Induction of selenium-glutathione peroxidase by stimulation of metabolic hydrogen peroxide production in vivo

Abstract The effects of bacterial neuraminidase on production of hydrogen peroxide (H2O2) and killing of Staphylococcus aureus by human polymorphonuclear leukocytes (PMN) were studied. The concentration of H2O2 was measured by the disappearance of scopoletin fluorescence in the presence of horseradish peroxidase. The results indicated that desialylation of human PMN inhibited the stimulation of H2O2 production during phagocytosis. It also markedly impaired the killing of S. aureus. Impaired killing of S. aureus by desialylated PMN was due to impaired intracellular killing rather than defective phagocytosis.

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Hydrogen peroxide production and killing of Staphylococcus aureus by human polymorphonuclear leukocytes

Blood ◽

10.1182/blood.v49.3.437.bloodjournal493437 ◽

1977 ◽

Vol 49 (3) ◽

pp. 437-444

Author(s):

MF Tsan ◽

KH Douglass ◽

PA McIntyre

Keyword(s):

Hydrogen Peroxide ◽

Staphylococcus Aureus ◽

Horseradish Peroxidase ◽

Polymorphonuclear Leukocytes ◽

H2o2 Production ◽

Intracellular Killing ◽

Hydrogen Peroxide Production ◽

Production Of Hydrogen ◽

Human Polymorphonuclear Leukocytes ◽

Stimulation Of

The effects of bacterial neuraminidase on production of hydrogen peroxide (H2O2) and killing of Staphylococcus aureus by human polymorphonuclear leukocytes (PMN) were studied. The concentration of H2O2 was measured by the disappearance of scopoletin fluorescence in the presence of horseradish peroxidase. The results indicated that desialylation of human PMN inhibited the stimulation of H2O2 production during phagocytosis. It also markedly impaired the killing of S. aureus. Impaired killing of S. aureus by desialylated PMN was due to impaired intracellular killing rather than defective phagocytosis.

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Hydrogen Peroxide Production by Monoamine Oxidase during Ischemia-Reperfusion in the Rat Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1993.15 ◽

1993 ◽

Vol 13 (1) ◽

pp. 125-134 ◽

Cited By ~ 80

Author(s):

Steven G. Simonson ◽

Jing Zhang ◽

Andrew T. Canada ◽

Ying-Fu Su ◽

Helene Benveniste ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Monoamine Oxidase ◽

Rat Brain ◽

Ischemia Reperfusion ◽

Mao Inhibitors ◽

Hydrogen Peroxide Production ◽

Threefold Increase ◽

Brain Reperfusion ◽

Improvement In Survival

Monoamine oxidase (MAO) as a source of hydrogen peroxide (H2O2) was evaluated during ischemiareperfusion in vivo in the rat brain. H2O2 production was assessed with and without inhibition of MAO during and after 15 min of ischemia. Metabolism of H2O2 by catalase during ischemia and reperfusion was measured in forebrain homogenates using aminotriazole (ATZ), an irreversible H2O2-dependent inhibitor of catalase. Catecholamine and glutathione concentrations in forebrain were measured with and without MAO inhibitors. During ischemia, forebrain blood flow was reduced to 8% of baseline and H2O2 production decreased as measured at the microperoxisome. During reperfusion, a rapid increase in H2O2 generation occurred within 5 min as measured by a threefold increase in oxidized glutathione (GSSG). The H2O2-dependent rates of ATZ inactivation of catalase between control and ischemia–reperfusion were similar, indicating that H2O2 was more available to glutathione peroxidase than to catalase in this model. MAO inhibitors eliminated the biochemical indications of increased H2O2 production and increased the catecholamine concentrations. Mortality was 67% at 48 h after ischemiareperfusion, and there was no improvement in survival after inhibition of MAO. We conclude that MAO is an important source of H2O2 generation early in brain reperfusion, but inhibition of the enzyme does not improve survival in this model despite ablating H2O2 production.

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Lichen Metabolites Modulate Hydrogen Peroxide and Nitric Oxide in Mouse Macrophages

Zeitschrift für Naturforschung C ◽

10.1515/znc-2009-9-1010 ◽

2009 ◽

Vol 64 (9-10) ◽

pp. 664-672 ◽

Cited By ~ 5

Author(s):

Iracilda Z. Carlos ◽

Marcela B. Quilles ◽

Camila B. A. Carli ◽

Danielle C. G. Maia ◽

Fernanda P. Benzatti ◽

...

