The Respiratory Burst of Phagocytic Cells: Facts and Problems

A 47 kDa phosphoprotein is involved in the respiratory-burst oxidase of phagocytic cells. After stimulation of neutrophils with phorbol myristate acetate, this phosphoprotein was identified in both the cytosol and membranes. Peptide mapping of the two forms resulted in identical patterns of phosphopeptides. Dose-response curves for accumulation of phosphoprotein in the two sites were very similar, whereas the detection of the phosphoprotein in the cytosol preceded that in the membranes. The membrane-associated 47 kDa phosphoprotein was absent from the neutrophils of patients with X-chromosome-linked chronic granulomatous disease, which lack cytochrome b-245, and intermediate levels were detected in the membranes of their heterozygote carrier mothers. Activation of the neutrophil oxidase system appears to be dependent upon phosphorylation of the cytosolic 47 kDa protein and its association with cytochrome b-245 in the membranes. It is probably the cytosolic factor required for reconstitution of the active oxidase in cell-free systems.

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A Comparative Study of the Respiratory Burst Produced by the Phagocytic Cells of Marine Invertebrates

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1994.tb33586.x ◽

1994 ◽

Vol 712 (1 Primordial Im) ◽

pp. 330-331 ◽

Cited By ~ 7

Author(s):

KAREN L. BELL ◽

VALERIE J. SMITH

Keyword(s):

Comparative Study ◽

Respiratory Burst ◽

Marine Invertebrates ◽

Phagocytic Cells

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The influence of microcystin-LR on fish phagocytic cells

Human & Experimental Toxicology ◽

10.1177/09603271060080075 ◽

2007 ◽

Vol 26 (7) ◽

pp. 603-607 ◽

Cited By ~ 20

Author(s):

A. Sierosławska ◽

A. Rymuszka ◽

A. Bownik ◽

T. Skowroński

Keyword(s):

Respiratory Burst ◽

Burst Activity ◽

Phagocytic Cell ◽

Phagocytic Cells ◽

Respiratory Burst Activity ◽

Superoxide Anion Production ◽

Cell Functions ◽

Fish Blood ◽

Dose Dependent

The in vitro influence of microcystin-LR (MC-LR) on rainbow trout phagocytic cell functions was studied. The cells isolated from the fish blood were exposed on MC-LR at the concentrations of 1, 5, 10, 20 μg/mL. The viability of the cells after 2, 4 and 24 hour incubation with MC-LR was studied as well as phagocytic cell ability measured as zymozan particle phagocytosis and metabolic activity measured as respiratory burst activity. The toxin caused time- and dose-dependent viability decrease, the strongest after cell exposure on 10 and 20 μg/mL and observed only after 24 hours incubation when 1 μg/mL was applied. The phagocytic ability was elevated in the presence of MC-LR at the dose of 5 μg/mL. MC-LR had also modulatory influence on respiratory burst activity. While the two lower doses caused the stimulation of the parameter, the two higher ones diminished superoxide anion production in the triggered cells. The results show the potency of the toxin to influence the fish phagocytic cell functions. Human & Experimental Toxicology (2007) 26: 603—607.

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PENGARUH PAJANAN LOGAM KADMIUM (Cd) TERHADAP KADAR PEROKSIDA (H2O2), KADAR MALODIALDEHID (MDA) DAN KADAR METIL GLIOKSAL (MG) PADA HATI TIKUS PUTIH (Rattus novergicus)

EnviroScienteae ◽

10.20527/es.v12i1.1099 ◽

2016 ◽

Vol 12 (1) ◽

pp. 43 ◽

Cited By ~ 1

Author(s):

Siti Juliati ◽

Emmy Sri Mahreda ◽

Triawanti Triawanti ◽

Eko Suhartono

Keyword(s):

