scholarly journals Effect of 7-nitroindazoleon superoxide production and MnSOD activity in threat brain following kainate-induced neurotoxicity

2008 ◽  
Vol 60 (1) ◽  
pp. 25-32
Author(s):  
Lidija Radenovic
Keyword(s):  
Time Course ◽  
Neurological Diseases ◽  
Brain Structures ◽  
Brain Regions ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Mnsod Activity ◽  
Font Color

We investigated the effect of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on superoxide concentration as well its influence on mitochondrial MnSOD activity since this activity is associated with the production of reactive oxygen species after kainate-induced neurotoxicity. The time course of in vivo oxidative damage in different brain regions was investigated. Measurements were performed at different times (5 min, 15 min, 2 h, 48 h, and 7 days) in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. Our results indicated that 7-NI had no statistically significant influence on superoxide concentrations in the tested brain structures compared to the control values. However, superoxide concentrations after kainate-induced neurotoxicity returned to the control values after pretreatment with 7-NI in all tested brain structures. Regarding the activity of MnSOD, our results demonstrated statistically significant increase 7 days after intrahippocampal KA treatment in all tested brain structures after pretreatment with 7-NI. The obtained results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS150330033E">10.2298/ABS150330033E</a><u></b></font>

scholarly journals Retraction: 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor in vivo prevents kainate-induced intrahippocampal neurotoxicity. Radenovic L, Selakovic V, Bozic B. Arch Biol Sci. 2005;57(2)75-81. DOI: 10.2298/ABS0502075R

2016 ◽  
Vol 68 (3) ◽  
pp. 691-691
Author(s):  
E Editorial
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Nitrite Concentration ◽  
Nitric Oxide Synthase Inhibitor ◽  
Retracted Article ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Font Color

The article: 7-Nitroindazole, a selective neuronal nitric oxide synthase inhibitor in vivo prevents kainate-induced intrahippocampal neurotoxicity. Radenovic L, Selakovic V, Bozic B. Arch Biol Sci. 2005;57(2)75-81, repeats data already published in: 7-Nitroindazole reduces nitrite concentration in rat brain after intrahippocampal kainate-induced seizure. Radenovic L, Vasiljevic I, Selakovic V, Jovanovic M. Comp Biochem Physiol Pt. C. 2003;135 443-50, without any referencing. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0502075R">10.2298/ABS0502075R</a></b></u>

scholarly journals 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitore in vivo, prevents kainate-induced intrahippocampal neurotoxicity

2005 ◽  
Vol 57 (2) ◽  
pp. 75-81 ◽  
Author(s):  
Lidija Radenovic ◽  
Vesna Selakovic ◽  
Biljana Bozic
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neurological Diseases ◽  
Neuronal Nitric Oxide Synthase ◽  
Nitrite Accumulation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Kainic Acid Injection ◽  
Synthase Inhibitor ◽  
Oxide Synthase

We investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. 7-nitroindazole can effectively inhibit NO synthesis in rat brain after kainate-induced neurotoxicity and suppressed nitrite accumulation. The present results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS160412036E">10.2298/ABS160412036E</a><u></b></font>

Abstract 18060: TRAIL Promotes Angiogenesis and Ischemia-Induced Neovascularisation via NOX4, H2O2 and Nitric Oxide-Dependent Mechanisms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Belinda A Di Bartolo ◽  
Sian P Cartland ◽  
Leonel Prado-Lourenco ◽  
Nor Saadah M Azahri ◽  
Thuan Thai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiogenic Factor ◽  
Tubule Formation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Therapeutic Implications ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
First Time

Background: Angiogenesis and neovascularization are essential processes that follow ischemia insults. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) not only induces endothelial cell (EC) death and inhibits angiogenesis, but also promotes EC migration, invasion and proliferation in vitro . These seemingly opposite effects make its role in angiogenesis in vivo unclear. Using TRAIL -/- and wild-type mice, we sought to determine the role of TRAIL in angiogenesis and neovascularisation. We also sought mechanisms in vitro . Methods and Results: Reduced vascularisation assessed by real-time in vivo 3D Vevo ultrasound imaging and CD31 staining was observed in TRAIL -/- mice 28 d after hindlimb ischemia. Moreover, reduced capillary formation and increased apoptosis was evident in TRAIL -/- muscles even at 3 d after ischemic surgery. We have previously shown that fibroblast growth factor-2 (FGF-2), a potent angiogenic factor, regulates TRAIL gene expression in vascular smooth muscle cells. Indeed, FGF-2 also regulates TRAIL expression in ECs, and FGF-2-inducible proliferation, migration and tubule formation was inhibited with siRNA targeting TRAIL. Notably, both FGF-2 and TRAIL significantly increased NOX4 expression. TRAIL-inducible angiogenic activity in ECs was inhibited with siRNAs targeting NOX4, and consistent with these, NOX4 mRNA was reduced in 3 d ischemic hindlimbs of TRAIL -/- mice. TRAIL stimulated intracellular H 2 O 2 levels in ECs, and TRAIL-inducible proliferation, migration and tubule formation was inhibited with not only PEG-catalase, a H 2 O 2 scavenger, but also blocked with L-NAME, a nitric oxide synthase inhibitor. Conclusions: This is the first demonstration showing that TRAIL promotes angiogenesis in vivo . We show for the first time that the TRAIL stimulates NOX4 expression to mediate nitric oxide-dependent angiogenic effects. This has significant therapeutic implications such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with CVD and diabetes.

