scholarly journals The impairment of superoxide dismutase coordinates the derepression of the PerR regulon in the response of Staphylococcus aureus to HOCl stress

Microbiology ◽  
2006 ◽  
Vol 152 (3) ◽  
pp. 855-861 ◽  
Author(s):  
Sami Maalej ◽  
Ines Dammak ◽  
Sam Dukan
Keyword(s):  
Staphylococcus Aureus ◽  
Superoxide Dismutase ◽  
Hypochlorous Acid ◽  
Antioxidant Properties ◽  
Exponential Phase ◽  
Dependent Manner ◽  
Wild Type ◽  
Sod Activity ◽  
Striking Result ◽  
Phosphoglycerate Dehydrogenase

The response of Staphylococcus aureus to hypochlorous acid (HOCl) exposure was investigated. HOCl challenges were performed on cultures interrupted in the exponential phase. Pretreatment with HOCl conferred resistance to hydrogen peroxide in a PerR-dependent manner. Derepression of the PerR regulon was observed at low HOCl concentration (survival >50 %), using several fusions of different stress promoters to lacZ reporter genes. At least four members of the PerR regulon (katA, mrgA, bcp and trxA) encoding proteins with antioxidant properties were strongly induced following exposure to various HOCl concentrations. A striking result was the link between the derepression of the PerR regulon and the decreased superoxide dismutase (SOD) activity following exposure to increased HOCl concentrations. The sodA mutant was more resistant than the wild-type and also had a higher level of 3-phosphoglycerate dehydrogenase (a measure of PerR regulon activity) without exposure to HOCl. Together, these results imply that derepression of PerR by HOCl is dependent on the level of SOD and protects exponentially arrested cells against HOCl stress.

scholarly journals Both Complement- and Fibrinogen-Dependent Mechanisms Contribute to Platelet Aggregation Mediated by Staphylococcus aureus Clumping Factor B

2007 ◽  
Vol 75 (7) ◽  
pp. 3335-3343 ◽  
Author(s):  
Helen Miajlovic ◽  
Anthony Loughman ◽  
Marian Brennan ◽  
Dermot Cox ◽  
Timothy J. Foster
Keyword(s):  
Staphylococcus Aureus ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Lag Time ◽  
Dependent Manner ◽  
Wild Type ◽  
Factor B ◽  
Fibrinogen Binding ◽  
Aggregation Of Platelets ◽  
Dependent Mechanism

ABSTRACT Staphylococcus aureus can stimulate activation and aggregation of platelets, which are thought to be factors in the development of infective endocarditis. Previous studies have identified clumping factor A (ClfA) and fibronectin binding proteins A and B (FnBPA and FnBPB) as potent platelet aggregators. These proteins are able to stimulate rapid platelet aggregation by either a fibrinogen- or a fibronectin-dependent process which also requires antibodies specific to each protein. Slower aggregation has been seen in other systems where specific fibrinogen binding ligands are absent and platelet aggregation is mediated by complement and specific antibodies. Bacteria expressing ClfB aggregate platelets with a longer lag time than ClfA or FnBPA and FnBPB. In order to investigate whether ClfB causes platelet aggregation in a complement- or fibrinogen-dependent manner, a non-fibrinogen-binding mutant of ClfB (ClfB Q235A) was constructed. Lactococcus lactis expressing ClfB Q235A was able to stimulate platelet aggregation in platelet-rich plasma without a significant increase in lag time. The requirements for platelet aggregation were investigated using gel-filtered platelets. Fibrinogen and specific anti-ClfB antibodies were found to be sufficient to allow platelet aggregation mediated by the wild-type ClfB protein. It seems that ClfB causes platelet aggregation by a fibrinogen-dependent mechanism. The non-fibrinogen-binding ClfB mutant was unable to stimulate platelet aggregation under these conditions. However, bacteria expressing ClfB Q235A caused platelet aggregation in a complement-dependent manner which required specific anti-ClfB antibodies.

