Formation of nanomolar concentrations of S-nitroso-albumin in human plasma by nitric oxide

Marley, Richard; Patel, Rakesh P.; Orie, Nelson N.; Ceaser, Erin K.; Darley‐Usmar, Victor; Moore, Kevin

doi:10.1016/s0891-5849(01)00627-x

Cited by 97 publications

(60 citation statements)

References 37 publications

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“…Nitrosothiols (RSNOs) may be formed by the reaction of • NO with thiol groups 25 (present in cysteine, homocysteine, and glutathione residues), and its concentration depends on the synthesis of • NO 45 . Nitrosothiols act promoting vasodilation and inhibition of platelet aggregation 45 .…”

Section: Discussionmentioning

confidence: 99%

“…Measurement of total S-nitrosothiols was performed according to Marley et al 25 with modifications. Aliquots of 500 µL of previously prepared plasma were double injected into the purge vessel of the • NO analyzer (NOA TM280 ) containing 16 mL of glacial acetic acid, 4 mL of KI 50 mg/mL, 1000 µL of decanol (antifoam agent), and 400 µL of CuSO 4 200 mM (this solution was exchanged every 8 injections).…”

Section: Methodsmentioning

confidence: 99%

“…Aliquots of 500 µL of previously prepared plasma were double injected into the purge vessel of the • NO analyzer (NOA TM280 ) containing 16 mL of glacial acetic acid, 4 mL of KI 50 mg/mL, 1000 µL of decanol (antifoam agent), and 400 µL of CuSO 4 200 mM (this solution was exchanged every 8 injections). The calibration curve was built based on S-nitroso-albumin synthesized according to Marley et al 25 .…”

Section: Methodsmentioning

confidence: 99%

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Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Pereira

Bertolami

Faludi

et al. 2003

Arq. Bras. Cardiol.

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Original ArticleCardiovascular diseases are less prevalent in premenopausal women and in those receiving hormone replacement therapy as compared with postmenopausal women and men 1 . This protective effect is attributed to estrogens, and one of the mechanisms of action may be related to the metabolism of plasma lipoproteins 2 .Estrogens reduce LDL-cholesterol and increase HDLcholesterol 3 . However, these changes in lipid profile only contribute to approximately 25% of the protective effect of estrogens 4 . Other potential mechanisms of action of estrogens may include protection against LDL oxidation 5 , reduction in lipoprotein(a), potentiation of fibrinolysis 6 , and increase in insulin sensitivity. In the arteries, estrogens improve vasodilating function, decrease calcification, secretion of cell adhesion molecules (E-selectin, ICAM-1, and VCAM-1), and formation of atherosclerotic lesions 7 .Direct action of estrogens on the arterial wall has also been demonstrated. The administration of estrogens for prolonged periods inhibits the deposition of cholesterol in the arteries and thickening of the intima in monkeys and rabbits fed an atherogenic diet 8 . However, the mechanisms determining the direct effects of estrogens on the arterial wall have not been completely elucidated. The hemodynamic effects may be partially measured by the activity of estrogens on the synthesis of endothelial nitric oxide 9 . Estrogens have been suggested to possibly improve endothelial function and decrease the risks of atherosclerosis in premenopausal women. Nitric oxide has its bioactivity reduced in postmenopausal women. However, it is not clear whether this occurs due to its lower production by nitric oxide synthase, or whether nitric oxide is inactivated by reaction with the superoxide radical also generated by endothelial cells, forming the peroxynitrite anion (ONOO -), which is a strong oxidizing agent.Peroxynitrite is decomposed into other reactive oxygen species ( fig. 1) 10 and reacts with tyrosine residues of proteins to form nitrotyrosine 11 . Although little is known NOx, nitrotyrosine, COx, CE 18:2 -OOH, and PC-OOH were higher in the postmenopausal period (33.8±22.3 µM; 230±130 nM; 55±19 ng/µL; 17±8.7 nM; 2775±460 nM, respectively) Objective -To assess the effect of endogenous estrogens on the bioavailability of nitric oxide (·NO) and in the formation of lipid peroxidation products in pre-and postmenopausal women. Methods -NOx and S-nitrosothiols were determined by gaseous phase chemiluminescence, nitrotyrosine was determined by ELISA, COx (cholesterol oxides) by gas chromatography, and cholesteryl linoleate hydroperoxides (CE 18:2 -OOH), trilinolein (TG 18:2 -OOH), and phospholipids (PC-OOH) by HPLC in samples of plasma. Results -The concentrations of

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Pereira

Bertolami

Faludi

et al. 2003

Arq. Bras. Cardiol.

