Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): implications for foam cell formation in atherosclerosis

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Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL) : implications for foam cell formation in atherosclerosis. / Ismael, Fahd O; Proudfoot, Julie M; Brown, Bronwyn E; van Reyk, David M; Croft, Kevin D; Davies, Michael Jonathan; Hawkins, Clare L.

In: Archives of Biochemistry and Biophysics, Vol. 573, 05.2015, p. 40-51.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Ismael, FO, Proudfoot, JM, Brown, BE, van Reyk, DM, Croft, KD, Davies, MJ & Hawkins, CL 2015, 'Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): implications for foam cell formation in atherosclerosis', Archives of Biochemistry and Biophysics, vol. 573, pp. 40-51. https://doi.org/10.1016/j.abb.2015.03.008

APA

Ismael, F. O., Proudfoot, J. M., Brown, B. E., van Reyk, D. M., Croft, K. D., Davies, M. J., & Hawkins, C. L. (2015). Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): implications for foam cell formation in atherosclerosis. Archives of Biochemistry and Biophysics, 573, 40-51. https://doi.org/10.1016/j.abb.2015.03.008

Vancouver

Ismael FO, Proudfoot JM, Brown BE, van Reyk DM, Croft KD, Davies MJ et al. Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): implications for foam cell formation in atherosclerosis. Archives of Biochemistry and Biophysics. 2015 May;573:40-51. https://doi.org/10.1016/j.abb.2015.03.008

Author

Ismael, Fahd O ; Proudfoot, Julie M ; Brown, Bronwyn E ; van Reyk, David M ; Croft, Kevin D ; Davies, Michael Jonathan ; Hawkins, Clare L. / Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL) : implications for foam cell formation in atherosclerosis. In: Archives of Biochemistry and Biophysics. 2015 ; Vol. 573. pp. 40-51.

Bibtex

@article{1bfa88745bb2441cb36ce10aff4d68e3,
title = "Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): implications for foam cell formation in atherosclerosis",
abstract = "Atherosclerosis is characterised by the accumulation of lipids within macrophages in the artery wall. Low-density lipoprotein (LDL) is the source of this lipid, owing to the uptake of oxidised LDL by scavenger receptors. Myeloperoxidase (MPO) released by leukocytes during inflammation produces oxidants that are implicated in atherosclerosis. Modification of LDL by the MPO oxidant hypochlorous acid (HOCl), results in extensive lipid accumulation by macrophages. However, the reactivity of the other major MPO oxidant, hypothiocyanous acid (HOSCN) with LDL is poorly characterised, which is significant given that thiocyanate is the favoured substrate for MPO. In this study, we comprehensively compare the reactivity of HOCl and HOSCN with LDL, and show key differences in the profile of oxidative damage observed. HOSCN selectively modifies Cys residues on apolipoprotein B100, and oxidises cholesteryl esters resulting in formation of lipid hydroperoxides, 9-hydroxy-10,12-octadecadienoic acid (9-HODE) and F2-isoprostanes. The modification of LDL by HOSCN results macrophage lipid accumulation, though generally to a lesser extent than HOCl-modified LDL. This suggests that a change in the ratio of HOSCN: HOCl formation by MPO from variations in plasma thiocyanate levels, will influence the nature of LDL oxidation in vivo, and has implications for the progression of atherosclerosis.",
author = "Ismael, {Fahd O} and Proudfoot, {Julie M} and Brown, {Bronwyn E} and {van Reyk}, {David M} and Croft, {Kevin D} and Davies, {Michael Jonathan} and Hawkins, {Clare L}",
note = "Copyright {\circledC} 2015. Published by Elsevier Inc.",
year = "2015",
month = "5",
doi = "10.1016/j.abb.2015.03.008",
language = "English",
volume = "573",
pages = "40--51",
journal = "Archives of Biochemistry and Biophysics",
issn = "0003-9861",
publisher = "Academic Press",

}

RIS

TY - JOUR

T1 - Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL)

T2 - implications for foam cell formation in atherosclerosis

AU - Ismael, Fahd O

AU - Proudfoot, Julie M

AU - Brown, Bronwyn E

AU - van Reyk, David M

AU - Croft, Kevin D

AU - Davies, Michael Jonathan

AU - Hawkins, Clare L

N1 - Copyright © 2015. Published by Elsevier Inc.

PY - 2015/5

Y1 - 2015/5

N2 - Atherosclerosis is characterised by the accumulation of lipids within macrophages in the artery wall. Low-density lipoprotein (LDL) is the source of this lipid, owing to the uptake of oxidised LDL by scavenger receptors. Myeloperoxidase (MPO) released by leukocytes during inflammation produces oxidants that are implicated in atherosclerosis. Modification of LDL by the MPO oxidant hypochlorous acid (HOCl), results in extensive lipid accumulation by macrophages. However, the reactivity of the other major MPO oxidant, hypothiocyanous acid (HOSCN) with LDL is poorly characterised, which is significant given that thiocyanate is the favoured substrate for MPO. In this study, we comprehensively compare the reactivity of HOCl and HOSCN with LDL, and show key differences in the profile of oxidative damage observed. HOSCN selectively modifies Cys residues on apolipoprotein B100, and oxidises cholesteryl esters resulting in formation of lipid hydroperoxides, 9-hydroxy-10,12-octadecadienoic acid (9-HODE) and F2-isoprostanes. The modification of LDL by HOSCN results macrophage lipid accumulation, though generally to a lesser extent than HOCl-modified LDL. This suggests that a change in the ratio of HOSCN: HOCl formation by MPO from variations in plasma thiocyanate levels, will influence the nature of LDL oxidation in vivo, and has implications for the progression of atherosclerosis.

AB - Atherosclerosis is characterised by the accumulation of lipids within macrophages in the artery wall. Low-density lipoprotein (LDL) is the source of this lipid, owing to the uptake of oxidised LDL by scavenger receptors. Myeloperoxidase (MPO) released by leukocytes during inflammation produces oxidants that are implicated in atherosclerosis. Modification of LDL by the MPO oxidant hypochlorous acid (HOCl), results in extensive lipid accumulation by macrophages. However, the reactivity of the other major MPO oxidant, hypothiocyanous acid (HOSCN) with LDL is poorly characterised, which is significant given that thiocyanate is the favoured substrate for MPO. In this study, we comprehensively compare the reactivity of HOCl and HOSCN with LDL, and show key differences in the profile of oxidative damage observed. HOSCN selectively modifies Cys residues on apolipoprotein B100, and oxidises cholesteryl esters resulting in formation of lipid hydroperoxides, 9-hydroxy-10,12-octadecadienoic acid (9-HODE) and F2-isoprostanes. The modification of LDL by HOSCN results macrophage lipid accumulation, though generally to a lesser extent than HOCl-modified LDL. This suggests that a change in the ratio of HOSCN: HOCl formation by MPO from variations in plasma thiocyanate levels, will influence the nature of LDL oxidation in vivo, and has implications for the progression of atherosclerosis.

U2 - 10.1016/j.abb.2015.03.008

DO - 10.1016/j.abb.2015.03.008

M3 - Journal article

VL - 573

SP - 40

EP - 51

JO - Archives of Biochemistry and Biophysics

JF - Archives of Biochemistry and Biophysics

SN - 0003-9861

ER -

ID: 134719417