Elaboration and use of nickel planar macrocyclic complex-based sensors for the direct electrochemical measurement of nitric oxide in biological media

Bedioui, Féthi; Trevin, Stéphane; Dvynck, Jacques; Lantoine, Frédérique; Brunet, Annie; Devynck, Marie‐Aude

doi:10.1016/s0956-5663(97)85338-9

Cited by 97 publications

(47 citation statements)

References 36 publications

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“…The identification of NO as the molecule responsible for the amperometric signal induced by histamine was assessed by inhibition of NO synthase by 1 mmol/L L-NMMA, as previously published. 23,24 In agreement with previous data obtained with the same electrode system, 22 NO oxidation at 37°C in PBS gave a dose-dependent, linear current response over the 5 to 50 nmol/L concentration range ( Figure 1). Similar electrochemical responses to NO were observed in the absence or presence of 60 g/mL 7-ketocholesterol, indicating the absence of a direct interaction between 7-ketocholesterol and NO (Figure 1).…”

Section: Measurement Of No Productionsupporting

confidence: 91%

“…To directly evaluate the concentrations of NO actually released by endothelial cells, we used a nickel porphyrin-and Nafion-coated carbon microfiber electrode that allows detection of low NO levels. 22,23,[32][33][34][35] Experiments of NO release were conducted on histamine-stimulated HUVECs, an experimental system in which the release of NO has been well documented. 24,25,34,35 The real-time measurement of NO by electrochemical detection revealed for the first time that both 7-ketocholesterol and 7␤-hydroxycholesterol directly reduced the amounts of NO released by stimulated HUVECs.…”

Section: Discussionmentioning

confidence: 99%

“…23 The sensitivity of electrodes varied from 0.7 to 2.7 nmol/L NO per pA (meanϮSD, 1.8Ϯ0.4 nmol/L NO per pA, nϭ6) with a detection limit varying from 4 to 6 nmol/L NO. The identification of NO as the molecule responsible for the amperometric signal induced by histamine was assessed by inhibition of NO synthase by 1 mmol/L L-NMMA, as previously published.…”

Section: Measurement Of No Productionmentioning

confidence: 99%

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Inhibition by Cholesterol Oxides of NO Release From Human Vascular Endothelial Cells

Deckert

Brunet

Lantoine

et al. 1998

ATVB

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Abstract-Recent studies have demonstrated that, unlike cholesterol, cholesterol oxidized at position 7 can reduce the maximal endothelium-dependent relaxation of isolated rabbit aortas (Circulation. 1997;95:723-731). The aim of the current study was to determine whether cholesterol oxides reduce the release of nitric oxide (NO) from human umbilical vein endothelial cells (HUVECs). The amount of NO released by histamine-stimulated HUVECs was determined by differential pulse amperometry using a nickel porphyrin-and Nafion-coated carbon microfiber electrode. The effects of cholesterol (preserved from oxidation by butylated hydroxytoluene), 7-ketocholesterol, 7␤-hydroxycholesterol, 5␣,6␣-epoxycholesterol, 19-hydroxycholesterol (60 g/mL), and ␣-lysophosphatidylcholine (10 g/mL) were compared. Pretreatment of HUVECs with cholesterol, 5␣,6␣-epoxycholesterol, or 19-hydroxycholesterol did not alter histamineactivated NO production. In contrast, pretreatment with 7-ketocholesterol or 7␤-hydroxycholesterol significantly decreased NO release. The inhibitory effect of 7-ketocholesterol was time and dose dependent and was maintained in the presence of L-arginine. In the absence of serum, lysophosphatidylcholine also reduced NO production. In ionomycin-stimulated cells, pretreatment with 7-ketocholesterol did not inhibit NO release. These results demonstrate that cholesterol derivatives oxidized at the 7 position, the main products of low density lipoprotein oxidation, reduce histamine-activated NO release in HUVECs. Such an inhibitory effect of cholesterol oxides may account, at least in part, for the ability of oxidized low density lipoprotein to reduce the endothelium-dependent relaxation of arteries. Key Words: human endothelial cells Ⅲ cholesterol oxides Ⅲ histamine Ⅲ NO production T he endothelium of blood vessels regulates vascular tone by releasing endothelium-derived relaxing and contracting factors.1-3 In particular, it has now been clearly established that the endothelium-dependent relaxation of arteries induced by acetylcholine or histamine involves the release of endothelium-derived relaxing factor, 1,4 identified as NO. 5,6 Recent studies have demonstrated that alterations in vascular reactivity can be associated with cardiovascular disorders [7][8][9][10] and that arteries from hypercholesterolemic and atherosclerotic patients exhibit marked attenuation of endothelium-dependent relaxation. 7,11,12 Although the impairment of arterial relaxation at an early stage of the atherosclerotic process may constitute a crucial step in disease progression, the related molecular mechanisms remain unclear. Several studies have demonstrated that LDLs, rather than native LDLs, can mimic the impairment of arterial relaxation observed in hyperlipidemia. [13][14][15][16] Whereas in some previous studies the inhibition of endothelium-dependent relaxation was attributed to LPC, 14,15,17 other studies did not support this view. 16,18 In particular, no significant relationship between the LPC content of LDLs and their ability to reduc...

