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PubMed1995

Azithromycin induces in vitro a time-dependent increase in the intracellular killing of Staphylococcus aureus by human polymorphonuclear leucocytes without damaging phagocytes.

Despite its clinical efficacy on intracellular pathogens, the in-vitro intracellular antimicrobial activity of azithromycin, has been shown to be absent or lower than expected from the intracellular concentrations reached. To test the possibility that the high intracellular concentrations of the drug could damage phagocytes, the present study evaluated the effects of azithromycin on (a) the intracellular killing of Staphylococcus aureus by human blood neutrophils (PMNs) and (b) the viability and the respiratory burst of PMNs. Using a fluorochrome assay, we assessed the phagocytosis and intracellular killing of S. aureus by PMNs preloaded with azithromycin, or by PMNs unloaded but with the drug in the culture medium. In addition, possible drug-induced damage to PMNs was evaluated measuring: (a) hydrogen peroxide (H2O2) production and (b) the percentages of PMNs dead at the end of the phagocytosis process. Compared to control PMNs without drug, a time-dependent enhancement in the intracellular killing was observed which was statistically significant after 60 min incubation. The increased intracellular killing was higher in suspensions of unloaded PMNs and azithromycin (P < 0.01) that in suspensions of preloaded PMNs (P < 0.05). This increased intracellular killing was not associated with increased proportions of dead phagocytes, either in preloaded or unloaded PMNs (P < 0.05, each comparison). Similarly no changes in the production of H2O2 by PMNs were observed in the presence of azithromycin. Thus, azithromycin induces a time-dependent increase in the bactericidal activity of human PMNs, without increasing the phagocyte self-killing or modifying H2O2 production.

Adolescent↗
PubMed1991

Synergistic induction of ovulation and prostaglandin synthesis in goldfish (Carassius auratus) follicles by sodium orthovanadate and hydrogen peroxide.

The effects of hydrogen peroxide (H2O2) and sodium orthovanadate (Na3VO4) on ovulation and prostaglandin (PG) production were investigated in goldfish (Carassius auratus) follicles. H2O2, at levels that did not stimulate ovulation, significantly increased the ability of Na3VO4 to induce ovulation. The enhancing effect of H2O2 on Na3VO4-induced (10 microM) ovulation was observed over a wide range of concentrations (0.3-19.2 ppm) but was maximal at 1.2-4.8 ppm. The H2O2 effect on ovulation diminished at concentrations greater than 4.8 ppm. Na3VO4 and H2O2 also stimulated prostaglandin E (PGE) and prostaglandin F (PGF) levels in incubates. An interactive effect of the two agents was significant only on PGE production. However, optimal H2O2/Na3VO4 concentrations for the stimulation of PG production were much higher than those for stimulating ovulation. In most incubations, Na3VO4-induced or Na3VO4/H2O2-induced ovulation was not inhibited by the cyclooxygenase inhibitor indomethacin (IM), but was blocked by the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA). Treatment of an Na3VO4/H2O2 mixture with catalase before the start of incubation totally abolished the enhancing effect of H2O2 on ovulation. This suggests that the enhancing effect of H2O2 on ovulation may not be a result of a chemical metabolite(s) produced by the two agents in mixture but rather is due to some direct effect of H2O2. This may have physiological significance in light of the published effects of H2O2 on various processes known to be involved in ovulation.

Animals↗
PubMed2002

Lactoperoxidase and hydrogen peroxide metabolism in the airway.

Hydrogen peroxide (H2O2) is known to play an important role in airway homeostasis. For this reason its levels and thus its synthesis and consumption are important mechanisms for controlling airway functions. We have identified the major macromolecular consumer of H2O2 in sheep airway secretions to be lactoperoxidase (LPO), a heme peroxidase previously studied in milk and saliva. This enzyme uses H2O2 to oxidize the anion thiocyanate to an antibiotic compound that prevents growth of bacteria, fungi, and viruses. LPO was isolated from sheep airways and proved to be a major constituent comprising about 1% of the soluble protein in airway secretions. The isolated airway LPO was catalytically active and displayed the enzymatic characteristics previously described for the enzyme isolated from bovine milk. Airway LPO activity was shown to increase the rate of bacterial clearance from sheep airways. The role of this enzyme in the airway host defense strongly suggests that an active H2O2 production system exists to supply appropriate substrate for the enzyme. The identity of this H2O2 synthesis system is an important, yet unknown feature of airway oxygen radical metabolism.

