Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Young, Lindon H.; Chen, Qian; Weis, Margaret T.

doi:10.5099/aj110100040

Cited by 8 publications

(9 citation statements)

References 32 publications

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“…Due to the limited availability of sensors and instrument limitations, controls and treatments were limited to two biological replicates (n = 2). Extracellular H 2 O 2 production was monitored continuously for 23 hours in each treatment and control culture using 2 mm H 2 O 2 sensors (World Precision Instruments, Sarasota, FL, USA) with output recorded by TBR4100/1025 Free Radical Analyzer58 (World Precision Instruments) as described in Young et al 59…”

Section: Methodsmentioning

confidence: 99%

Cell cycle arrest and biochemical changes accompanying cell death in harmful dinoflagellates following exposure to bacterial algicide IRI-160AA

Pokrzywinski

Tilney

Warner

et al. 2017

Sci Rep

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Bacteria may play a role in regulating harmful algal blooms, but little is known about the biochemical and physiological changes associated with cell death induced by algicidal bacteria. Previous work characterized an algicidal exudate (IRI-160AA) produced by Shewanella sp. IRI-160 that is effective against dinoflagellates, while having little to no effect on other phytoplankton species in laboratory culture experiments. The objective of this study was to evaluate biochemical changes associated with cell death and impacts on the cell cycle in three dinoflagellate species (Prorocentrum minimum, Karlodinium veneficum and Gyrodinium instriatum) after exposure to IRI-160AA. In this study, IRI-160AA induced cell cycle arrest in all dinoflagellates examined. Several indicators for programmed cell death (PCD) that are often observed in phytoplankton in response to a variety of stressors were also evaluated. Cell death was accompanied by significant increases in DNA degradation, intra- and extracellular ROS concentrations and DEVDase (caspase-3 like) protease activity, which have been associated with PCD in other phytoplankton species. Overall, results of this investigation provide strong evidence that treatment with the bacterial algicide, IRI-160AA results in cell cycle arrest and induces biochemical changes consistent with stress-related cell death responses observed in other phytoplankton.

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Section: Methodsmentioning

confidence: 99%

Cell cycle arrest and biochemical changes accompanying cell death in harmful dinoflagellates following exposure to bacterial algicide IRI-160AA

Pokrzywinski

Tilney

Warner

et al. 2017

Sci Rep

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“…Thereafter, one limb was subjected to ischemia/ reperfusion, while the other limb was used as a non-ischemic sham control in the same rat. The H 2 O 2 or NO microsensors (100 µm, World Precision Instruments [WPI] Inc., Sarasota, FL) were connected to a free radical analyzer (Apollo 4000, WPI Inc.) and inserted into a 24 gauge catheter placed inside each femoral vein, as previously described by Perkins et al [8] and reviewed by Young et al [26]. Ischemia in one hind limb was induced by clamping the femoral artery/vein for 20 min followed by 45 min of reperfusion.…”

Section: Hind Limb Ischemia/reperfusion In Vivo Proceduresmentioning

confidence: 99%

Apocynin Exerts Dose-Dependent Cardioprotective Effects by Attenuating Reactive Oxygen Species in Ischemia/Reperfusion

Chen¹,

C²,

Devine³

et al. 2016

Cardiovasc Pharm Open Access

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Ischemia/reperfusion results in cardiac contractile dysfunction and cell death partly due to increased reactive oxygen species and decreased endothelial-derived nitric oxide bioavailability. NADPH oxidase normally produces reactive oxygen species to facilitate cell signalling and differentiation; however, excessive release of such species following ischemia exacerbates cell death. Thus, administration of an NADPH oxidase inhibitor, apocynin, may preserve cardiac function and reduce infarct size following ischemia. Apocynin dose-dependently (40 μM, 400 μM and 1 mM) attenuated leukocyte superoxide release by 87 ± 7%. Apocynin was also given to isolated perfused hearts after ischemia, with infarct size decreasing to 39 ± 7% (40 μM), 28 ± 4% (400 μM; p < 0.01) and 29 ± 6% (1 mM; p < 0.01), versus the control's 46 ± 2%. This decrease correlated with improved final post-reperfusion left ventricular end-diastolic pressure, which decreased from 60 ± 5% in control hearts to 56 ± 5% (40 µM), 43 ± 4% (400 μM; p < 0.01) and 48 ± 5% (1 mM; p < 0.05), compared to baseline. Functionally, apocynin (13.7 mg/kg, I.V.) significantly reduced H 2 O 2 by nearly four-fold and increased endothelial-derived nitric oxide bioavailability by nearly four-fold during reperfusion compared to controls (p < 0.01), which was confirmed in in vivo rat hind limb ischemia/reperfusion models. These results suggest that apocynin attenuates ischemia/reperfusion-induced cardiac contractile dysfunction and infarct size by inhibiting reactive oxygen species release from NADPH oxidase.

