Effect of antioxidants on induction time of luminol luminescence elicited by 3-morpholinosydnonimine (SIN-1)

Pascual, Carlos; Reinhart, Konrad

doi:10.1002/(sici)1522-7243(199903/04)14:2<83::aid-bio517>3.0.co;2-w

Cited by 13 publications

(3 citation statements)

References 24 publications

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“…To study the antioxidant properties of the different single crystal surfaces we used a modification of a method described earlier. 18,19 The peroxynitrite donor 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1; Cayman Chemical, Ann Arbor, MI) was used as a cell-free ROS donor. SIN-1 spontaneously degrades to produce the oxygen free radicals superoxide anion and nitric oxide which rapidly react to form peroxynitrite (ONOO -).…”

Section: Surface Interaction With Ros Generated By Sin-1mentioning

confidence: 99%

Titanate biomaterials with enhanced antiinflammatory properties

Contreras

Sahlin

Frangos

2006

J Biomedical Materials Res

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While titanium implants are generally recognized as having excellent biocompatibility, the mechanistic basis for this has yet to be established. We previously demonstrated that TiO2, found on surfaces of titanium, has antioxidant properties that degrade the reactive oxygen species (ROS) which mediate the inflammatory response. We hypothesized that the antioxidant mechanism was similar to that known to mediate photocatalysis by titanium oxides. Specifically, we investigated whether the electronic or valence state of the surface titanium atoms mediates the catalytic degradation of ROS. Surface Ti(IV) atoms in TiO2 and SrTiO3 single crystal substrates were converted into Ti(III) while maintaining the bulk crystalline structure by vacuum annealing or Niobium doping. The degradation of both chemically-induced and neutrophil-derived ROS were significantly increased by changing the valence state of surface titanium. These results suggest that titanium-mediated degradation of ROS is through a catalytic mechanism. Furthermore, we describe a series of novel biomaterials that have antioxidant properties superior to those of titanium.

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Section: Surface Interaction With Ros Generated By Sin-1mentioning

confidence: 99%

Titanate biomaterials with enhanced antiinflammatory properties

Contreras

Sahlin

Frangos

2006

J Biomedical Materials Res

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“…To study the antioxidative properties of different surface coatings, we used a modified version of a method described earlier. 12,13 The peroxynitrite donor 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1; Cayman Chemical, Ann Arbor, MI) was used as a cell-free ROS donor. Forty microliter of 25 mM SIN-1 in dimethyl sulfoxide (DMSO; Sigma-Aldrich, St Louis, MO) was added to 960 L Dulbecco's phosphate-buffered saline (DPBS; Mediatech, Herndon, VA) containing 50 M luminol (Sigma-Aldrich).…”

Section: Surface Interaction With Ros Generated By Sin-1mentioning

confidence: 99%

Anti‐inflammatory properties of micropatterned titanium coatings

Sahlin

Contreras

Gaskill

et al. 2005

J Biomedical Materials Res

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Prolonged inflammation and reactive oxygen species (ROS) generated around an implanted biosensor are the primary causes of the foreign body response, including encapsulation of biosensor membranes. We have previously demonstrated that TiO2 surfaces reduce ROS. Here we investigated the potential of using the anti-inflammatory properties of TiO2 in the design of biosensor membranes with improved long-term in vivo transport properties. Micropatterned Ti films were sputtered onto quartz surfaces in a series of hexagonally distributed dots with identical coverage area of 23% and dot size ranging from 5 to 100 microm. The antioxidant effect of the surfaces was investigated using a cell-free peroxynitrite donor assay and assays of superoxide released from stimulated surface-adhering neutrophils and macrophages. In all three assays, the amount of ROS was monitored using luminol-amplified chemiluminescence. Patterned surfaces in all experimental models significantly decreased ROS compared to the etched surfaces. In the cell-free experiment, the ROS reduction was only dependent on fractional surface coverage. In the cell experiments, however, a dot-size-dependent ROS reduction was seen, with the largest reduction at the smallest dot-size surfaces. These results indicate that micropatterned surfaces with small dots covering only 23% of the surface area exhibit similar antioxidative effect as fully covered surfaces.

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“…In AD brain, the level of 3-nitrotyrosine is elevated markedly [9] and the elevation of 3-nitrotyrosine correlates positively with decreased cognitive functions of AD patients [12]. Moreover, uric acid (UA), a proposed endogenous ONOO ) scavenger [13][14][15], is decreased in a manner consistent with the increases of 3-nitrotyrosine [9]. ONOO ) induces tau nitration and thus inhibits its microtubule-binding activity in neuroblastoma N2a cell [16].…”

Section: Introductionmentioning

confidence: 98%

Melatonin arrests peroxynitrite‐induced tau hyperphosphorylation and the overactivation of protein kinases in rat brain

Yin¹,

Liu²,

Xu³

et al. 2006

Journal of Pineal Research

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The purpose of this study was to examine the in vivo effect of melatonin (MEL) on peroxynitrite-induced tau hyperphosphorylation and the involvement of glycogen synthase kinase-3beta (GSK-3beta) and mitogen-activated protein kinase (MAPK) families. Melatonin was injected into the right cerebroventricle of the rats 1 hr before the bilateral hippocampal injection of 3-morpholino-sydnonimine chloride (SIN-1), the recognized donor of peroxynitrite. Thereafter, the phosphorylation level of tau and the activity of the kinases were analyzed. The injection of SIN-1 induced hyperphosphorylation of tau at pS396 epitope with a concomitant activation of GSK-3beta and selective MAPK isoforms including p38alpha, p38beta, and p38delta but not p38gamma. The effect of peroxynitrite was confirmed using uric acid, a recognized scavenger of peroxynitrite. Preinjection of MEL significantly arrested the peroxynitrite-induced hyperphosphorylation of tau and the activation of GSK-3beta and MAPKs. Melatonin also ameliorated peroxynitrite-induced oxidative stress. We conclude that MEL can efficiently arrest peroxynitrite-induced tau hyperphosphorylation, and the underlying mechanism may involve scavenging the reactive species and suppressing the activated GSK-3beta and p38 MAPK family.

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Effect of antioxidants on induction time of luminol luminescence elicited by 3-morpholinosydnonimine (SIN-1)

Cited by 13 publications

References 24 publications

Titanate biomaterials with enhanced antiinflammatory properties

Titanate biomaterials with enhanced antiinflammatory properties

Anti‐inflammatory properties of micropatterned titanium coatings

Melatonin arrests peroxynitrite‐induced tau hyperphosphorylation and the overactivation of protein kinases in rat brain

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