scholarly journals Key role of hydrogen peroxide in antimicrobial activity of spring,Honeydew maquisand chestnut grove Corsican honeys onPseudomonas aeruginosaDNA

2018 ◽  
Vol 66 (5) ◽  
pp. 427-433 ◽  
Author(s):  
J.-P. Poli ◽  
E. Guinoiseau ◽  
A. Luciani ◽  
Y. Yang ◽  
M.-J. Battesti ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Antimicrobial Activity

Hydrogen peroxide inhibits IL-12 p40 induction in macrophages by inhibiting c-rel translocation to the nucleus through activation of calmodulin protein

Blood ◽  
2006 ◽  
Vol 107 (4) ◽  
pp. 1513-1520 ◽  
Author(s):  
Nooruddin Khan ◽  
Sheikh Showkat Rahim ◽  
Chandra Sekhar Boddupalli ◽  
Sheikh Ghousunnissa ◽  
Samavedan Padma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Immune Response ◽  
Antimicrobial Activity ◽  
The Body ◽  
Interleukin 12 ◽  
Oxygen Species ◽  
H2o2 Treatment ◽  
Ifn Γ

Although the antimicrobial activity of reactive oxygen species (ROSs) is well defined, the role of ROSs in regulating the immune response of the body is not well understood. We now provide evidence that hydrogen peroxide (H2O2), a major component of ROSs, inhibits interleukin-12 (IL-12) p40 and IL-12 p70 induction in murine macrophages and catalase pretreatment prevents H2O2-mediated down-regulation of IL-12. Endogenous accumulation of H2O2/ROSs in macrophages treated with alloxan resulted in IL-12 p40 inhibition. Although nuclear expression of both p50 and p65 NF-κB increased on H2O2 exposure, nuclear c-rel level was inhibited. Overexpression of c-rel restored IL-12 p40 on stimulation with lipopolysaccharide plus IFN-γ during H2O2 treatment. H2O2 did not inhibit c-rel induction in cytosol; however, it prevented the transport of c-rel from cytosol to the nucleus. H2O2 activated calmodulin (CaM) protein in the cytosol, which subsequently sequestered c-rel in the cytosol preventing its transport to the nucleus. The CaM inhibitor trifIuoperazine increased both nuclear c-rel and IL-12 p40 levels in H2O2-treated macrophages, emphasizing a role of CaM in these processes. H2O2/ROSs thus down-regulate IL-12 induction in macrophages by a novel pathway inhibiting c-rel translocation to the nucleus through activation of CaM protein.

scholarly journals 1727. Sustained Antimicrobial Activity of a Novel Disinfectant Against Healthcare Pathogens

2018 ◽  
Vol 5 (suppl_1) ◽  
pp. S55-S55 ◽  
Author(s):  
William Rutala ◽  
Maria Gergen ◽  
Emily Sickbert-Bennett ◽  
Deverick J Anderson ◽  
David Weber
Keyword(s):  
Hydrogen Peroxide ◽  
Antimicrobial Activity ◽  
Stainless Steel ◽  
The Novel ◽  
Log10 Reduction ◽  
Final Time ◽  
E Coli ◽  
Environmental Surfaces ◽  
The Mean