Further investigation of the mechanism of Vitreoscilla hemoglobin (VHb) protection from oxidative stress in Escherichia coli

Biologia ◽  
2011 ◽  
Vol 66 (5) ◽  
Author(s):  
Meltem Akbas ◽  
Tugrul Doruk ◽  
Serhat Ozdemir ◽  
Benjamin Stark
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Stationary Phase ◽  
Exponential Phase ◽  
Vitreoscilla Hemoglobin ◽  
Sod Activity ◽  
E Coli ◽  
Hydrogen Peroxide Treatment

AbstractIn Escherichia coli, Vitreoscilla hemoglobin (VHb) protects against oxidative stress, perhaps, in part, by oxidizing OxyR. Here this protection, specifically VHb-associated effects on superoxide dismutase (SOD) and catalase levels, was examined. Exponential or stationary phase cultures of SOD+ or SOD− E. coli strains with or without VHb and oxyR antisense were treated with 2 mM hydrogen peroxide without sublethal peroxide induction, and compared to untreated control cultures. The hydrogen peroxide treatment was toxic to both SOD+ and SOD− cells, but much more to SOD− cells; expression of VHb in SOD+ strains enhanced this toxicity. In contrast, the presence of VHb was generally associated in the SOD+ background with a modest increase in SOD activity that was not greatly affected by oxyR antisense or peroxide treatment. In both SOD+ and SOD− backgrounds, VHb was associated with higher catalase activity both in the presence and absence of peroxide. Contrary to its stimulatory effects in stationary phase, in exponential phase oxyR antisense generally decreased VHb levels.

scholarly journals Yeast as a biosensor for antioxidants: simple growth tests employing a Saccharomyces cerevisiae mutant defective in superoxide dismutase.

2005 ◽  
Vol 52 (3) ◽  
pp. 679-684 ◽  
Author(s):  
Ewa Zyracka ◽  
Renata Zadrag ◽  
Sabina Kozioł ◽  
Anna Krzepiłko ◽  
Grzegorz Bartosz ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Superoxide Dismutase ◽  
Wild Type Strain ◽  
Solid Medium ◽  
Protective Action ◽  
Antioxidant Properties ◽  
Wild Type ◽  
High Concentration ◽  
Simple Growth ◽  
Antioxidant Effects

Mutants of Saccharomyces cerevisiae devoid of Cu,Zn-superoxide dismutase are hypersensitive to a range of oxidants, hyperbaric oxygen and hyperosmotic media, show lysine and methionine auxotrophy when grown under the atmosphere of air and have a shortened replicative life span when compared to the wild-type strain. Ascorbate and other antioxidants can ameliorate these defects, which may be a basis of simple tests sensing the presence of antioxidants. In particular, tests of growth on solid medium (colony formation) in the absence of methionine and/or lysine, or in the presence of 0.8 M NaCl can be useful for detection and semiquantitative estimation of compounds of antioxidant properties. Hypoxic atmosphere was found to increase the sensitivity of detection of antioxidants. The test of abolishment of lysine auxotrophy showed a concentration dependence of the antioxidant effects of cysteine and N-acetylcysteine which, however, lost their protective action at high concentration, in contrast to glutathione which was effective also at higher concentrations.

Increased susceptibility to exacerbated liver injury in hypercholesterolemic ApoE-deficient mice: potential involvement of oxysterols

2009 ◽  
Vol 296 (3) ◽  
pp. G553-G562 ◽  
Author(s):  
Natàlia Ferré ◽  
Marcos Martínez-Clemente ◽  
Marta López-Parra ◽  
Ana González-Périz ◽  
Raquel Horrillo ◽  
...  
Keyword(s):  
Liver Injury ◽  
Smooth Muscle Actin ◽  
Cell Types ◽  
Dependent Manner ◽  
Wild Type ◽  
Sod Activity ◽  
Concentration Dependent Manner ◽  
Oil Red O Staining ◽  
Cytochrome P 450 ◽  
Oxidized Products

