High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase

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High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase. / Morgan, Philip E; Pattison, David I; Talib, Jihan; Summers, Fiona A; Harmer, Jason A; Celermajer, David S; Hawkins, Clare Louise; Davies, Michael Jonathan.

In: Free Radical Biology & Medicine, Vol. 51, No. 9, 01.11.2011, p. 1815-22.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Morgan, PE, Pattison, DI, Talib, J, Summers, FA, Harmer, JA, Celermajer, DS, Hawkins, CL & Davies, MJ 2011, 'High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase', Free Radical Biology & Medicine, vol. 51, no. 9, pp. 1815-22. https://doi.org/10.1016/j.freeradbiomed.2011.08.008

APA

Morgan, P. E., Pattison, D. I., Talib, J., Summers, F. A., Harmer, J. A., Celermajer, D. S., ... Davies, M. J. (2011). High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase. Free Radical Biology & Medicine, 51(9), 1815-22. https://doi.org/10.1016/j.freeradbiomed.2011.08.008

Vancouver

Morgan PE, Pattison DI, Talib J, Summers FA, Harmer JA, Celermajer DS et al. High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase. Free Radical Biology & Medicine. 2011 Nov 1;51(9):1815-22. https://doi.org/10.1016/j.freeradbiomed.2011.08.008

Author

Morgan, Philip E ; Pattison, David I ; Talib, Jihan ; Summers, Fiona A ; Harmer, Jason A ; Celermajer, David S ; Hawkins, Clare Louise ; Davies, Michael Jonathan. / High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase. In: Free Radical Biology & Medicine. 2011 ; Vol. 51, No. 9. pp. 1815-22.

Bibtex

@article{916eb73280ad487c826ecdcaaa11afc8,
title = "High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase",
abstract = "Smokers have an elevated risk of atherosclerosis but the origins of this elevated risk are incompletely defined, though evidence supports an accumulation of the oxidant-generating enzyme myeloperoxidase (MPO) in the inflamed artery wall. We hypothesized that smokers would have a high level of thiocyanate (SCN(-)), a preferred substrate for MPO, which in turn would predispose to thiol oxidation, an established independent risk factor for atherosclerosis. In this study it is shown that on exposure to MPO/H(2)O(2), thiols on plasma proteins from nonsmokers were increasingly oxidized with increasing added SCN(-) concentrations. Plasma from smokers contained significantly higher endogenous levels of SCN(-) than that from nonsmokers (131±31 vs 40±24 μM, P<0.0001). When plasma from smokers and nonsmokers was exposed to MPO/H(2)O(2)-stimulated oxidation, a strong positive correlation (r=0.8139, P<0.0001) between the extent of thiol oxidation and the plasma SCN(-) concentrations was observed. Computational calculations indicate a changeover from HOCl to HOSCN as the major MPO-generated oxidant in plasma, with increasing SCN(-) levels. These data indicate that plasma SCN(-) levels are a key determinant of the extent of thiol oxidation on plasma proteins induced by MPO, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage to proteins in smokers.",
keywords = "Adult, Female, Humans, Male, Oxidation-Reduction, Peroxidase, Smoking, Sulfhydryl Compounds, Thiocyanates",
author = "Morgan, {Philip E} and Pattison, {David I} and Jihan Talib and Summers, {Fiona A} and Harmer, {Jason A} and Celermajer, {David S} and Hawkins, {Clare Louise} and Davies, {Michael Jonathan}",
note = "Copyright {\circledC} 2011 Elsevier Inc. All rights reserved.",
year = "2011",
month = "11",
day = "1",
doi = "10.1016/j.freeradbiomed.2011.08.008",
language = "English",
volume = "51",
pages = "1815--22",
journal = "Free Radical Biology & Medicine",
issn = "0891-5849",
publisher = "Elsevier",
number = "9",

}

RIS

TY - JOUR

T1 - High plasma thiocyanate levels in smokers are a key determinant of thiol oxidation induced by myeloperoxidase

AU - Morgan, Philip E

AU - Pattison, David I

AU - Talib, Jihan

AU - Summers, Fiona A

AU - Harmer, Jason A

AU - Celermajer, David S

AU - Hawkins, Clare Louise

AU - Davies, Michael Jonathan

N1 - Copyright © 2011 Elsevier Inc. All rights reserved.

PY - 2011/11/1

Y1 - 2011/11/1

N2 - Smokers have an elevated risk of atherosclerosis but the origins of this elevated risk are incompletely defined, though evidence supports an accumulation of the oxidant-generating enzyme myeloperoxidase (MPO) in the inflamed artery wall. We hypothesized that smokers would have a high level of thiocyanate (SCN(-)), a preferred substrate for MPO, which in turn would predispose to thiol oxidation, an established independent risk factor for atherosclerosis. In this study it is shown that on exposure to MPO/H(2)O(2), thiols on plasma proteins from nonsmokers were increasingly oxidized with increasing added SCN(-) concentrations. Plasma from smokers contained significantly higher endogenous levels of SCN(-) than that from nonsmokers (131±31 vs 40±24 μM, P<0.0001). When plasma from smokers and nonsmokers was exposed to MPO/H(2)O(2)-stimulated oxidation, a strong positive correlation (r=0.8139, P<0.0001) between the extent of thiol oxidation and the plasma SCN(-) concentrations was observed. Computational calculations indicate a changeover from HOCl to HOSCN as the major MPO-generated oxidant in plasma, with increasing SCN(-) levels. These data indicate that plasma SCN(-) levels are a key determinant of the extent of thiol oxidation on plasma proteins induced by MPO, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage to proteins in smokers.

AB - Smokers have an elevated risk of atherosclerosis but the origins of this elevated risk are incompletely defined, though evidence supports an accumulation of the oxidant-generating enzyme myeloperoxidase (MPO) in the inflamed artery wall. We hypothesized that smokers would have a high level of thiocyanate (SCN(-)), a preferred substrate for MPO, which in turn would predispose to thiol oxidation, an established independent risk factor for atherosclerosis. In this study it is shown that on exposure to MPO/H(2)O(2), thiols on plasma proteins from nonsmokers were increasingly oxidized with increasing added SCN(-) concentrations. Plasma from smokers contained significantly higher endogenous levels of SCN(-) than that from nonsmokers (131±31 vs 40±24 μM, P<0.0001). When plasma from smokers and nonsmokers was exposed to MPO/H(2)O(2)-stimulated oxidation, a strong positive correlation (r=0.8139, P<0.0001) between the extent of thiol oxidation and the plasma SCN(-) concentrations was observed. Computational calculations indicate a changeover from HOCl to HOSCN as the major MPO-generated oxidant in plasma, with increasing SCN(-) levels. These data indicate that plasma SCN(-) levels are a key determinant of the extent of thiol oxidation on plasma proteins induced by MPO, and implicate HOSCN as an important mediator of inflammation-induced oxidative damage to proteins in smokers.

KW - Adult

KW - Female

KW - Humans

KW - Male

KW - Oxidation-Reduction

KW - Peroxidase

KW - Smoking

KW - Sulfhydryl Compounds

KW - Thiocyanates

U2 - 10.1016/j.freeradbiomed.2011.08.008

DO - 10.1016/j.freeradbiomed.2011.08.008

M3 - Journal article

C2 - 21884783

VL - 51

SP - 1815

EP - 1822

JO - Free Radical Biology & Medicine

JF - Free Radical Biology & Medicine

SN - 0891-5849

IS - 9

ER -

ID: 129669499