Animals↗
PubMed1999

Catalase activity and hydrogen peroxide levels are inversely correlated in maize scutella during seed germination.

Temporal patterns of hydrogen peroxide (H2O2) levels and total catalase activity are presented for post-imbibition scutella from six maize inbred lines expressing variable catalase activity. In all lines examined, H2O2 levels were highest during the initial days post-imbibition (1-2 dpi) and decreased thereafter, while total catalase activity was lowest during early dpi (1-2 dpi) and reached maximal activity at 4-6 dpi. In three of the six lines tested, a simple inverse correlation between catalase activity and H2O2 level was significant by Spearman's rank (P < 0.01). In addition to the general decline in H2O2 level throughout the dpi period, a reproducible increase in H2O2 level was observed at 4-5 dpi in five of six lines examined. Mutant lines lacking CAT-3 activity demonstrated a temporal shift in the occurrence of this increase. The role of total catalase (and individual isozymes) in controlling H2O2 levels during germination and the role of H2O2 as a potential regulator of catalase expression during germination are discussed.

Catalase↗
PubMed2001

Killing of Schistosoma mansoni sporocysts by hemocytes from resistant Biomphalaria glabrata: role of reactive oxygen species.

The fate of Schistosoma mansoni (Trematoda) sporocysts in its molluscan host Biomphalaria glabrata (Gastropoda) is determined by circulating phagocytes (hemocytes). When the parasite invades a resistant snail, it is attacked and destroyed by hemocytes, whereas in a susceptible host it remains unaffected. We used 3 inbred strains of B. glabrata: 13-16-R1 and 10-R2, which are resistant to the PR-1 strain of S. mansoni, and M-line Oregon (MO), which is susceptible to PR-1. In an in vitro killing assay using plasma-free hemocytes from these strains, the rate of parasite killing corresponded closely to the rate by which S. mansoni sporocysts are killed in vivo. Hemocytes from resistant snails killed more than 80% of S. mansoni sporocysts within 48 hr, whereas sporocyst mortality in the presence of hemocytes from susceptible snails was <10%. Using this in vitro assay, we assessed the involvement of reactive oxygen species (ROS) produced by resistant hemocytes, during killing of S. mansoni sporocysts. Inhibition of NADPH oxidase significantly reduced sporocyst killing by 13-16-R1 hemocytes, indicating that ROS play an important role in normal killing. Reduction of hydrogen peroxide (H2O2) by including catalase in the killing assay increased parasite viability. Reduction of superoxide (O2-), however, by addition of superoxide dismutase or scavenging of hydroxyl radicals (*OH) and hypochlorous acid (HOCl) by addition of hypotaurine did not alter the rate of sporocyst killing by resistant hemocytes. We conclude that H2O2 is the ROS mainly responsible for killing.

Animals↗
PubMed1984

Direct measurement of hydrogen peroxide release from rat alveolar macrophages: artifactual effect of horseradish peroxidase.

Investigators disagree on the amount of hydrogen peroxide (H2O2) released by resting and stimulated alveolar macrophages. The method commonly used to measure H2O2 release involves horseradish peroxidase (HRP)-catalyzed oxidation of scopoletin by H2O2. We describe an artifact in this method that may explain the seemingly inconsistent data reported by other investigators. Release of H2O2 and luminol-catalyzed chemiluminescence are stimulated in rat alveolar macrophages by type II HRP at concentrations normally used in the HRP-scopoletin method. The amount of H2O2 released depends upon the length of time the cells are preincubated at 37.5 degrees C and the time at which type II HRP is added. After stimulation with type II HRP, the cells do not release additional H2O2 upon exposure to zymosan particles. Myeloperoxidase, an alternative catalyst to type II HRP, does not stimulate H2O2 release and, therefore, can be used to measure H2O2 release from rat alveolar macrophages. Using myeloperoxidase, resting H2O2 release is negligible; after zymosan stimulation, 6.14 (+/- 0.87) X 10(-6) nmoles/cell X 10 min is released. In addition, more pure HRP preparations (types VI, VII, VIII, and IX) do not stimulate alveolar macrophages to release H2O2 and can be used to monitor zymosan-induced H2O2 release. As our data indicate that type II HRP stimulates H2O2 release from rat and guinea pig alveolar macrophages, it is not the catalyst of choice for this assay. In conclusion, our data explain the conflicting results found in the literature and indicate that rat alveolar macrophages release minimal amounts of H2O2 at rest and can be stimulated by zymosan.

Animals↗
PubMed1992

Glomerular injury induced by hydrogen peroxide: modifying influence of ACE inhibitors.