The contribution of metabolic factors to the severity of liver disease is not completely understood. In this study, apolipoprotein E-deficient (ApoE−/−) mice were evaluated to define potential effects of hypercholesterolemia on the severity of carbon tetrachloride (CCl4)-induced liver injury. Under baseline conditions, hypercholesterolemic ApoE−/− mice showed increased hepatic oxidative stress (SOD activity/4-hydroxy-2-nonenal immunostaining) and higher hepatic TGF-β1, MCP-1, and TIMP-1 expression than wild-type control mice. After CCl4 challenge, ApoE−/− mice exhibited exacerbated steatosis (Oil Red O staining), necroinflammation (hematoxylin-eosin staining), macrophage infiltration (F4/80 immunohistochemistry), and fibrosis (Sirius red staining and α-smooth muscle actin immunohistochemistry) and more severe liver injury [alanine aminotransferase (ALT) and aspartate aminotransferase] than wild-type controls. Direct correlations were identified between serum cholesterol and hepatic steatosis, fibrosis, and ALT levels. These changes did not reflect the usual progression of the disease in ApoE−/− mice, since exacerbated liver injury was not present in untreated age-paired ApoE−/− mice. Moreover, hepatic cytochrome P-450 expression was unchanged in ApoE−/− mice. To explore potential mechanisms, cell types relevant to liver pathophysiology were exposed to selected cholesterol-oxidized products. Incubation of hepatocytes with a mixture of oxysterols representative of those detected by GC-MS in livers from ApoE−/− mice resulted in a concentration-dependent increase in total lipoperoxides and SOD activity. In hepatic stellate cells, oxysterols increased IL-8 secretion through a NF-κB-independent mechanism and upregulated TIMP-1 expression. In macrophages, oxysterols increased TGF-β1 secretion and MCP-1 expression in a concentration-dependent manner. Oxysterols did not compromise cell viability. Taken together, these findings demonstrate that hypercholesterolemic mice are sensitized to liver injury and that cholesterol-derived products (i.e., oxysterols) are able to induce proinflammatory and profibrogenic mechanisms in liver cells.

scholarly journals Safranal Treatment Improves Hyperglycemia, Hyperlipidemia and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

2013 ◽  
Vol 16 (2) ◽  
pp. 352 ◽  
Author(s):  
Saeed Samarghandian ◽  
Abasalt Borji ◽  
Mohammad Bagher Delkhosh ◽  
Fariborz Samini
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Antioxidant Properties ◽  
Diabetic Rats ◽  
Dependent Manner ◽  
Protective Effects ◽  
Total Lipids ◽  
Sod Activity ◽  
Chemically Induced ◽  
Antioxidant Defense Systems

Purpose. Clinical research has confirmed the efficacy of several plant extracts in the modulation of oxidative stress associated with diabetes mellitus. Findings indicate that safranal has antioxidant properties. The aim of the present study was the evaluation of possible protective effects of safranal against oxidative damage in diabetic rats. Methods. In this study, the rats were divided into the following groups of 8 animals each: control, untreated diabetic, three safranal (0.25, 0.50, 0.75 mg/kg/day)-treated diabetic groups. Diabetes was induced by streptozotocin (STZ) in rats. STZ was injected intraperitoneally at a single dose of 60 mg/kg for diabetes induction. Safranal (intraperitoneal injection) was administered 3 days after STZ administration; these injections were continued to the end of the study (4 weeks). At the end of the 4-week period, blood was drawn for biochemical assays. In order to determine the changes of cellular antioxidant defense systems, antioxidant enzymes including glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were measured in serum. Moreover we also measured serum nitric oxide (NO) and serum malondialdehyde (MDA) levels, a marker of lipid peroxidation.  Results. STZ-induced diabetes caused an elevation (p < 0.001) of blood glucose, MDA, NO, total lipids, triglycerides and cholesterol, with reduction of GSH level and CAT and SOD activities. The results indicated that the significant elevation in the blood glucose, MDA, NO, total lipids, triglycerides, cholesterol and reduction of glutathione level and CAT and SOD activity were ameliorated in the safranal–treated diabetic groups compared with the untreated groups, in a dose dependent manner (p < 0.05, p<0.01, p < 0.001). Conclusion. These results suggest that safranal has antioxidant properties and improves chemically-induced diabetes and its complications by modulation of oxidative stress. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

Influence of Plasmids on Catalase and Superoxide Dismutase Activities in Listeria monocytogenes

1995 ◽  
Vol 58 (9) ◽  
pp. 955-959 ◽  
Author(s):  
LOWELL L. ISOM ◽  
ALI H. AHMED ◽  
SCOTT E. MARTIN
Keyword(s):  
Superoxide Dismutase ◽  
Listeria Monocytogenes ◽  
Gradient Centrifugation ◽  
Plasmid Copy Number ◽  
Activity Levels ◽  
Wild Type ◽  
Cadmium Resistance ◽  
Sod Activity ◽  
Plasmid Copy ◽  
Cscl Density Gradient