Abstract Background Environmental contamination plays an important role in the transmission of MRSA, VRE, and C. difficile. Suboptimal compliance with hand hygiene or inappropriate glove use can result in indirect transfer of these pathogens to patients. This study evaluates a novel disinfectant that claims to kill microbes on surfaces for ≥24 hours. Methods We investigated the persistent antimicrobial activity of a novel disinfectant using an EPA protocol for sustained disinfecting activity. In brief, surfaces are inoculated, treated with the novel disinfectant, allowed to dry, and then abraded using a standardized abrasion machine under multiple alternating wet and dry wipe conditions (N = 12) interspersed with 6 re-inoculations. After 24 hours, the surface was re-inoculated a final time and ability of the disinfectant to kill ≥99.9% of 9 test microbes within 5 minutes was measured on 3 test surfaces (glass, formica, and stainless steel). Results The novel disinfectant demonstrated a 3–5 log10 reduction in 5 minutes when testing S. aureus, VRE, C. auris, CRE E. coli and antibiotic-sensitive strains of E. coli, and Enterobacter sp. (table). The disinfectant demonstrated lower killing for CRE isolates of Enterobacter sp. and K. pneumoniae, and for antibiotic-sensitive K. pneumoniae (~2 log10 reduction in 5 minutes). When the novel disinfectant was compared with 3 other commonly used disinfectants using the same methodology with S. aureus, the mean log10 reductions were: 4.4 (novel disinfectant); 0.9 (quat-alcohol); 0.2 (improved hydrogen peroxide); and 0.1 (chlorine). Conclusion Persistent disinfectants may reduce or eliminate the problem of recontamination and minimize the role of environmental surfaces in transmission of healthcare pathogens. Disclosures W. Rutala, PDI: Consultant and Speaker’s Bureau, Consulting fee and Speaker honorarium. D. Weber, PDI: Consultant, Consulting fee

The role of intracanal medicaments in inhibition of bacteria isolated from root canals of infected primary molars

2019 ◽  
Vol 14 (1) ◽  
pp. 92
Author(s):  
Dr. Maha Abdul- Kareem Mahmood ◽  
Dr. Huda Elias Ali ◽  
Dr. Haraa Khairi Abdul-Kadher
Keyword(s):  
Antimicrobial Activity ◽  
Streptococcus Mutans ◽  
Normal Saline ◽  
Root Canal ◽  
Primary Teeth ◽  
Primary Molars ◽  
Root Canals ◽  
Etiologic Agents ◽  
Micro Organisms

Microbes are considered as the primary etiologic agents in endodontic diseases.Disinfection of the root canal is obtained by the combined effect of biomechanicalpreparation, irrigation and intra canal medicament. The aim of the present study wasto assess the antimicrobial activity of intracanal medicaments (formocresol andEndosepton) against two micro organisms (Streptococcus mutans and staphylococcusaureus) isolated from 15 necrotic pulps of primary molars indicated for pulpectomyprocedure. The samples were cultured, and purified using microbiological evaluation.Broth dilution test was performed in our study by preparing test tubes containing10 ml of BHI broth (pH. 7) which then inoculated with strains of the tested bacteriaand incubated at 37 C° for 24 h. After over night incubaction, ten fold dilution weremade in test tubes containing 9 ml of normal saline by adding 1 ml of the inoculum tothe first tube . Then from dilution 10-1 , 0.1 ml of cell suspension was added to 9.9 mlof formocresol and endosepton, then 0.1 ml was taken and spread on duplicates ofBHI agar plates at different intervals and incubated aerobically for 24 h. at 37 C°.Colonies on the plates were counted after incubation and CFU/mL (colony formingunit) was calculated. Our results indicating that there were no significant differencesbetween the intracanal medicaments, but there were high significant differencesbetween the intervals time of the study. We concluded that both materials had greatantibacterial effect against the pathogens commonly isolated from necrotic pulpaltissue of primary teeth.

The role of copper ions in hydrogen peroxide bleaching: Their origin, removal, and effect on pulp quality

TAPPI Journal ◽  
2012 ◽  
Vol 11 (7) ◽  
pp. 37-46 ◽  
Author(s):  
PEDRO E.G. LOUREIRO ◽  
SANDRINE DUARTE ◽  
DMITRY V. EVTUGUIN ◽  
M. GRAÇA V.S. CARVALHO
Keyword(s):  
Hydrogen Peroxide ◽  
Copper Ions ◽  
Peroxide Bleaching ◽  
Metals Removal ◽  
Peroxide Decomposition ◽  
Equipment Corrosion ◽  
And Performance ◽  
And Control ◽  
Main Effects