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Section: Measurement Of No Productionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Measurement Of No Productionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition by Cholesterol Oxides of NO Release From Human Vascular Endothelial Cells

Deckert

Brunet

Lantoine

et al. 1998

ATVB

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“…Electrochemical NO-sensing electrodes allow for real-time detection of NO with high sensitivity and selectivity [11][12][13][14] . However, as the signal amplitude and sensitivity of electrochemical sensors are generally proportional to the electroactive surface area of the electrodes 13 , it is often difficult to simultaneously achieve high sensitivity and high-spatial resolution.…”

mentioning

confidence: 99%

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

et al. 2013

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Real-time monitoring of nitric oxide concentrations is of central importance for probing the diverse roles of nitric oxide in neurotransmission, cardiovascular systems and immune responses. Here we report a new design of nitric oxide sensors based on hemin-functionalized graphene field-effect transistors. With its single atom thickness and the highest carrier mobility among all materials, graphene holds the promise for unprecedented sensitivity for molecular sensing. The non-covalent functionalization through p-p stacking interaction allows reliable immobilization of hemin molecules on graphene without damaging the graphene lattice to ensure the highly sensitive and specific detection of nitric oxide. Our studies demonstrate that the graphene-hemin sensors can respond rapidly to nitric oxide in physiological environments with a sub-nanomolar sensitivity. Furthermore, in vitro studies show that the graphene-hemin sensors can be used for the detection of nitric oxide released from macrophage cells and endothelial cells, demonstrating their practical functionality in complex biological systems.

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“…Direct detection of NO is performed through the oxidation of NO on the surface of a working electrode producing Faradaic redox current [168]. Metallophthalocyanine and metalloporphyrins are preferred in electrochemistry among the widely used catalyst metal complexes of porphyrins [190][191][192][193][194] and phthalocyanines [195][196][197][198], due to their similarity and to the metalloporphyrins' mimicking the properties of the naturally occurring metalloporphyrin complexes. They enable NO detection even at concentrations in the nM range [168].…”

Section: No Detection and Interaction Studiesmentioning

confidence: 99%

ATR-FTIR Spectroscopy of Membrane Bound Ras Protein

Adıgüzel¹,

Güldenhaupt²,

Kötting³

et al. 2007

GBM Annual Spring Meeting Mosbach 2007

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Elaboration and use of nickel planar macrocyclic complex-based sensors for the direct electrochemical measurement of nitric oxide in biological media

Cited by 97 publications

References 36 publications

Inhibition by Cholesterol Oxides of NO Release From Human Vascular Endothelial Cells

Inhibition by Cholesterol Oxides of NO Release From Human Vascular Endothelial Cells

Real-time electrical detection of nitric oxide in biological systems with sub-nanomolar sensitivity

ATR-FTIR Spectroscopy of Membrane Bound Ras Protein

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