Lipid Peroxidation ◽

Heavy Metal ◽

Liver Damage ◽

Respiratory Burst ◽

Statistical Test ◽

White Mouse ◽

Cadmium Exposure ◽

Phagocytic Cells ◽

Amadori Product ◽

Cd Exposure

Cadmium and its compounds are used for various industrial interests. However, the accumulation of cadmium in liver will lead to liver damage. This research aims to analyze the effect of the long exposure of cadmium to wards the levels of H2O2, MDA and MG in white-mouse livers. The number of white-mouse livers used in this research were 24 male mouses which were divided into four treatments of cadmium exposure for zero, two, four and six weeks. After the surgeries, the levels of H2O2, MDA and MG of the white-mouse livers were measured using spectrophotometer UV – VIS. The results showed that there were significant differences in the levels of H2O2 between treatment without exposure to Cd and that exposure. The levels of H2O2 increased respectively 3.164 mmol, 11.076 mmol, 16.292 mmol and 31.588 mmol at the weeks of 0, 2, 4, and 6. The results of the Kruskal-Wallis statistical test (p = 0.000; p <0.05), stated that the long exposure of Cd increased significantly the level of H2O2 in the white-mouse livers. The level of MDA of the white-mouse livers also increased consecutively in the week of 0, 2, 4, and 6 as much as 211.5 μM, 230.6 μM, 269.2 μM and 533 μM. The results of the Kruskal-Wallis statistical test (p = 0.000; p <0.05) showed that the Cd exposure could significantly increase the MDA levels in white-mouse livers. This happened because the Cd exposure activated the phagocytic cells to perform respiratory burst resulting in the accumulation of peroxide compounds. The increased Peroxide with Fe metal that existed in the cytoplasm triggered the lipid peroxidation in the membrane producing the MDA compounds. In addition, the results also showed the increased levels of liver MG consecutively in week 0, 2, 4, and 6 as much as 20.039 %, 24.055 %, 27.985 % and 33.87 % . The results of the Kruskal - Wallis statistical test (p = 0.001 ; p < 0.05), showed that the Cd exposure increased significantly the level of MG which was caused by the metal Cd increased the glycation reaction, i.e., the reaction between glucose and proteins to form Amadori product. At the time of the Amadory formation, the formation of 2,3- enediol which was are easily oxidized by the presence of Cd and oxygen to produce MG occurred. It can be concluded that the exposure of heavy metal cadmium (Cd) for 6 weeks may increase the levels of H2O2, MDA and MG

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The respiratory burst of phagocytic cells is associated with a rise in vacuolar pH

Nature ◽

10.1038/290406a0 ◽

1981 ◽

Vol 290 (5805) ◽

pp. 406-409 ◽

Cited By ~ 272

Author(s):

Anthony W. Segal ◽

Michael Geisow ◽

Rodolfo Garcia ◽

Angela Harper ◽

Robert Miller

Keyword(s):

Respiratory Burst ◽

Phagocytic Cells ◽

Vacuolar Ph

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Inhibitory Effect of Interferon-α on Respiratory Burst and Glucose Metabolism in Phagocytic Cells

Journal of Interferon Research ◽

10.1089/jir.1994.14.11 ◽

1994 ◽

Vol 14 (1) ◽

pp. 11-16 ◽

Cited By ~ 5

Author(s):

MANUEL CONDE ◽

JOSEFA ANDRADE ◽

FRANCISCO J. BEDOYA ◽

FRANCISCO SOBRINO

Keyword(s):

Glucose Metabolism ◽

Respiratory Burst ◽

Inhibitory Effect ◽

Interferon Α ◽

Phagocytic Cells

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A new X-linked variant of chronic granulomatous disease characterized by the existence of a normal clone of respiratory burst-competent phagocytic cells

Blood ◽

10.1182/blood.v85.1.231.bloodjournal851231 ◽

1995 ◽

Vol 85 (1) ◽

pp. 231-241 ◽

Cited By ~ 43

Author(s):

RC Woodman ◽

PE Newburger ◽

P Anklesaria ◽

RW Erickson ◽

J Rae ◽

...

Keyword(s):

Chronic Granulomatous Disease ◽

Progenitor Cells ◽

Respiratory Burst ◽

Burst Activity ◽

Granulomatous Disease ◽

Phagocytic Cells ◽

Respiratory Burst Activity ◽

Myeloid Progenitor ◽

Nbt Reduction ◽

O2 Production

Chronic granulomatous disease (CGD) is characterized by recurrent infections, and is usually associated with a complete inability of phagocytic cells to generate superoxide anion (O2-). Rarely, variant forms of CGD have been reported in which there is reduced, but detectable, O2- production by phagocytic cells. We describe three adult males in two kindreds with a unique form of X-linked cytochrome b558- deficient (X91-) CGD not previously reported. All three patients had two distinct populations of phagocytic cells, with one subset capable of normal respiratory burst activity and the other larger subset inactive, as in classic CGD (X91 (0)). The respiratory burst activity in neutrophils purified from each patient was approximately 10% of normal as determined by O2- production, O2 consumption, cytochrome b558 spectroscopy, and membrane oxidase activity using a cell-free activation system. In contrast with other patients with X91(-)-variant CGD, the unique feature of these patients is the presence of a small but significant population (5% to 15%) of circulating neutrophils and monocytes with completely normal respiratory burst activity as assessed by nitroblue tetrazolium (NBT) reduction and flow-cytometric measurement of dihydrorhodamine oxidation. NBT reduction of peripheral blood granulocyte-macrophage progenitor cells also showed the presence of a subset of colonies derived from myeloid progenitor cells that had normal respiratory burst capabilities. A mosaic XX chromosome karyotype and an unstable oxidase complex that might occur during myeloid maturation were both excluded as possible explanations. In these families, the molecular defect in the gp91-phox gene, which is currently under investigation, appears to prevent expression of the gene in the majority of neutrophils, but not in a small subset. Our studies suggest that commitment to either a respiratory burst-competent or -incompetent phagocytic cell occurs at the level of the myeloid progenitor cell.

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