal cryodamage to human sperm during cryopreservation.

Cryopreservation of human sperm, now generally required in donor insemination programs, adversely affects the sperm in terms of standard sperm evaluation parameters and fertilizing ability. The freeze-thaw process appears to produce sublethal damage that appears only after a delay. The authors hypothesized that cryopreservation enhanced peroxidation of sperm membrane lipids, based on previous studies of sperm lipid peroxidation, which showed that the effects of peroxidative damage became evident only after a delay, depending on the peroxidation rate. The effect of cryopreservation on the phospholipid content, the composition of the acyl moieties of the phospholipids, and the activities of the peroxidation protective enzymes, superoxide dismutase (SOD) and glutathione peroxidase plus reductase, in human sperm were examined to test the hypothesis. Parallel determinations were made of the percent motility, the average path velocity of the motile cells, and the time to loss of motility under specified aerobic incubation conditions, which gives a good estimate of the lipid peroxidation rate. The phospholipid content decreases after cryopreservation, with loss of phosphatidylcholine and phosphatidylethanolamine being the more pronounced. Polyunsaturated acyl moieties were also preferentially lost. This loss pattern is observed also from lipid peroxidation. The activities of glutathione peroxidase plus reductase remained unchanged. The sperm SOD activities varied widely between samples before cryopreservation. In all samples there was a decline in SOD activity after freeze-thaw, but the extent of the decline was also widely variable. The time to loss of motility declined in parallel with SOD activity, and a strong correlation (R2 greater than 0.9) between SOD activity and time to loss of motility was found for all samples, before and after freeze-thaw. The authors conclude that cryopreservation does enhance lipid peroxidation in human sperm, as hypothesized, and that this enhancement is mediated at least in part by the loss of SOD activity occurring during the process.

Adult↗
PubMed2006

[Vitamin C decreases MMP-9 synthesis induced by hydrogen peroxide in an in vitro chorioamniotic membrane model].

OBJECTIVE: To evaluate the hydrogen peroxide ability to induce the synthesis of matrix metalloproteinase-9 (MMP-9) in an in vitro chorioamniotic membrane model. MATERIAL AND METHODS: An experimental, transversal, analytic and prospective study was made. From amniotic membranes (n = 13) of term labour pregnant women chorionic and chorioamniotic explants were prepared; these were stimulated with hydrogen peroxide [200 mcM]. A group of explants were cultured with vitamin C, 48 hours prior to the hydrogen peroxide stimulus. Twenty-four hours after hydrogen peroxide stimulus the supernatants were collected and metalloproteinase-9 production was determined by zymography methods. RESULTS: Hydrogen peroxide induced the synthesis of metalloproteinase-9 in chorionic and chorioamniotic membranes. When chorionic and chorioamniotic membranes were cultured with vitamin C prior to the hydrogen peroxide stimulus, the MMP-9 production diminished (p < 0.05; Dunn's method). CONCLUSIONS: Hydrogen peroxide induced the synthesis of metalloproteinase-9 in chorionic and chorioamniotic membranes. When chorionic and chorioamniotic membranes were cultured with vitamin C, 48 hours prior to peroxide hydrogen stimulus, the metalloproteinase-9 production diminished with statistical significance.

Ascorbic Acid↗
PubMed1990

Lipid peroxidation inactivates rat liver microsomal glycerol-3-phosphate acyl transferase. Effect of iron and copper salts and carbon tetrachloride.

Lipid peroxidation is known to affect the activity of several enzymes including microsomal enzymes such as glucose-6-phosphatase; but its effect on the enzymes of lipid biosynthesis has not been investigated. Glycerol-3-phosphate acyltransferase (GPAT) represents the first committed step and probably the rate limiting step in glycerolipid synthesis and thus may be a good candidate for study. Rat liver microsomal GPAT was assayed after preincubating the microsomes under conditions known to induce peroxidation. In 30 min, 10 microM Fe2+ can diminish the activity by as much as 80%. The inactivating effect can be blocked to different extents by several antioxidants, while ascorbic acid enhances it. These effects, along with the concomitant measurement of lipid peroxidation, indicate that microsomal GPAT activity is inactivated by lipid peroxidation in a sensitive and rapid fashion. This is further confirmed by the inactivating effect of carbon tetrachloride, which is known to induce lipid peroxidation in microsomes. Fe3+ also inactivates the enzyme, but at a higher concentration. Copper salts inactivate GPAT by a mechanism apparently different from that of iron. The mechanism might involve a direct sulfhydryl modification by copper and lipid peroxidation apparently different from that induced by iron. It is suggested that the inactivation of GPAT by lipid peroxidation could accelerate the process of membrane disintegration caused by lipid peroxidation in pathological conditions involving free radical-mediated tissue injury.

