On radical production by PMA-stimulated neutrophils as monitored by luminol-amplified chemiluminescence

Samuni, Amram; Krishna, C. Murali; Cook, John A.; Black, Christopher D. V.; Russo, Angelo

doi:10.1016/0891-5849(91)90037-4

Cited by 31 publications

(14 citation statements)

References 27 publications

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“…we found that L-012 emits a considerably stronger signal (~900 times higher), in agreement with a previous in vitro study [51]. The comparatively low chemiluminescence emission of luminol may be partially caused by the fact that the luminol signal is pH dependent showing a reduction at low pH, which often occurs at sites of inflammation [52]. Further, the results of H 2 O 2 concentration-dependent chemiluminescence for L-012 show good agreement with a previous study in which ROS-mediated L-012 chemiluminescence are generated by xanthine oxidase [51].…”

Section: Discussionsupporting

confidence: 91%

Noninvasive assessment of localized inflammatory responses

Zhou

Tsai

Hong

et al. 2012

Free Radical Biology and Medicine

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Inflammatory diseases are associated with the accumulation of activated inflammatory cells, particularly polymorphonuclear neutrophils (PMN), which release reactive oxygen species (ROS) to eradicate foreign bodies and microorganisms. To assess the location and extent of localized inflammatory responses, L-012, a highly-sensitive chemiluminescence probe, was employed to non-invasively monitor the production of ROS. We find that L-012-associated chemiluminescence imaging can be used to identify and to quantify the extent of inflammatory responses. Furthermore, regardless of differences among animal models, there is a good linear relationship between chemiluminescence intensity and PMN numbers surrounding inflamed tissue. Depletion of PMN substantially diminished L-012-associated chemiluminescence in vivo. Finally, L-012-associated chemiluminescence imaging was found to be a powerful tool for assessing implant-mediated inflammatory responses by measuring chemiluminescent intensities at the implantation sites. These results support the use of L-012 for monitoring the kinetics of inflammatory responses in vivo via the detection and quantification of ROS production.

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Section: Discussionsupporting

confidence: 91%

Noninvasive assessment of localized inflammatory responses

Zhou

Tsai

Hong

et al. 2012

Free Radical Biology and Medicine

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“…6B). This result is in a good agreement with previously published data (Mills et al, 1980;Dahlgren et al, 1985;Panasenko et al, 1991;Samuni et al, 1991). The stimulator, however, increased the current response of the azurin-modified electrode only moderately ( …”

Section: Production From Neutrophilssupporting

confidence: 83%

Electrochemical characterization and application of azurin-modified gold electrodes for detection of superoxide

Shleev

Wetterö

Magnusson

et al. 2006

Biosensors and Bioelectronics

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The interaction of superoxide radicals with Pseudomonas aeruginosa azurin in solution and in adsorbed form was characterized using spectrophotometric and electrochemical techniques. It was determined that the rate constant for the reduction of azurin by superoxide ion in solution was about 10 5 M -1 s -1 , being 2-3 times lower than the constant for cytochrome c. To prepare superoxide sensitive electrode azurin was immobilised on the surface of gold electrodes. Cyclic voltammetry measurements revealed that the best electron transfer between the protein and the electrode is realised at short-chain thiol, viz. 3,3'-dithiobis(sulfosuccinimidylpropionate,)-(DTSSP-) modified gold. The formal potential of the redox protein on the DTSSP-modified electrode was found to be 380 mV vs. NHE being 100 mV more positive if compared to the standard redox potential of the T1 site of azurin fromPseudomonas aeruginosa. The heterogeneous electron transfer rate constant was determined to be in the range 2-6 s −1 for the azurin adsorbed on the DTSSP-modified gold electrodes.Based on the electrochemical measurements the sensitivity of the biosensor towards superoxide was calculated to be 6. biosensor displayed a response to chemically and enzymatically generated superoxide, and adequate sensitivity to assess the biological response of stimulated human neutrophils.

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“…This suggests that the reaction is not terminated by the inactivation of the XO but by consumption of the substrate. Despite these observations, the actual duration of ROI formation may be underestimated, since recent observations revealed that luminol may fail to detect long-term chemiluminescence activity [25].…”

Section: Resultsmentioning

confidence: 99%

Oxygen radicals generated by the enzyme xanthine oxidase lyse rat pancreatic islet cells in vitro

et al. 1992

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Summary. The endothelium-associated enzyme xanthine oxidase is known to generate reactive oxygen intermediates which may damage the surrounding tissue. We investigated whether reactive oxygen intermediates released by xanthine oxidase exert a toxic effect on isolated rat islet cells. The xanthine oxidase (25 mU/ml)/hypoxanthine (0.5 mmol/1) system released reactive oxygen intermediates in vitro as detected by luminol in a chemiluminescence analysing system. The addition of nicotinamide inhibited the release of reactive oxygen intermediates in a dose-dependent manner (50 % inhibition at 20 retool/l). Exposure of islet cells to enzyme generated reactive oxygen intermediates caused lysis of 39 % of the cells within 15 h. Monitoring the mitochondrial function of islet cells by the conversion of tetrazolium bromide to its formazan product revealed a significant reduction of the respiratory activity down to 51% of that of the controls by 30 min after the initiation of the xanthine oxidase reaction. Mitochondrial dysfunction preceded plasma membrane damage. The addition of nicotinamide, a radical scavenger and inhibitor of the DNA repair enzyme poly(ADP-ribose) synthetase protected the islet cells from lysis and partially preserved their mitochondrial activity in the presence of reactive oxygen intermediates. We conclude that activation of the endothelial enzyme xanthine oxidase, known to be induced by mediators of immune cells or by episodes of ischaemia and reperfusion causes islet cell damage with subsequent cell death in early phases of pancreatic islet cell destruction.

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On radical production by PMA-stimulated neutrophils as monitored by luminol-amplified chemiluminescence

Cited by 31 publications

References 27 publications

Noninvasive assessment of localized inflammatory responses

Noninvasive assessment of localized inflammatory responses

Electrochemical characterization and application of azurin-modified gold electrodes for detection of superoxide

Oxygen radicals generated by the enzyme xanthine oxidase lyse rat pancreatic islet cells in vitro

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