Two of nine strains of Listeria monocytogenes examined were found to contain plasmid DNA. Strain 19112 contained a 31.1 kb plasmid and strain 7644 contained a 49.4 kb plasmid. Each of the strains was cured of its plasmid by heat treatment at 46°C. Both the wild-type and plasmid-negative forms of each strain were screened for cadmium resistance. The 31.1 kb plasmid of L. monocytogenes 19112 was shown to confer resistance to cadmium. Listeria monocytogenes 7644 did not show resistance to cadmium. The plasmids for both strains were isolated and purified by CsCl density-gradient centrifugation. Each plasmid was electroporated back into the respective plasmid-negative strain. The catalase (CA) and superoxide dismutase (SOD) activities were determined for the wild type, plasmid-negative and electroporated strains. There was a significant decrease in CA and SOD activities upon loss of the plasmid from each strain of L. monocytogenes. Strain 19112 showed a 36% decrease in CA activity and an 81% decrease in SOD activity as a result of plasmid removal. Strain 7644 showed a 22% decrease in both CA and SOD activities following plasmid loss. Catalase and SOD activity levels increased for both strains following reinsertion of the plasmid through electroporation. Catalase and SOD activity levels of L. monocytogenes 7644 were higher for the transformed strain than those of the wild type. Catalase and SOD activity levels of transformed L. monocytogenes 19112 were less than in the corresponding wild type. It appears that plasmids in L. monocytogenes strains 19112 and 7644 may be involved in influencing the regulation of the production of CA and SOD. Plasmid copy number may influence the level of activity of these enzymes.

Protection against bleomycin-induced lung injury by IL-18 in mice

2005 ◽  
Vol 289 (2) ◽  
pp. L280-L287 ◽  
Author(s):  
Akemi Nakatani-Okuda ◽  
Haruyasu Ueda ◽  
Shin-ichiro Kashiwamura ◽  
Atsuo Sekiyama ◽  
Akira Kubota ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Messenger Rna ◽  
Lavage Fluid ◽  
Protective Role ◽  
Myeloperoxidase Activity ◽  
Wild Type ◽  
Sod Activity ◽  
Alveolar Epithelial ◽  
Lung Injuries ◽  
Macrophage Colony

The role of interleukin (IL)-18 in the protection from interstitial pneumonia and pulmonary fibrosis induced by bleomycin (BLM) was investigated by comparing the severity of BLM-induced lung injuries between wild-type and C57BL/6 mice with a targeted knockout mutation of the IL-18 gene (IL-18−/− mice). IL-18−/− mice showed much worse lung injuries than wild-type mice, as assessed by the survival rate, histological images, and leukocyte infiltration in the bronchoalveolar lavage fluid and myeloperoxidase activity. In wild-type mice, administration of IL-18 before BLM instillation resulted in suppression of lung injuries, increases in the hydroxyproline content, and decreases in the granulocyte-macrophage colony-stimulating factor content in the lung. Preadministration of IL-18 also resulted in prevention of the reduction of the lung IL-10 content caused by BLM-induced damage of alveolar epithelial. BLM instillation suppressed superoxide dismutase (SOD) activity in IL-18−/− mice to a greater extent than in wild-type mice. Pretreatment of IL-18 augmented Mn-containing superoxide dismutase (Mn-SOD) messenger RNA expression and SOD activity in the lung and prevented the reduction of SOD activity caused by BLM in both wild-type and IL-18−/− mice. These results suggest that IL-18 plays a protective role against BLM-induced lung injuries by upregulating a defensive molecule, Mn-SOD.

scholarly journals Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiaopeng Tian ◽  
Chunhong Zhao ◽  
Jinbo Guo ◽  
Shurui Xie ◽  
Fengrong Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bile Duct ◽  
Hepatic Fibrosis ◽  
Transforming Growth Factor ◽  
Bile Duct Ligation ◽  
Antioxidant Properties ◽  
Dependent Manner ◽  
Sod Activity ◽  
Duct Ligation ◽  
Clinical Benefits