The sensitivity of isolated glomeruli from normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SHR) strains to oxidant stress was studied by determining the incidence of pyknosis, karyohexis and karyolysis after incubation with different concentrations of hydrogen peroxide (H2O2) (4.7 x 10(-9) - 10(-3) M). Even though the proportion of glomeruli containing nuclei that demonstrated these features increased progressively with increasing concentrations of H2O2, the number of severely damaged glomeruli was relatively small even at concentrations of 4.7 x 10(-3) M. Examination of the surface epithelial cells of glomeruli using scanning electron microscopy revealed no evidence of disturbance of the macroscopic or podocyte structure or, of increased blebbing after H2O2-treatment. These data suggest damage to nuclei is an early result of ROS stress on glomeruli. Preincubation of WKY glomeruli with captopril or lisinopril resulted in a significant drop in the proportion of WKY glomeruli demonstrating structural damage after oxidant stress. In contrast, preincubation of SHR glomeruli with lisinopril had no effect on oxidant-induced changes in the morphology of SHR glomeruli, whereas captopril effected a significant increase in the proportion of glomeruli demonstrating damage at all concentration of H2O2.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Glomerular macrophages produce reactive oxygen species in experimental glomerulonephritis.

The production of reactive oxygen species by intraglomerular macrophages was assessed in a macrophage dependent model of diffuse proliferative glomerulonephritis in rabbits. Glomerular macrophages were obtained from isolated nephritic glomeruli by short term (60 min) culture. Control macrophage populations were simultaneously obtained from peripheral blood (blood monocytes) and lung lavage fluid (alveolar macrophages). Superoxide anion (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH.) production was assessed. Glomerular macrophage production of O2- (48.9 +/- 5.5 nmol/hr/10(6) cells), H2O2 (4.4 +/- 2.5 nmol/hr/10(6) cells) and OH. (57.8 +/- 4.7 U/hr/10(6) cells) was significantly greater than the production of reactive oxygen species seen with control monocyte populations: alveolar macrophages, O2- 9.8 +/- 2.0 nmol/hr/10(6) cells; H2O2 0.6 +/- 0.3 nmol/hr/10(6) cells; OH. 11.0 +/- 1.8 U/hr/10(6) cells; blood monocytes, O2- 8.6 +/- 1.4 nmol/hr/10(6) cells; OH. 9.9 +/- 1.2 U/hr/10(6) cells, (all P less than 0.05 cf. glom macs). Hydrogen peroxide production by blood monocytes (1.6 +/- 0.9 nmol/hr/10(6) cells) was less than glomerular macrophages, however this difference was not statistically significant. The enhanced production of reactive oxygen species by glomerular macrophages in this macrophage dependent model of glomerulonephritis suggests that these mononuclear cells are locally activated within the glomerulus following recruitment from the circulation. Reactive oxygen species production by glomerular macrophages may contribute to their ability to induce glomerular basement membrane injury in this disease.

Animals↗
PubMed1999

The auxin, hydrogen peroxide and salicylic acid induced expression of the Arabidopsis GST6 promoter is mediated in part by an ocs element.

Glutathione S-transferases (GSTs) are multi-functional enzymes that play critical roles in a number of plant stress responses. Ocs elements are enhancer sequences found in some pathogen and GST promoters. We previously isolated an Arabidopsis GST gene, called GST6, which contained an ocs-like element. Here we tested the role this putative ocs element plays in GST6 expression in response to auxin, salicylic acid (SA) and hydrogen peroxide (H2O2) using a transient assay and transgenic Arabidopsis. The requirement for the ocs element for basal and/or induced expression varied between the transient and transgenic studies, and in different plant tissues. The GST6 promoter showed the largest induction in roots following treatment with SA (84-fold) or H2O2 (122-fold), and the effect of mutating the ocs element was most pronounced in root tissue. However, in no case did mutation of the ocs element abolish GST6 expression, suggesting that other promoter element(s) are also important. Using the transient assay, other promoter element(s) critical for GST6 expression were identified that may also help mediate the activity of the ocs element. The finding that the ocs element plays a role in the transcriptional response of a plant GST gene to SA and H2O2 has potential significance for the plant defense response, where SA and H2O2 play critical roles.

Arabidopsis↗
PubMed1998

Pharmacological enhancement of cutaneous flap survival with topical dimethyl sulphoxide and hydrogen peroxide.