This study puts particular emphasis on the role of copper ions in the performance of hydrogen peroxide bleaching (P-stage). Owing to their variable levels across the bleaching line due to washing filtrates, bleaching reagents, and equipment corrosion, these ions can play a major role in hydrogen peroxide decomposition and be detrimental to polysaccharide integrity. In this study, a Cu-contaminated D0(EOP)D1 prebleached pulp was subjected to an acidic washing (A-stage) or chelation (Q-stage) before the alkaline P-stage. The objective was to understand the isolated and combined role of copper ions in peroxide bleaching performance. By applying an experimental design, it was possible to identify the main effects of the pretreatment variables on the extent of metals removal and performance of the P-stage. The acid treatment was unsuccessful in terms of complete copper removal, magnesium preservation, and control of hydrogen peroxide consumption in the following P-stage. Increasing reaction temperature and time of the acidic A-stage improved the brightness stability of the D0(EOP)D1AP bleached pulp. The optimum conditions for chelation pretreatment to maximize the brightness gains obtained in the subsequent P-stage with the lowest peroxide consumption were 0.4% diethylenetriaminepentaacetic acid (DTPA), 80ºC, and 4.5 pH.

An ESR study of the peroxidase reaction catalyzed by human methaemoglobin and methaemoglobin-haptoglobin complex

1991 ◽  
Vol 56 (4) ◽  
pp. 923-932
Author(s):  
Jana Stejskalová ◽  
Pavel Stopka ◽  
Zdeněk Pavlíček
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Amino Acid ◽  
Peroxidase Activity ◽  
Amino Acid Analysis ◽  
Superoxide Radical ◽  
Esr Spectra ◽  
The Other ◽  
Delocalized Electron

The ESR spectra of peroxidase systems of methaemoglobin-ascorbic acid-hydrogen peroxide and methaemoglobin-haptoglobin complex-ascorbic acid-hydrogen peroxide have been measured in the acetate buffer of pH 4.5. For the system with methaemoglobin an asymmetrical signal with g ~ 2 has been observed which is interpreted as the perpendicular region of anisotropic spectrum of superoxide radical. On the other hand, for the system with methaemoglobin-haptoglobin complex the observed signal with g ~ 2 is symmetrical and is interpreted as a signal of delocalized electron. After realization of three repeatedly induced peroxidase processes the ESR signal of the perpendicular part of anisotropic spectrum of superoxide radical is distinctly diminished, whereas the signal of delocalized electron remains practically unchanged. An amino acid analysis of methaemoglobin along with results of the ESR measurements make it possible to derive a hypothesis about the role of haptoglobin in increasing of the peroxidase activity of methaemoglobin.

Inhibition of the water channel aquaporin-1 prevents myocardial remodeling by blocking the transmembrane transport of hydrogen peroxide

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Montiel ◽  
R Bella ◽  
L Michel ◽  
E Robinson ◽  
J.C Jonas ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cardiac Hypertrophy ◽  
Cardiac Myocytes ◽  
Cardiac Remodeling ◽  
Cardiac Myocyte ◽  
Water Channel ◽  
Transmembrane Transport ◽  
Funding Source ◽  
Water Pore

