Simultaneous monitoring of nitric oxide, oxyhemoglobin and deoxyhemoglobin from small areas of the rat brain by in vivo visible spectroscopy and a least-square approach

Martín, Felipe A; Rojas-Dı́az, David; Luis-García, Ma. Luz; González–Mora, José Luis; Castellano, Miguel A.

doi:10.1016/j.jneumeth.2004.04.036

Cited by 4 publications

(4 citation statements)

References 15 publications

(17 reference statements)

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“…MRE also caused a dose-dependent inhibition of nitric oxide ( Figure 1 ): it is evident a nitric oxide scavenger activity (78.08 ± 3.24% at 200 μ g/mL). It is well known that nitric oxide is involved in many physiological processes and it is also implicated in inflammation, cancer, and other pathological conditions [ 30 , 31 ]. NO has both cytoprotective and cytotoxic role.…”

Section: Resultsmentioning

confidence: 99%

Antioxidant and Proapoptotic Activities ofSclerocarya birrea[(A. Rich.) Hochst.] Methanolic Root Extract on the Hepatocellular Carcinoma Cell Line HepG2

Armentano

Bisaccia

Miglionico

et al. 2015

BioMed Research International

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The main goal of this study was to characterize the in vitro antioxidant activity and the apoptotic potential of S. birrea methanolic root extract (MRE). Among four tested extracts, obtained with different solvents, MRE showed the highest content of polyphenols, flavonoids, and tannins together with antioxidant activities tested with superoxide, nitric oxide, ABTS, and beta-carotene bleaching assays. Moreover, the cytotoxic effect of MRE was evaluated on the hepatocarcinoma cell line HepG2. In these cells, MRE treatment induced apoptosis and generated reactive oxygen species (ROS) in dose-dependent manner. The cytotoxic effect promoted by MRE was prevented by pretreatment of HepG2 cells with N-acetyl-L-cysteine (NAC), suggesting that oxidative stress was pivotal in MRE-mediated cell death. Moreover, we showed that the MRE treatment induced the mitochondrial membrane depolarization and the cytochrome c release from mitochondria into the cytosol. It suggests that the apoptosis occurred in a mitochondrial-dependent pathway. Interestingly, MRE showed a sensibly lower cytotoxicity, associated with a low increase of ROS, in normal human dermal fibroblasts compared to HepG2 cells. It is suggested that the methanolic root extract of S. Birrea is able to selectively increase intracellular ROS levels in cancer cells, promoting cell death.

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Section: Resultsmentioning

confidence: 99%

Antioxidant and Proapoptotic Activities ofSclerocarya birrea[(A. Rich.) Hochst.] Methanolic Root Extract on the Hepatocellular Carcinoma Cell Line HepG2

Armentano

Bisaccia

Miglionico

et al. 2015

BioMed Research International

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“…When macrophages contact a foreign agent or sense a particular stimulus, they might become activated and this process occurs by different pathways [15–17]. Mediators are synthesized or their relative concentration modified, causing abnormal cellular functions [18,19].…”

Section: Introductionmentioning

confidence: 99%

Macrophage activation, phagocytosis and intracellular calcium oscillations induced by scorpion toxins fromTityus serrulatus

Petricevich

Reynaud²,

Cruz³

et al. 2008

Clinical and Experimental Immunology

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SummaryThe research described here is focused upon studying the activation of mice peritoneal macrophages when submitted to in vitro effects of Tityus serrulatus scorpion venom and its major toxic peptides. Several functional events were analysed, such as: cytotoxicity, spreading, extent of phagocytosis, vacuole formation and changes of internal calcium concentration. Among the main results observed, when macrophages are subjected to the effects of soluble venom of Tityus serrulatus scorpion venom, a partially purified fraction (FII) or a pure toxin (Ts1), are an increment in the percentage of phagocytosis and vacuole formation, a decrement of the spreading ability, accompanied by oscillations of internal calcium concentration. The net results demonstrate that scorpion venom or its major toxins are effective stimulators of macrophage activity; the effect of whole soluble venom or partially purified fractions is due to the toxic peptides, seen here clearly with Ts1. The possible involvement of Na + -channels in these events is discussed. A basic understanding of the underlying molecular mechanisms responsible for macrophage activation should serve as a foundation for novel drug development aimed at modulating macrophage activity.

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“…changes in cerebral regions. 29 In vivo microdialysis is accepted as a means to simultaneously estimate NO molecules and hemodynamic parameters in human and rat brains. 30 Cosby et al further demonstrated in human circulation that vasodilation of rat aortic rings and formation of both NO gas and NO-modified hemoglobin resulted from nitrite reductase activity on deoxyhemoglobin and deoxygenated erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…They demonstrated that the infusion of NO is directly associated with dynamic changes in hemoglobin, deoxyhemoglobin, etc. changes in cerebral regions 29 . In vivo microdialysis is accepted as a means to simultaneously estimate NO molecules and hemodynamic parameters in human and rat brains 30 .…”

Section: Discussionmentioning

confidence: 99%

Acute ischemic stroke induces magnetic resonance susceptibility signs dominated by endothelial nitric oxide synthase activation

Chen

Chang

Lin

et al. 2020

Magnetic Resonance in Med

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Purpose: Acute ischemic stroke induces deoxyhemoglobin accumulation around the ischemic region while activating endothelial nitric oxide synthase (eNOS) coupling and the subsequent release of nitric oxide (NO). Because deoxyhemoglobin is a natural NO spin trap, its interplay with NO could be prominent during acute stroke. Its interaction with NO has been shown to induce overt paramagnetic signals in vitro; our goal was to investigate whether this interplay can be detected using MRI. Methods: To verify the in vivo image effects using the deoxyhemoglobin-NO interaction during acute stroke, eNOS states were manipulated in an animal model of acute ischemia, and the susceptibility signals, cerebral perfusion, and infarction were assessed noninvasively via MR susceptibility weighted imaging (SWI). Results: Occlusion of the right middle cerebral artery increased eNOS coupling and susceptibility signals in the ischemic cortex while abolishing regional cerebral blood flow. Pharmacological eNOS blockage led to weakened susceptibility signals in the ischemic cortex as well as worsened tissue survival. Consistently, abolishment of eNOS coupling through genetic editing reduced the regional susceptibility signals in the ischemic cortex, causing large infarcts. Conclusion: Upregulation of eNOS during acute ischemia sustains tissue viability through the interaction between NO and deoxyhemoglobin. This interplay can be traced in vivo using SWI and can be considered a sensitive marker revealing the delicate oxygenation status of the ischemic tissue, therefore, guiding the management of acute stroke in clinical settings.

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Simultaneous monitoring of nitric oxide, oxyhemoglobin and deoxyhemoglobin from small areas of the rat brain by in vivo visible spectroscopy and a least-square approach

Cited by 4 publications

References 15 publications

Antioxidant and Proapoptotic Activities ofSclerocarya birrea[(A. Rich.) Hochst.] Methanolic Root Extract on the Hepatocellular Carcinoma Cell Line HepG2

Antioxidant and Proapoptotic Activities ofSclerocarya birrea[(A. Rich.) Hochst.] Methanolic Root Extract on the Hepatocellular Carcinoma Cell Line HepG2

Macrophage activation, phagocytosis and intracellular calcium oscillations induced by scorpion toxins fromTityus serrulatus

Acute ischemic stroke induces magnetic resonance susceptibility signs dominated by endothelial nitric oxide synthase activation

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