The present study was designed to investigate, in a rabbit model, the value of topical application of a solution of hydrogen peroxide (H2O2) 8% + dimethyl sulphoxide (DMSO) 50% in order to reduce ischaemic failure in random skin flaps. Two parallel, cephalad-based para-midline random cutaneous flap (10 cm x 2.5 cm) were elevated and resutured in place on the dorsum of 40 New Zealand rabbits. The 80 flaps thus obtained were then randomly divided into one control group and three experimental groups of 20 flaps each. Flaps from the control group (Group A) were topically treated with saline, while flaps from experimental Group B were treated with H2O2 8%, flaps from experimental Group C with DMSO 50%, and flaps from experimental Group D with a solution of 50% DMSO + 8% H2O2. Each solution was topically applied to the flaps, 20 ml three times a day for 7 days, starting in the immediate postoperative period. Transcutaneous oxygen tension (PtcO2) measurements were carried out in all flaps 72 h after flap elevation. The percentage of surviving skin area of each flap was determined by planimetry 7 days after flap elevation. The mean surviving area of the Group A (control) flaps was 71%, the mean surviving area of the Group B (H2O2-treated) flaps was 72%, the mean surviving area of the Group C (DMSO-treated) flaps was 76%, and that of the Group D (DMSO+H2O2-treated) flaps was 92%. While no statistically significant differences were found between the survival rates of both the flaps treated with H2O2 or DMSO alone and that of the control group, the mean surviving rate of the DMSO+H2O2 treated flaps (+20%) was statistically higher than that of the control flaps. Similarly, a statistically significant difference has been found between the mean PtcO2 values of the DMSO+H2O2 flaps and those of the other three groups of flaps.

Animals↗
PubMed1979

Defective hydrogen peroxide production in chronic granulocytic leukaemia neutrophils.

Hydrogen peroxide (H2O2) production by polymorphonuclear neutrophils (PMN) during phagocytosis was fluorometrically vestimated over an incubation period of 80 min during which dead Candida guilliermondii were ingested. Ten patients with chronic granulocytic leukaemia (CGL) were tested and compared with 15 normal subjects. The production of H2O2 by CGL neutrophils was about 29% of normal. There was no correlation between H2O2 production and the impaired killing of Candida guilliermondii by the neutrophils of CGL patients.

Candida↗
PubMed1996

Benzene metabolites enhance reactive oxygen species generation in HL60 human leukemia cells.

Benzene is myelotoxic and leukemogenic in humans. The mechanisms leading to these effects, however have not been fully elucidated. One of the underlying mechanisms is believed to be the oxidative damage caused by its metabolites. A comparative study was undertaken to examine the relationships between reactive oxygen species (ROS) production, lipid peroxidation and subsequent cytotoxicity induced by five major benzene metabolites. The generation of ROS by benzene metabolites was demonstrated by the significant and dose-dependent increase of intracellular ROS formation in HL60 human promyelocytic leukemia cells in vitro. 1,4-Benzoquinone (BQ) was found to be the most potent metabolite in induction of ROS formation, followed by 1,2,4-benzenetriol (BT) and to a lesser extent, phenol (PH) and trans, trans-muconaldehyde (MD). No significant effect was observed when the cells were treated with trans, trans-muconic acid (MA). The enhancement of ROS production by BQ was effectively inhibited by the addition of catalase, deferoxamine (DFO) and dimethyl sulfoxide (DMSO), but unchanged by superoxide dismutase (SOD), suggest that hydrogen peroxide (H2O2) and hydroxyl radicals (OH) are the two major forms of ROS involved. The results also demonstrate that the ability of benzene metabolites in enhancing ROS generation is closely correlated to their capacity in causing lipid peroxidation and subsequent cytotoxicity. These findings together with earlier parallel observations on DNA damage suggest that ROS play an important role in the mechanism of carcinogenesis induced by benzene metabolites.

Aldehydes↗
PubMed1989

Induction of stress proteins in cultured human RPE-derived cells.

The expression and induction of stress protein families were examined in cultured human fetal retinal pigment epithelial (RPE)-derived cells. These stress proteins (SPs) include the heat-shock proteins (HSPs) that have been shown to be highly inducible following treatment by heat, amino acid analogues, and various chemical oxidants. Three sets of proteins with molecular weights of 70, 84, and 110 kilodaltons were elevated simultaneously from constitutive levels after treatment with azetidine-2-carboxylic acid (AzC), an amino acid analogue of proline. Further experiments demonstrated that incubation of cultured human fetal RPE-derived cells with hydrogen peroxide (H2O2) at concentrations ranging from 10(-5) M to 10(-3) M for 30 minutes to 60 minutes did not elevate the levels of the common families of HSPs as with AzC. These results indicate that cultured human fetal RPE-derived cells are capable of elevated HSP biosynthesis after AzC exposure but appear resistant to H2O2 treatment.