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“…The short half-life of NO can be prolonged by reaction with sulfhydryl groups of proteins or low molecular thiols to form more stable, biologically active S-nitrosothiols (23,32). Although the actual concentration in the circulation is debated, S-nitrosothiols are known to be formed in vivo (8,10,17,31,33,39) and are proposed to mediate diverse biological responses (7, 9). Among the circulating S-nitrosothiols, S-nitrosoalbumin is an important species and may act as reservoir of NO (8,31,34,35).…”

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confidence: 99%

Functional characterization of two S-nitroso-l-cysteine transporters, which mediate movement of NO equivalents into vascular cells

Sheng¹,

Whorton²

2007

American Journal of Physiology-Cell Physiology

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Li S, Whorton AR. Functional characterization of two S-nitroso-Lcysteine transporters, which mediate movement of NO equivalents into vascular cells. Am J Physiol Cell Physiol 292: C1263-C1271, 2007. First published November 8, 2006; doi:10.1152/ajpcell.00382.2006.-System L amino acid transporters have been shown to be responsible for cellular uptake of S-nitroso-L-cysteine (L-CSNO). In this study, we examined the characteristics of L-CSNO uptake in Xenopus laevis oocytes expressing system L transporters and found that uptake increased only when both 4F2 heavy chain (4F2HC) and either L-type amino acid transporter 1 (LAT1) or LAT2 light chain were coexpressed. The K m for transport was 57 Ϯ 8 M for 4F2HC-LAT1 and 520 Ϯ 52 M for 4F2HC-LAT2. Vascular endothelial and smooth muscle cells were shown to express transcripts for 4F2HC and for both LAT1 and LAT2. Transport of L-CSNO into red blood cells, endothelial cells, and smooth muscle cells was inhibited by 2-aminobicyclo(2.2.1)heptane-2-carboxylic acid (BCH) and by large neutral amino acids demonstrating functional system L transporters in each cell type. Uptake of L-CSNO led to accumulation of cellular S-nitrosothiols and inhibition of both growth factor-induced ERK phosphorylation and TNF-␣-mediated IB degradation. Similar effects were seen when cells were incubated simultaneously with S-nitrosoalbumin and L-cysteine but not with D-cysteine or with S-nitrosoalbumin alone. In each case, nitrosylation of proteins and cellular responses were blocked by BCH. Together, these data suggest that transmembrane movement of nitric oxide (NO) equivalents from the plasma albumin NO reservoir is mediated by cysteine, which serves as a carrier. The mechanism requires transnitrosylation from S-nitrosoalbumin to free cysteine and activity of system L transporters, thereby providing a unique pathway for cellular responses to S-nitrosoalbumin. nitric oxide; nitrosothiols; system L transporter; endothelial cells; smooth muscle cells; red blood cells NITRIC OXIDE (NO) has been implicated in numerous cellular functions, from vascular smooth muscle relaxation to regulation of gene expression (11,19,26). The short half-life of NO can be prolonged by reaction with sulfhydryl groups of proteins or low molecular thiols to form more stable, biologically active S-nitrosothiols (23,32). Although the actual concentration in the circulation is debated, S-nitrosothiols are known to be formed in vivo (8,10,17,31,33,39) and are proposed to mediate diverse biological responses (7, 9). Among the circulating S-nitrosothiols, S-nitrosoalbumin is an important species and may act as reservoir of NO (8,31,34,35). The physiological roles for S-nitrosoalbumin or mechanisms for transfer of NO equivalents from this circulating S-nitrosoprotein to vascular tissues are not known. However, mobilization of NO bioactivity from S-nitrosoalbumin by low-molecular-weight thiols leads to vasorelaxation (13, 29), and low-molecularweight thiols are involved in the ability of S-nitrosoalbumin to inhibit platelet function...

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“…16 -18 Pharmacodynamic studies have demonstrated a short half-life of Ϸ6 to 7 minutes. 19 In the present randomized double-blind treatment study, we examined the hypothesis that GSNO reduces cerebral embolization, as detected by transcranial Doppler ultrasound, in patients after carotid angioplasty.…”

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confidence: 99%

S -Nitrosoglutathione Reduces Asymptomatic Embolization After Carotid Angioplasty

et al. 2002

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Background-The major complication of carotid angioplasty is embolic stroke, which may occur after balloon inflation and deflation or in the early postintervention period. Platelet adhesion and aggregation to the angioplasty site with subsequent embolization seems to plays a major role in early postangioplasty embolization and stroke. During this period, asymptomatic embolic signals can be detected in patients by transcranial Doppler ultrasound despite aspirin and heparin treatment. S-Nitrosoglutathione (GSNO) is a nitric oxide donor that appears to have relative platelet specificity. We evaluated its effectiveness in reducing embolization after carotid angioplasty. Methods and Results-Sixteen patients undergoing carotid angioplasty and stenting for symptomatic Ն70% internal carotid artery stenosis were randomized in a double-blind manner to GSNO or placebo given after surgery for 90 minutes. All patients were pretreated with aspirin and given heparin for 24 hours after the procedure. Transcranial Doppler recordings were made from the ipsilateral middle cerebral artery for 1 hour before treatment and at 0 to 3, 6, and 24 hours after treatment. GSNO resulted in a rapid reduction in the frequency of embolic signals of 95% at 0 to 3 hours and 100% at 6 hours (Pϭ0.007 and Pϭ0.01 versus placebo, respectively). In the placebo group, 2 patients experienced ipsilateral stroke after the angioplasty. No cerebrovascular events occurred in the GSNO group. Conclusions-S-Nitrosoglutathione

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Formation of nanomolar concentrations of S-nitroso-albumin in human plasma by nitric oxide

Cited by 97 publications

References 37 publications

Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Lipid peroxidation and nitric oxide inactivation in postmenopausal women

Functional characterization of two S-nitroso-l-cysteine transporters, which mediate movement of NO equivalents into vascular cells

S -Nitrosoglutathione Reduces Asymptomatic Embolization After Carotid Angioplasty

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