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“…Prior to baseline measurement, experimental animals received a single dose of triacsin C (100 µg/kg) with or without L-NAME (non-selective NOS inhibitor, 30 mg/kg), 1400W (highly selective iNOS inhibitor, 10 µg/kg), or SMTC (a selective nNOS inhibitor, 1.2 mg/kg) while the controls were treated with vehicle (5% DMSO in normal saline). The NO levels during reperfusion were expressed as the relative difference of NO between I/R and sham limb as previously described (38). This technology allows for the real-time measurement of NO in blood [39].…”

Section: Global Cardiac Ischemiamentioning

confidence: 99%

“…Both femoral arteries and veins were exteriorized and NO microsensors (100 μm, World Precision Instruments (WPI) Inc., Sarasota, FL) were inserted into both femoral veins via 24 gauge catheters as previously described [37,38]. Following a 15-minute baseline measurement, one femoral artery/vein was clamped for 20 minutes while the contralateral limb served as the sham control.…”

Section: Global Cardiac Ischemiamentioning

confidence: 99%

Triacsin C, a Fatty Acyl CoA Synthetase Inhibitor, Improves Cardiac Performance Following Global Ischemia

Blakeman¹,

Chen²,

Tolson³

et al. 2012

Am. J. Biomed. Sci.

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The role of fatty acyl CoA synthetase (FACS) in ischemia/reperfusion (I/R) injury has not been well established. Our earlier studies showed that triacsin C, a selective FACS inhibitor, decreases endothelial nitric oxide synthase (eNOS) palmitoylation and increases nitric oxide (NO) in cultured human coronary endothelial cells. In the present study, we tested the hypothesis that triacsin C would reduce infarct size and improve post-reperfusion cardiac function by increasing vascular NO. In isolated rat hearts, triacsin C, given during the first 5 minutes of reperfusion, significantly reduced infarct size and attenuated cardiac dysfunction during reperfusion. N G -nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 50 µM) completely abolished the protective effects of triacsin C. In the ischemic hind limb model, triacsin C significantly increased intravascular NO concentration during reperfusion, an effect that was blocked by L-NAME or S-methyl-L-thiocitrulline (SMTC, a selective neuronal NOS inhibitor), but not by 1400W (a highly selective iNOS inhibitor). Lastly, triacsin C significantly reduced L-NAME induced leukocyte rolling, adhesion, and transmigration in rat mesenteric circulation, as measured by intravital microscopy. In summary, this study provides novel evidence showing that triacsin C reduces myocardial infarct size, attenuates loss of post-reperfusion cardiac function, increases intravascular NO concentration and inhibits leukocyte recruitment. These pharmacologic properties suggest that triacsin C may be useful as an adjunct to Am.

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Direct Measurement of Hydrogen Peroxide (H2O2) or Nitric Oxide (NO) Release: A Powerful Tool to Assess Real-time Free Radical Production in Biological Models

Cited by 8 publications

References 32 publications

Cell cycle arrest and biochemical changes accompanying cell death in harmful dinoflagellates following exposure to bacterial algicide IRI-160AA

Cell cycle arrest and biochemical changes accompanying cell death in harmful dinoflagellates following exposure to bacterial algicide IRI-160AA

Apocynin Exerts Dose-Dependent Cardioprotective Effects by Attenuating Reactive Oxygen Species in Ischemia/Reperfusion

Triacsin C, a Fatty Acyl CoA Synthetase Inhibitor, Improves Cardiac Performance Following Global Ischemia

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