Azetidinecarboxylic Acid↗
PubMed1982

The involvement of hydroxyl radical derived from hydrogen peroxide in lignin degradation by the white rot fungus Phanerochaete chrysosporium.

The possible involvement of hydrogen peroxide (H2O2)-derived hydroxyl radical (.OH) in lignin degradation ([14C]lignin leads to 14CO2) by Phanerochaete chrysosporium was investigated. When P. chrysosporium was grown in low nitrogen medium (2.4 mM N), an increase in the specific activity for H2O2 production in cell extracts was observed to coincide with the appearance of ligninolytic activity and both activities appeared after the culture entered stationary phase. The production of .OH in ligninolytic cultures of P. chrysosporium was demonstrated by alpha-keto-gamma-methiolbutyric acid-dependent formation of ethylene. Hydrogen peroxide-dependent .OH formation was also shown in cell extracts of ligninolytic cultures. The radical species was demonstrated to be .OH by the .OH-dependent hydroxylation of p-hydroxybenzoic acid to form protocatechuic acid and by using 5,5-dimethyl-1-pyrroline-N-oxide and detecting the production of the nitroxide radical of 5,5-dimethyl-1-pyrroline-N-oxide by EPR. These reactions were inhibited by .OH-scavenging agents and were stimulated when azide was added to inhibit endogenous catalase. Lignin degradation by P. chrysosporium was markedly suppressed in the presence of the .OH-scavenging agents mannitol, benzoate, and the nonspecific radical scavenging agent butylated hydroxytoluene. The above results indicate that .OH derived from H2O2 is involved in lignin biodegradation by P. chrysosporium.

Agaricales↗
PubMed1997

Transient Ca2+ changes in endothelial cells induced by low doses of reactive oxygen species: role of hydrogen peroxide.

Cultured human and rat endothelial cells were used to study cellular toxicity and Ca2+ signalling upon exposure to reactive oxygen species. Superoxide and hydrogen peroxide (O2.-/H2O2) were produced by the hypoxanthine/xanthine oxidase system (HX/XO) and caused intracellular Ca2+ concentration ([Ca2+]i) to rise steadily when activities above 2 mU/ml were used. These Ca2+ increases were also measured when the glucose/glucose oxidase (G/GO) system above 5 mU/ml was used to produce hydrogen peroxide (H2O2). Gross morphological changes appeared to parallel elevated [Ca2+]i levels preceding cell death. However, when HX/XO or G/GO were used at non toxic doses rapid and transient changes in [Ca2+]i were measured. These treatments did not alter subsequent receptor mediated Ca2+ signalling induced by ATP (10 microM) or histamine (100 microM). Superoxide dismutase (50 U/ml), which dismutates O2.- into H2O2 also had no influence, whereas catalase (50 U/ml), which removes H2O2, completely diminished transient [Ca2+]i responses. H2O2 added directly was able to induce similar Ca2+ transients when concentrations of at least 500 microM were used. Buffering trace amounts of iron (o-phenanthroline; 200 microM) in order to inhibit .OH radical formation was not effective to alter Ca2+ changes. Experiments performed in Ca(2+)-free buffer showed a similar rise in [Ca2+]i and readdition of Ca2+ to the extracellular medium indicated the activation of store operated Ca2+ entry. Blocking Ca(2+)-ATPases of the endoplasmatic reticulum with thapsigargin (1 microM) inhibited ROS induced transient increases and cells preincubated with pertussis toxin (200 nM) showed unchanged Ca2+ transients after exposure to both enzyme systems. Phospholipase C inhibitor U73122 (2 microM) effectively reduced hydrogen peroxide induced emptying of intracellular stores. Taken together, we demonstrate that enzymatically produced non-toxic H2O2 rather than O2.- or .OH causes calcium signalling from thapsigargin sensitive stores, and activates store operated Ca2+ entry at least partially by activating phospholipase C. These changes clearly differ from pathological 'oxidative stress' associated with a progressive increase in [Ca2+]i.

Animals↗
PubMed1998

Protective effects of nicergoline against hydrogen peroxide toxicity in rat neuronal cell line.

