Correlation between release of reactive oxygen intermediates and inhibition of toxoplasma multiplication in mouse peritoneal and alveolar macrophages and kidney cells after in vitro incubation with obioactin, lonomycin a, muramyl dipeptide, lipopolysaccharide or toxoplasma lysate antigen

1987 ◽  
Vol 264 (3-4) ◽  
pp. 446-454
Author(s):  
Atsushi Saito ◽  
Haruhisa Sakurai ◽  
Toshio Saito ◽  
Shuichi Taji ◽  
Tadatoshi Miyagami ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Muramyl Dipeptide ◽  
Reactive Oxygen ◽  
Kidney Cells ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates ◽  
In Vitro Incubation

scholarly journals Coxiella burnetiiAcid Phosphatase Inhibits the Release of Reactive Oxygen Intermediates in Polymorphonuclear Leukocytes

2010 ◽  
Vol 79 (1) ◽  
pp. 414-420 ◽  
Author(s):  
J. Hill ◽  
J. E. Samuel
Keyword(s):  
Acid Phosphatase ◽  
Nadph Oxidase ◽  
Polymorphonuclear Leukocytes ◽  
Q Fever ◽  
Reactive Oxygen ◽  
Host Cells ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates

ABSTRACTCoxiella burnetii, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication ofC. burnetiiduring infection has been shown to be increased by decreasing oxidative stress using p47phox −/−and iNOS−/−micein vivoand by pharmacologic inhibitorsin vitro. Building upon this model, we investigated the role polymorphonuclear leukocytes (PMN) play in the control of infection, since NADPH oxidase-mediated release of reactive oxygen intermediates (ROI) is a primary bactericidal mechanism for these cells that is critical for early innate clearance. Earlier studies suggested thatC. burnetiiactively inhibited release of ROI from PMN through expression of an unidentified acid phosphatase (ACP). Recent genomic annotations identified one open reading frame (CBU0335) which may encode a Sec- and type II-dependent secreted ACP. To test this model, viableC. burnetiipropagated in tissue culture host cells or axenic media,C. burnetiiextracts, or purified recombinant ACP (rACP) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA). The release of ROI was inhibited when PMN were challenged with viableC. burnetii,C. burnetiiextracts, or rACP but not when PMN were challenged with electron beam-inactivatedC. burnetii. C. burnetiiextracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN membranes, suggesting a molecular mechanism responsible for this inhibition. These data support a model in whichC. burnetiieludes the primary ROI killing mechanism of activated PMN by secreting at least one acid phosphatase.

H2O2-Induced Apoptosis of Thymocytes Involves Mobilization of Divalent Cations

2002 ◽  
Vol 15 (3) ◽  
pp. 195-200 ◽  
Author(s):  
A. Acharya
Keyword(s):  
Divalent Cations ◽  
Reactive Oxygen ◽  
Time Dependent ◽  
Dependent Manner ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates ◽  
Thymocyte Apoptosis ◽  
Induced Apoptosis

More than 90% of thymocytes undergo apoptosis while undergoing differentiation in the thymus. Although several factors act in concert to induce thymocyte apoptosis, it remains speculative if reactive oxygen intermediates produced by thymic macrophages may play a role in this process. The present investigation was carried out to determine if H2O2 is capable of inducing apoptosis of thymocytes in vitro. It was observed that H2O2 could induce apoptosis of thymocytes in vitro in a dose and time dependent manner. It was further found that H2O2-induced thymocyte apoptosis was dependent on the mobilization of divalent cations. The result of this study will help further in the understanding of the mechanism of H2O2 - induced apoptosis.

Reactive oxygen in skeletal muscle. I. Intracellular oxidant kinetics and fatigue in vitro

1992 ◽  
Vol 73 (5) ◽  
pp. 1797-1804 ◽  
Author(s):  
M. B. Reid ◽  
K. E. Haack ◽  
K. M. Franchek ◽  
P. A. Valberg ◽  
L. Kobzik ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
High Frequency ◽  
Low Frequency ◽  
Reactive Oxygen ◽  
Muscular Contraction ◽  
Fiber Bundles ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates ◽  
Low Frequency Fatigue

We hypothesized that muscle fiber bundles produce reactive oxygen intermediates and that reactive oxidant species contribute to muscular fatigue in vitro. Fiber bundles from rat diaphragm were mounted in chambers containing Krebs-Ringer solution. In studies of intracellular oxidant kinetics, bundles were loaded with 2′,7′-dichlorofluorescin, a fluorochrome that emits at 520 nm when oxidized; emissions were quantified using a fluorescence microscope. Emissions from unstimulated muscles increased over time (P < 0.001). Accumulation of fluorescence was slowed by addition of catalase (P < 0.001) or superoxide dismutase (P < 0.001) and was accelerated by repetitive muscular contraction (P < 0.05). To determine effects of reactive oxygen intermediates on fatigue, curarized bundles were stimulated to contract isometrically; force was measured. Catalase, superoxide dismutase, and dimethyl sulfoxide were screened for effects on low- and high-frequency fatigue. Antioxidants inhibited low-frequency fatigue [after 5 min of repetitive contractions, force at 30 Hz was 20% greater than control (P < 0.015)] and increased the variability of fatigue at 30 Hz (P < 0.03). Antioxidants did not alter high-frequency (200-Hz) fatigue. We conclude that 1) diaphragm fiber bundles produce reactive oxygen intermediates, including O2-. and H2O2; 2) muscular contraction increases intracellular oxidant levels; and 3) reactive oxygen intermediates promote low-frequency fatigue in this preparation.