Acyltransferases↗
PubMed1990

Hydrogen peroxide-induced base damage in deoxyribonucleic acid.

Aqueous solutions of calf thymus deoxyribonucleic acid (DNA) were exposed to hydrogen peroxide in the presence of air. Base products formed in DNA were identified and quantitated following acid hydrolysis and trimethylsilylation using gas chromatography-mass spectrometry. The yields of these products were dependent upon the hydrogen peroxide concentration, and increased in the following order: 8-hydroxyadenine, cytosine glycol, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, 8-hydroxyguanine, thymine glycol, and 4,6-diamino-5-formamidopyrimidine. Previous studies have shown that these compounds are typically formed in DNA in aqueous solution by hydroxyl radicals generated by ionizing radiation. Hydrogen peroxide is thought to participate in a Fenton-like reaction with transition metals, which are readily bound to DNA in trace quantities, resulting in the production of hydroxyl radicals close to the DNA. This proposed mechanism was examined by exposing DNA to hydrogen peroxide either in the presence of a hydroxyl radical scavenger or following pretreatment of DNA with metal-ion chelators. The results indicate that trace quantities of transition metal ions can react readily with hydrogen peroxide to produce radical species. The production of radical species was monitored by determining the altered bases that resulted from the reaction between radicals and DNA. The yields of the base products were reduced by 40 to 60% with 10 mmol dm-3 of dimethyl sulfoxide. A 100-fold increase in the concentration of dimethyl sulfoxide did not result in a further reduction in hydrogen peroxide-induced base damage. DNA which was freed from bound metal ions by pretreatment with metal ion chelators followed by exhaustive dialysis was found to be an ineffective substrate for hydrogen peroxide. The yields of base products measured in this DNA were at background levels. These results support the role of metal ions bound to DNA in the site-specific formation of highly reactive radical species, most likely hydroxyl radicals, in hydrogen peroxide-induced damage to the bases in DNA.

Base Sequence↗
PubMed1989

Metmyoglobin promotes arachidonic acid peroxidation at acid pH.

The ability of metmyoglobin and other heme proteins to promote peroxidation of arachidonic acid under acidic conditions was investigated. Incubation of metmyoglobin with arachidonic acid resulted in a pH-dependent increase in lipid peroxidation as measured by the formation of thiobarbituric acid reactive products and oxygen consumption. Increased peroxidation was observed at pH levels below 6.0, reaching a plateau between pH 5.5 and 5.0. At comparable heme concentrations, metmyoglobin was more efficient than oxymyoglobin, methemoglobin, or ferricytochrome c in promoting arachidonic acid peroxidation. Metmyoglobin also promoted peroxidation of 1-palmityl-2-arachidonyl phosphatidylcholine and methylarachidonate but at significantly lower rates than arachidonic acid. Addition of fatty acid-free albumin inhibited arachidonic acid peroxidation in a molar ratio of 6 to 1 (arachidonic acid:albumin). Both ionic and non-ionic detergents inhibited metmyoglobin-dependent arachidonic acid peroxidation under acidic conditions. The anti-oxidants butylated hydroxytoluene and nordihydroguaiaretic acid and low molecular weight compounds with reduced sulfhydryl groups inhibited the reaction. However, mannitol, benzoic acid, and deferoxamine were without significant effect. Visible absorption spectra of metmyoglobin following reaction with arachidonic acid showed minimal changes consistent with a low level of degradation of the heme protein during the reaction. These observations support the hypothesis that metmyoglobin and other heme proteins can promote significant peroxidation of unsaturated fatty acids under conditions of mildly acidic pH such as may occur at sites of inflammation and during myocardial ischemia and reperfusion. This may be the result of enhanced aggregation of the fatty acid and/or interaction of the fatty acid with heme under acidic conditions.

Antioxidants↗
PubMed1989

Candidacidal activity of the neutrophil myeloperoxidase system can be protected from excess hydrogen peroxide by the presence of ammonium ion.