We examined the effects of nicergoline on hydrogen peroxide (H2O2)-induced neurotoxicity in cultured rat neuronal cell line (B50). H2O2 induced death of B50 cells in a dose-dependent manner. The H2O2-induced neuronal cell death was significantly decreased in B50 cells maintained in the presence of nicergoline. We compared the levels of antioxidants (glutathione, catalase and superoxide dismutase) in nicergoline-treated and untreated B50 cells. Lipid peroxidation products (thiobarbituric acid reactive substances, TBARS) levels were also measured. Cultures treated with nicergoline had higher levels of catalase activity. TBARS level was significantly lower in nicergoline-treated cells than in untreated cells. Our results suggest that nicergoline may induce the up-regulation of intracellular antioxidant defences and protect the neuronal cells against oxidative stress.

Animals↗
PubMed1998

Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase.

HDL levels are inversely related to the risk of developing atherosclerosis. In serum, paraoxonase (PON) is associated with HDL, and was shown to inhibit LDL oxidation. Whether PON also protects HDL from oxidation is unknown, and was determined in the present study. In humans, we found serum HDL PON activity and HDL susceptibility to oxidation to be inversely correlated (r2 = 0.77, n = 15). Supplementing human HDL with purified PON inhibited copper-induced HDL oxidation in a concentration-dependent manner. Adding PON to HDL prolonged the oxidation lag phase and reduced HDL peroxide and aldehyde formation by up to 95%. This inhibitory effect was most pronounced when PON was added before oxidation initiation. When purified PON was added to whole serum, essentially all of it became HDL-associated. The PON-enriched HDL was more resistant to copper ion-induced oxidation than was control HDL. Compared with control HDL, HDL from PON-treated serum showed a 66% prolongation in the lag phase of its oxidation, and up to a 40% reduction in peroxide and aldehyde content. In contrast, in the presence of various PON inhibitors, HDL oxidation induced by either copper ions or by a free radical generating system was markedly enhanced. As PON inhibited HDL oxidation, two major functions of HDL were assessed: macrophage cholesterol efflux, and LDL protection from oxidation. Compared with oxidized untreated HDL, oxidized PON-treated HDL caused a 45% increase in cellular cholesterol efflux from J-774 A.1 macrophages. Both HDL-associated PON and purified PON were potent inhibitors of LDL oxidation. Searching for a possible mechanism for PON-induced inhibition of HDL oxidation revealed PON (2 paraoxonase U/ml)-mediated hydrolysis of lipid peroxides (by 19%) and of cholesteryl linoleate hydroperoxides (by 90%) in oxidized HDL. HDL-associated PON, as well as purified PON, were also able to substantially hydrolyze (up to 25%) hydrogen peroxide (H2O2), a major reactive oxygen species produced under oxidative stress during atherogenesis. Finally, we analyzed serum PON activity in the atherosclerotic apolipoprotein E-deficient mice during aging and development of atherosclerotic lesions. With age, serum lipid peroxidation and lesion size increased, whereas serum PON activity decreased. We thus conclude that HDL-associated PON possesses peroxidase-like activity that can contribute to the protective effect of PON against lipoprotein oxidation. The presence of PON in HDL may thus be a major contributor to the antiatherogenicity of this lipoprotein.

Animals↗
PubMed2000

Elevated oxidative stress in skin of B6C3F1 mice affects dermal exposure to metal working fluid.

Metal working fluids (MWFs) are widely used in industry for metal cutting, drilling, shaping, lubricating, and milling. Potential for dermal exposure to MWFs exists for a large number of men and women via aerosols and splashing during the machining operations. It has been reported earlier that occupational exposure to MWFs causes allergic and irritant contact dermatitis. Previously, we showed that dermal exposure of female and male B6C3F1 mice to 5% MWFs for 3 months resulted in accumulation of mast cells and elevation of histamine in the skin. Topical exposure to MWF also resulted in elevated oxidative stress in the liver of both sexes and the testes in males. The goal of this study was to evaluate the interaction between oxidative stress in the skin and topical application of MWF. Oxidative stress in skin ofB6C3F1 mice of both sexes was generated by intradermal injection ofthe hydrogen peroxide (H2O2) -producing enzyme, glucose oxidase with polyethylene glycol (GOD+PEG). In mice given GOD+PEG, topical treatment with MWF (200 microl, 30%, for 1, 3, or 7 days) resulted in a mixed inflammatory cell response, accumulation of peroxidative products, and reduction of GSH content in the skin. Such changes were not observed with MWF treatment alone. These data indicate that oxidative stress can enhance dermal inflammation caused by occupational exposure to MWF.

Administration, Cutaneous↗