scholarly journals Involvement of Reactive Oxygen Intermediates in Spontaneous and CD95(Fas/APO-1)–Mediated Apoptosis of Neutrophils

Blood ◽  
1997 ◽  
Vol 89 (5) ◽  
pp. 1748-1753 ◽  
Author(s):  
Yoshihito Kasahara ◽  
Kazuyuki Iwai ◽  
Akihiro Yachie ◽  
Kunio Ohta ◽  
Akihiro Konno ◽  
...  
Keyword(s):  
Signal Transduction Pathway ◽  
Reactive Oxygen ◽  
Reactive Oxygen Intermediates ◽  
Transduction Pathway ◽  
Spontaneous Apoptosis ◽  
Oxygen Intermediates ◽  
Hereditary Defect ◽  
Oxidative Products

Apoptosis is well known to be mediated by oxidative stress. To evaluate the functional role of reactive oxygen intermediates (ROI) produced by neutrophils, we compared the rates of apoptosis in neutrophils isolated from normal donors and from patients with chronic granulomatous disease (CGD), a hereditary defect in ROI production. Spontaneous cell death in CGD neutrophils in vitro was significantly inhibited relative to normal neutrophils. The acceleration of apoptosis induced by anti-Fas monoclonal antibody (MoAb) in CGD neutrophils was much slower than that seen in normal neutrophils. These findings suggest that the apoptosis of neutrophils may be mediated by endogenous oxidative products. This suggestion was confirmed by observation that apoptosis of normal neutrophils was markedly inhibited by reduction of intracellular levels of hydrogen peroxide (H2O2 ). The inhibition of apoptosis in normal neutrophils by adding catalase occurred regardless of the presence of anti-Fas MoAb. H2O2 increased both spontaneous apoptosis and Fas-mediated apoptosis of the CGD neutrophils in proportion to that seen in normal neutrophils. Although several factors that mediate the apoptosis of neutrophils remain to be determined, these results suggest that ROI are major mediators of the apoptosis in neutrophils and may be involved in Fas-mediated signal transduction pathway.

scholarly journals Involvement of Reactive Oxygen Intermediates in Spontaneous and CD95(Fas/APO-1)–Mediated Apoptosis of Neutrophils

Blood ◽  
1997 ◽  
Vol 89 (5) ◽  
pp. 1748-1753 ◽  
Author(s):  
Yoshihito Kasahara ◽  
Kazuyuki Iwai ◽  
Akihiro Yachie ◽  
Kunio Ohta ◽  
Akihiro Konno ◽  
...  
Keyword(s):  
Signal Transduction Pathway ◽  
Reactive Oxygen ◽  
Reactive Oxygen Intermediates ◽  
Transduction Pathway ◽  
Spontaneous Apoptosis ◽  
Oxygen Intermediates ◽  
Hereditary Defect ◽  
Oxidative Products

Abstract Apoptosis is well known to be mediated by oxidative stress. To evaluate the functional role of reactive oxygen intermediates (ROI) produced by neutrophils, we compared the rates of apoptosis in neutrophils isolated from normal donors and from patients with chronic granulomatous disease (CGD), a hereditary defect in ROI production. Spontaneous cell death in CGD neutrophils in vitro was significantly inhibited relative to normal neutrophils. The acceleration of apoptosis induced by anti-Fas monoclonal antibody (MoAb) in CGD neutrophils was much slower than that seen in normal neutrophils. These findings suggest that the apoptosis of neutrophils may be mediated by endogenous oxidative products. This suggestion was confirmed by observation that apoptosis of normal neutrophils was markedly inhibited by reduction of intracellular levels of hydrogen peroxide (H2O2 ). The inhibition of apoptosis in normal neutrophils by adding catalase occurred regardless of the presence of anti-Fas MoAb. H2O2 increased both spontaneous apoptosis and Fas-mediated apoptosis of the CGD neutrophils in proportion to that seen in normal neutrophils. Although several factors that mediate the apoptosis of neutrophils remain to be determined, these results suggest that ROI are major mediators of the apoptosis in neutrophils and may be involved in Fas-mediated signal transduction pathway.

Sign in / Sign up

Export Citation Format

Share Document