Excessive concentrations of hydrogen peroxide inhibit the neutrophil myeloperoxidase system, presumably by inactivating the hypochlorous acid produced by this system. Ammonium ion generated by neutrophils and other cells can react with hypochlorous acid to produce monochloramine, an oxidant with good microbicidal activity, but relative resistance to inactivation by other compounds. In an assay based on the oxidation of 5-thio-2-nitrobenzoic acid, hydrogen peroxide reacted more readily with sodium hypochlorite (used as a source of hypochlorous acid) than with monochloramine. Also, in this assay Candida albicans yeast inactivated the oxidant activity of hypochlorous acid more completely than they did that of monochloramine. The killing of Candida by sodium hypochlorite, as determined in a standard colony count microbicidal assay, was inhibited by equimolar and greater concentrations of hydrogen peroxide; killing of this organism by monochloramine was not affected by a tenfold excess concentration of hydrogen peroxide. In microbicidal assays using 4 mU of myeloperoxidase and optimal or excessive concentrations of hydrogen peroxide or glucose and glucose oxidase to generate hydrogen peroxide, the excessive concentrations inhibited killing of Candida, but not Staphylococcus aureus. The inhibition of Candida killing could be reversed by addition of ammonium ion to convert hypochlorous acid to monochloramine. These results indicate that for certain organisms such as C albicans, conversion of hypochlorous acid to monochloramine by reactions with ammonium ion may extend the range of hydrogen peroxide concentrations under which killing by the myeloperoxidase system can occur by protecting the necessary microbicidal oxidants from inactivation by excess hydrogen peroxide.

Ammonia↗
PubMed1988

Halothane-induced liver injury as a consequence of enhanced microsomal lipid peroxidation in guinea pigs.

We investigated the role of microsomal lipid peroxidation in halothane hepatotoxicity in guinea pigs. Animals were exposed to halothane, isoflurane or enflurane. Enhancement of microsomal lipid peroxidation was specific to halothane. The time-course of lipid peroxidation and hepatic damage following a single exposure to halothane was investigated by measuring the thiobarbituric acid (TBA)reactive products, serum transaminase activity, reduced glutathione (GSH) concentration and histopathological examination. Microsomal lipid peroxidation was enhanced most rapidly and preceded GSH depletion and hepatic injury. Metyrapone, an inhibitor of cytochrome P-450, and N-tert-butyl-alpha-phenylnitrone (BPN), a radical trapping agent, inhibited halothane-induced lipid peroxidation and the incidence and severity of liver injury. The metabolism of halothane was considered to be inhibited by metyrapone and the reactivity of radical intermediates was considered to be decreased by BPN. Microsomal lipid peroxidation was initiated by radical metabolites of halothane but did not result from GSH depletion. Inhibition of microsomal lipid peroxidation reduced the halothane hepatotoxicity. These results demonstrated that the halothane-induced liver injury was caused by microsomal lipid peroxidation in guinea pigs.

Administration, Inhalation↗
PubMed1987

Oxygen radicals stimulate intracellular proteolysis and lipid peroxidation by independent mechanisms in erythrocytes.

Exposure of red blood cells to oxygen radicals can induce hemoglobin damage and stimulate protein degradation, lipid peroxidation, and hemolysis. To determine if these events are linked, rabbit erythrocytes were incubated at 37 degrees C with various oxygen radical-generating systems and antioxidants. Protein degradation, measured by the production of free alanine, increased more than 11-fold in response to xanthine (X) + xanthine oxidase (XO). A similar increase in proteolysis occurred when the cells were incubated with acetaldehyde plus XO, with ascorbic acid plus iron (Asc + Fe), or with hydrogen peroxide (H2O2) alone. Upon addition of XO, increased proteolysis was evident within 5 min and was linear for up to 5 h. In contrast, lipid peroxidation, as shown by the production of malonyldialdehyde, conjugated dienes, or lipid hydroperoxides was observed only after 2 h of incubation with X + XO, acetaldehyde + XO, or H2O2. Ascorbate plus Fe2+ induced both protein degradation and lipid peroxidation; however, the addition of various antioxidants (urate, xanthine, glucose, or butylated hydroxytoluene) decreased lipid peroxidation without affecting proteolysis. Thus, these processes seem to occur by distinct mechanisms. Furthermore, at low concentrations of XO, protein degradation was clearly increased in the absence of detectable lipid peroxidation products. Hemolysis occurred only in a small number of cells (9%) and followed the appearance of lipid peroxidation products. Thus, an important response of red cells to oxygen radicals is rapid degradation of damaged cell proteins. Increased proteolysis seems to occur independently of membrane damage and to be a more sensitive indicator of cell exposure to oxygen radicals than is lipid peroxidation.

Acetaldehyde↗