Background.The sympathetic nervous system (SNS) is responsible for hepatic stellate cells (HSCs) activation and the accumulation of collagen that occurs in hepatic fibrogenesis. Carvedilol has been widely used for the complication of hepatic cirrhosis in the clinic. Furthermore, it has powerful antioxidant properties. We assessed the potential antifibrotic effects of carvedilol and the underlying mechanisms that may further enhance its clinical benefits.Methods.Using a bile duct ligation rat model of hepatic fibrosis, we studied the effects of carvedilol on the fibrosis, collagen deposition, and oxidative stress based on histology, immunohistochemistry, western blot, and RT-PCR analyses.Results.Carvedilol attenuated liver fibrosis, as evidenced by reduced hydroxyproline content and the accumulation of collagen, downregulated TIMP-1 and TIMP-2, and upregulated MMP-13. MMP-2 was an exception, which was decreased after carvedilol treatment for 2 weeks and upregulated after carvedilol treatment for 4 weeks. Carvedilol reduced the activation of HSCs, decreased the induction of collagen, transforming growth factor-β1, and MDA content, and strengthened the SOD activity. The antifibrotic effects were augmented as dosages increased.Conclusions.The study indicates that carvedilol attenuated hepatic fibrosis in a dose-dependent manner. It can decrease collagen accumulation and HSCs activation by the amelioration of oxidative stress.

scholarly journals Growth-phase dependence of susceptibility to antimicrobial peptides in Staphylococcus aureus

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1786-1797 ◽  
Author(s):  
Miki Matsuo ◽  
Yuichi Oogai ◽  
Fuminori Kato ◽  
Motoyuki Sugai ◽  
Hitoshi Komatsuzawa
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Surface ◽  
Antimicrobial Peptides ◽  
Stationary Phase ◽  
Surface Charge ◽  
Growth Phase ◽  
Exponential Phase ◽  
Dependent Manner ◽  
Phase Dependence ◽  
Cell Surface Charge

Bacterial cell surface charge is responsible for susceptibility to cationic antimicrobial peptides. Previously, Staphylococcus aureus dlt and mprF were identified as factors conferring a positive charge upon cell surfaces. In this study, we investigated the regulation of cell surface charge during growth. Using a group of S. aureus MW2 mutants, which are gene-inactivated in 15 types of two-component systems (TCSs), we tested dltC and mprF expression and found that two TCSs, aps and agr, were associated with dltC and mprF expression in a growth phase-dependent manner. The first of these, aps, which had already been identified as a sensor of antimicrobial peptides and a positive regulator of dlt and mprF expression, was expressed strongly in the exponential phase, while its expression was significantly suppressed by agr in the stationary phase, resulting in higher expression of dltC and mprF in the exponential phase and lower expression in the stationary phase. Since both types of expression affected the cell surface charge, the susceptibility to antimicrobial peptides and cationic antibiotics was changed during growth. Furthermore, we found that the ability to sense antimicrobial peptides only functioned in the exponential phase. These results suggest that cell surface charge is tightly regulated during growth in S. aureus.

scholarly journals Identification and Characterization of a Second Superoxide Dismutase Gene (sodM) fromStaphylococcus aureus

2001 ◽  
Vol 183 (11) ◽  
pp. 3399-3407 ◽  
Author(s):  
Michelle Wright Valderas ◽  
Mark E. Hart
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Amino Acid ◽  
Amino Acid Sequence ◽  
Stationary Phases ◽  
Potassium Cyanide ◽  
Exponential Phase ◽  
Sod Activity ◽  
Protein Amino Acid ◽  
Sequence Comparisons

ABSTRACT A gene encoding superoxide dismutase (SOD), sodM, fromS. aureus was cloned and characterized. The deduced amino acid sequence specifies a 187-amino-acid protein with 75% identity to the S. aureus SodA protein. Amino acid sequence comparisons with known SODs and relative insensitivity to hydrogen peroxide and potassium cyanide indicate that SodM most likely uses manganese (Mn) as a cofactor. The sodM gene expressed from a plasmid rescued an Escherichia coli double mutant (sodA sodB) under conditions that are otherwise lethal. SOD activity gels ofS. aureus RN6390 whole-cell lysates revealed three closely migrating bands of activity. The two upper bands were absent in asodM mutant, while the two lower bands were absent in asodA mutant. Thus, the middle band of activity most likely represents a SodM-SodA hybrid protein. All three bands of activity increased as highly aerated cultures entered the late exponential phase of growth, SodM more so than SodA. Viability of the sodAand sodM sodA mutants but not the sodM mutant was drastically reduced under oxidative stress conditions generated by methyl viologen (MV) added during the early exponential phase of growth. However, only the viability of the sodM sodA mutant was reduced when MV was added during the late exponential and stationary phases of growth. These data indicate that while SodA may be the major SOD activity in S. aureus throughout all stages of growth, SodM, under oxidative stress, becomes a major source of activity during the late exponential and stationary phases of growth such that viability and growth of an S. aureus sodA mutant are maintained.

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