Keyword(s):

Nitric Oxide ◽

Hydrogen Peroxide ◽

Phenol Red ◽

Hydrogen Peroxide Production ◽

Griess Reagent ◽

Mouse Macrophages ◽

Lichen Metabolites ◽

Oxidation Of Phenol ◽

Peritoneal Macrophage Cells ◽

Stimulation Of

The activities of perlatolic acid (1), atranorin (2), and lecanoric acid (3) and their derivatives, such as orsellinates and β-methyl orsellinates obtained by alcoholysis, were assessed for stimulation of the release of hydrogen peroxide and nitric oxide in cultures of peritoneal macrophage cells from mice. The hydrogen peroxide production was estimated by oxidation of phenol red, while the Griess reagent was used to determine the nitric oxide production. 1 and 4-methoxy-ethyl orsellinate (XVII) were the compounds that induced the greatest release of H2O2, whereas n-pentyl orsellinate (IV), iso-propyl orsellinate (V), sec-butyl orsellinate (VI), and XVII induced a small release of NO. These results indicate that lichen products and their derivatives have potential immune-modulating activities

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Lactate dehydrogenases amplify reactive oxygen species in cancer cells in response to oxidative stimuli

Signal Transduction and Targeted Therapy ◽

10.1038/s41392-021-00595-3 ◽

2021 ◽

Vol 6 (1) ◽

Author(s):

Hao Wu ◽

Yuqi Wang ◽

Minfeng Ying ◽

Chengmeng Jin ◽

Jiangtao Li ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Cancer Cells ◽

Hela Cells ◽

Hydrogen Peroxide Production ◽

Physiological Relevance ◽

4T1 Cells ◽

Lactate Dehydrogenases ◽

Transfer Chain

AbstractPrevious studies demonstrated that superoxide could initiate and amplify LDH-catalyzed hydrogen peroxide production in aqueous phase, but its physiological relevance is unknown. Here we showed that LDHA and LDHB both exhibited hydrogen peroxide-producing activity, which was significantly enhanced by the superoxide generated from the isolated mitochondria from HeLa cells and patients’ cholangiocarcinoma specimen. After LDHA or LDHB were knocked out, hydrogen peroxide produced by Hela or 4T1 cancer cells were significantly reduced. Re-expression of LDHA in LDHA-knockout HeLa cells partially restored hydrogen peroxide production. In HeLa and 4T1 cells, LDHA or LDHB knockout or LDH inhibitor FX11 significantly decreased ROS induction by modulators of the mitochondrial electron transfer chain (antimycin, oligomycin, rotenone), hypoxia, and pharmacological ROS inducers piperlogumine (PL) and phenethyl isothiocyanate (PEITC). Moreover, the tumors formed by LDHA or LDHB knockout HeLa or 4T1 cells exhibited a significantly less oxidative state than those formed by control cells. Collectively, we provide a mechanistic understanding of a link between LDH and cellular hydrogen peroxide production or oxidative stress in cancer cells in vitro and in vivo.

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Intracerebroventricular injection of oxidant and antioxidant molecules affects long-term potentiation in urethane anaesthetized rats

Physiological Research ◽

10.33549/physiolres.930973 ◽

2008 ◽

pp. 269-273

Author(s):

A Viggiano ◽

E Viggiano ◽

M Monda ◽

A Viggiano ◽

S Ascione ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Dentate Gyrus ◽

Long Term Potentiation ◽

Control Group ◽

High Frequency Stimulation ◽

Perforant Pathway ◽

Term Potentiation ◽

Stimulation Of

Production of superoxide anions in the incubation medium of hippocampal slices can induce long-term potentiation (LTP). Other reactive oxygen species (ROS) such as hydrogen peroxide are able to modulate LTP and are likely to be involved in aging mechanisms. The present study explored whether intracerebroventricular (ICV) injection of oxidant or antioxidant molecules could affect LTP in vivo. With this aim in mind, field excitatory post-synaptic potentials (fEPSPs) elicited by stimulation of the perforant pathway were recorded in the dentate gyrus of the hippocampal formation in urethane-anesthetized rats. N-acetyl-Lcysteine, hydrogen peroxide (H2O2) or hypoxanthine/xanthineoxidase solution (a superoxide producing system) were administrated by ICV injection. The control was represented by a group injected with saline ICV. Ten minutes after the injection, LTP was induced in the granule cells of the dentate gyrus by high frequency stimulation of the perforant pathway. Neither the H2O2 injection or the N-acetyl-L-cysteine injection caused any variation in the fEPSP at the 10-min post-injection time point, whereas the superoxide generating system caused a significant increase in the fEPSP. Moreover, at 60 min after tetanic stimulation, all treatments attenuated LTP compared with the control group. These results show that ICV administration of oxidant or antioxidant molecules can modulate LTP in vivo in the dentate gyrus. Particularly, a superoxide producing system can induce potentiation of the synaptic response. Interestingly, ICV injection of oxidants or antioxidants prevented a full expression of LTP compared to the saline injection.

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