Abstract Background Pathological remodeling of the myocardium has long been known to involve oxidant signaling, but so far, strategies using systemic anti-oxidants have generally failed to prevent it. Aquaporins are a family of transmembrane water channels with thirteen isoforms currently known. Some isoforms have been implicated in oxidant signaling. AQP1 is the most abundant aquaporin in cardiovascular tissues but its specific role in cardiac remodeling remains unknown. Purpose We tested the role of AQP1 as a key regulator of oxidant-mediated cardiac remodeling amenable to targeted pharmacological therapy. Methods We used mice with genetic deletion of Aqp1 (and wild-type littermate), as well as primary isolates from the same mice and human iPSC/Engineered Heart Tissue to test the role of AQP1 in pro-hypertrophic signaling. Human cardiac myocyte-specific (PCM1+) expression of AQP's and genes involved in hypertrophic remodeling was studied by RNAseq and bioinformatic GO pathway analysis. Results RNA sequencing from human cardiac myocytes revealed that the archetypal AQP1 is a major isoform. AQP1 expression correlates with the severity of hypertrophic remodeling in patients with aortic stenosis. The AQP1 channel was detected at the plasma membrane of human and mouse cardiac myocytes from hypertrophic hearts, where it colocalizes with the NADPH oxidase-2 (NOX2) and caveolin-3. We show that hydrogen peroxide (H2O2), produced extracellularly, is necessary for the hypertrophic response of isolated cardiac myocytes and that AQP1 facilitates the transmembrane transport of H2O2 through its water pore, resulting in activation of oxidant-sensitive kinases in cardiac myocytes. Structural analysis of the amino acid residues lining the water pore of AQP1 supports its permeation by H2O2. Deletion of Aqp1 or selective blockade of AQP1 intra-subunit pore (with Bacopaside II) inhibits H2O2 transport in mouse and human cells and rescues the myocyte hypertrophy in human induced pluripotent stem cell-derived engineered heart muscle. This protective effect is due to loss of transmembrane transport of H2O2, but not water, through the intra-subunit pore of AQP1. Treatment of mice with clinically-approved Bacopaside extract (CDRI08) inhibitor of AQP1 attenuates cardiac hypertrophy and fibrosis. Conclusion We provide the first demonstration that AQP1 functions as an aqua-peroxiporin in primary rodent and human cardiac parenchymal cells. We show that cardiac hypertrophy is mediated by the transmembrane transport of H2O2 through the AQP1 water channel. Our studies open the way to complement the therapeutic armamentarium with specific blockers of AQP1 for the prevention of adverse remodeling in many cardiovascular diseases leading to heart failure. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): FRS-FNRS, Welbio

scholarly journals The Unexpected Role of Se VI Species in Epoxidations with Benzeneseleninic Acid and Hydrogen Peroxide

2020 ◽  
Vol 132 (11) ◽  
pp. 4313-4317
Author(s):  
Kai N. Sands ◽  
Emerita Mendoza Rengifo ◽  
Graham N. George ◽  
Ingrid J. Pickering ◽  
Benjamin S. Gelfand ◽  
...  
Keyword(s):  
Hydrogen Peroxide

scholarly journals Distribution of Lactoferrin Is Related with Dynamics of Neutrophils in Bacterial Infected Mice Intestine

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1496 ◽  
Author(s):  
Li Liang ◽  
Zhen-Jie Wang ◽  
Guang Ye ◽  
Xue-You Tang ◽  
Yuan-Yuan Zhang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Activity ◽  
Mucosal Immunity ◽  
Mrna Levels ◽  
Iron Binding ◽  
E Coli ◽  
New Knowledge ◽  
Activated Neutrophils ◽  
Binding Glycoprotein

Lactoferrin (Lf) is a conserved iron-binding glycoprotein with antimicrobial activity, which is present in secretions that recover mucosal sites regarded as portals of invaded pathogens. Although numerous studies have focused on exogenous Lf, little is known about its expression of endogenous Lf upon bacterial infection. In this study, we investigated the distribution of Lf in mice intestine during Escherichia coli (E. coli) K88 infection. PCR and immunohistology staining showed that mRNA levels of Lf significantly increased in duodenum, ileum and colon, but extremely decreased in jejunum at 8 h and 24 h after infection. Meanwhile, endogenous Lf was mostly located in the lamina propria of intestine villi, while Lf receptor (LfR) was in the crypts. It suggested that endogenous Lf-LfR interaction might not be implicated in the antibacterial process. In addition, it was interesting to find that the infiltration of neutrophils into intestine tissues was changed similarly to Lf expression. It indicated that the variations of Lf expression were rather due to an equilibrium between the recruitment of neutrophils and degranulation of activated neutrophils. Thus, this new knowledge will pave the way to a more effective understanding of the role of Lf in intestinal mucosal immunity.

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