Nitric oxide synthase inhibition reverses arteriolar hyporesponsiveness to catecholamines in septic rats

1993 ◽  
Vol 264 (2) ◽  
pp. H660-H663 ◽  
Author(s):  
S. M. Hollenberg ◽  
R. E. Cunnion ◽  
J. Zimmerberg
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cecal Ligation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Norepinephrine Concentration ◽  
Synthase Inhibitor ◽  
The Right ◽  
Oxide Synthase ◽  
Concentration Response Curve

Induction of nitric oxide synthase by cytokines has been hypothesized as a mechanism of the hyporesponsiveness to catecholamines that occurs in clinical septic shock. We measured responses of resistance arterioles in rat cremaster muscle to topically suffused norepinephrine in vivo with the use of image-shearing videomicroscopy. Rats made septic by cecal ligation and puncture were compared with controls that underwent sham ligation. The norepinephrine concentration-response curve was shifted to the right in septic rats [50% effective concentration (EC50) 9.1 +/- 5.4 vs. 0.10 +/- 0.02 microM, P < 0.05]. Contractions at doses of 10(-9), 10(-8), and 10(-7) M norepinephrine were 26, 41, and 38%, respectively, of sham controls. Superfusion of the muscle with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine at 100 microM restored the arteriolar responsiveness of the septic rats (EC50 0.14 +/- 0.07 vs. 6.8 +/- 3.1 microM, P < 0.05). This effect was reversed with superfusion of excess (1 mM) L-arginine. These experiments demonstrate impaired vasoconstriction in response to norepinephrine in resistance arterioles of septic rats in vivo. NG-monomethyl-L-arginine reversed this hyporesponsiveness, implying that nitric oxide synthase may mediate the decreased catecholamine responsiveness associated with sepsis.

In vivo production of nitric oxide correlates with NMDA-induced cerebral hyperemia in newborn sheep

1995 ◽  
Vol 269 (1) ◽  
pp. H215-H221 ◽  
Author(s):  
F. J. Northington ◽  
J. R. Tobin ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Nitric Oxide Synthase Inhibitor ◽  
Oxide Production ◽  
Adenosine Receptor Agonist ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Hydrogen Clearance

Stimulation of N-methyl-D-aspartate (NMDA) receptors in brain increases nitric oxide production in vitro. We tested the hypothesis that nitric oxide participates in the increase in local cerebral blood flow (CBF) caused by infusion of NMDA in anesthetized newborn sheep. We used the combined hydrogen clearance and microdialysis technique for simultaneous measurement of local CBF, infusion of drugs, and measurement of interstitial levels of L-[14C]citrulline in the parietal cortex. Release of L-[14C]citrulline into the dialysate during continuous infusion of L-[14C]arginine was used as a marker of nitric oxide production in vivo. Citrulline recovery and CBF were measured hourly during a 4-h infusion of cerebrospinal fluid containing either 1) no additional drugs, 2) 1 mM NMDA, 3) 1 mM NG-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor), 4) 1 mM NMDA + 1 mM L-NAME, 5) 0.1 mM 2-chloroadenosine (adenosine receptor agonist), or 6) 0.1 mM 2-chloroadenosine + 1 mM L-NAME. At 240 min of perfusion, CBF (ml.min-1.100 g-1; means +/- SE) was as follows: control 52 +/- 3, NMDA 116 +/- 11, L-NAME 32 +/- 5, NMDA+L-NAME 40 +/- 4,2-chloroadenosine 201 +/- 63, and 2-chloroadenosine+L-NAME 129 +/- 18. Citrulline recovery (fmol/min) at 240 min of perfusion was as follows: control 38 +/- 12, NMDA 149 +/- 21, L-NAME 9 +/- 1, NMDA+L-NAME 39 +/- 5, 2-chloroadenosine 13 +/- 5, and 2-chloroadenosine+L-NAME 17 +/- 1.(ABSTRACT TRUNCATED AT 250 WORDS)

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