Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells

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Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells. / Lloyd, Mitchell M; Grima, Michael A; Rayner, Benjamin S; Hadfield, Katrina A; Davies, Michael Jonathan; Hawkins, Clare Louise.

In: Free Radical Biology & Medicine, Vol. 65, 12.2013, p. 1352-62.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Lloyd, MM, Grima, MA, Rayner, BS, Hadfield, KA, Davies, MJ & Hawkins, CL 2013, 'Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells', Free Radical Biology & Medicine, vol. 65, pp. 1352-62. https://doi.org/10.1016/j.freeradbiomed.2013.10.007

APA

Lloyd, M. M., Grima, M. A., Rayner, B. S., Hadfield, K. A., Davies, M. J., & Hawkins, C. L. (2013). Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells. Free Radical Biology & Medicine, 65, 1352-62. https://doi.org/10.1016/j.freeradbiomed.2013.10.007

Vancouver

Lloyd MM, Grima MA, Rayner BS, Hadfield KA, Davies MJ, Hawkins CL. Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells. Free Radical Biology & Medicine. 2013 Dec;65:1352-62. https://doi.org/10.1016/j.freeradbiomed.2013.10.007

Author

Lloyd, Mitchell M ; Grima, Michael A ; Rayner, Benjamin S ; Hadfield, Katrina A ; Davies, Michael Jonathan ; Hawkins, Clare Louise. / Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells. In: Free Radical Biology & Medicine. 2013 ; Vol. 65. pp. 1352-62.

Bibtex

@article{915e380fe8054c68a77ef85cf0f36db0,
title = "Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells",
abstract = "In the immune response, hypohalous acids are generated by activated leukocytes via the release of myeloperoxidase and the formation of H2O2. Although these oxidants have important bactericidal properties, they have also been implicated in causing tissue damage in inflammatory diseases, including atherosclerosis. Hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN) are the major oxidants formed by myeloperoxidase under physiological conditions, with the ratio of these oxidants dependent on diet and smoking status. HOCl is highly reactive and causes marked cellular damage, but few data are available on the effects of HOSCN on mammalian cells. In this study, we have compared the actions of HOCl and HOSCN on human coronary artery endothelial cells (HCAEC). HOCl reacts rapidly with the cells, resulting in extensive cell death by both apoptosis and necrosis, with necrosis dominating at higher oxidant doses. In contrast, HOSCN is consumed more slowly, with cell death occurring only by apoptosis. Exposure of HCAEC to HOCl and HOSCN induces changes in mitochondrial membrane permeability, which, in the case of HOSCN, is associated with mitochondrial release of proapoptotic factors, including cytochrome c, apoptosis-inducing factor, and endonuclease G. With each oxidant, apoptosis appears to be caspase-independent, with the inactivation of caspases 3/7 observed, and pretreatment of the cells with the caspase inhibitor Z-VAD-fmk having no effect on the extent of cell death. Loss of cellular thiols, depletion of glutathione, and the inactivation of thiol-dependent enzymes, including glyceraldehyde-3-phosphate dehydrogenase, were seen with both oxidants, though to a much greater extent with HOCl. The ability of myeloperoxidase-derived oxidants to induce endothelial cell apoptosis may contribute to the formation of unstable lesions in atherosclerosis. The results with HOSCN may be particularly significant for smokers, who have elevated plasma levels of SCN(-), the precursor of this oxidant.",
keywords = "Amino Acid Chloromethyl Ketones, Apoptosis, Apoptosis Inducing Factor, Atherosclerosis, Caspase 3, Caspase 7, Caspase Inhibitors, Cell Line, Cell Survival, Coronary Vessels, Cytochromes c, Endodeoxyribonucleases, Endothelial Cells, Glutathione, Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating), Humans, Hydrogen Peroxide, Hypochlorous Acid, Mitochondrial Membranes, Necrosis, Oxidation-Reduction, Permeability, Peroxidase, Sulfhydryl Compounds, Thiocyanates",
author = "Lloyd, {Mitchell M} and Grima, {Michael A} and Rayner, {Benjamin S} and Hadfield, {Katrina A} and Davies, {Michael Jonathan} and Hawkins, {Clare Louise}",
note = "{\circledC} 2013 Elsevier Inc. All rights reserved.",
year = "2013",
month = "12",
doi = "10.1016/j.freeradbiomed.2013.10.007",
language = "English",
volume = "65",
pages = "1352--62",
journal = "Free Radical Biology & Medicine",
issn = "0891-5849",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Comparative reactivity of the myeloperoxidase-derived oxidants hypochlorous acid and hypothiocyanous acid with human coronary artery endothelial cells

AU - Lloyd, Mitchell M

AU - Grima, Michael A

AU - Rayner, Benjamin S

AU - Hadfield, Katrina A

AU - Davies, Michael Jonathan

AU - Hawkins, Clare Louise

N1 - © 2013 Elsevier Inc. All rights reserved.

PY - 2013/12

Y1 - 2013/12

N2 - In the immune response, hypohalous acids are generated by activated leukocytes via the release of myeloperoxidase and the formation of H2O2. Although these oxidants have important bactericidal properties, they have also been implicated in causing tissue damage in inflammatory diseases, including atherosclerosis. Hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN) are the major oxidants formed by myeloperoxidase under physiological conditions, with the ratio of these oxidants dependent on diet and smoking status. HOCl is highly reactive and causes marked cellular damage, but few data are available on the effects of HOSCN on mammalian cells. In this study, we have compared the actions of HOCl and HOSCN on human coronary artery endothelial cells (HCAEC). HOCl reacts rapidly with the cells, resulting in extensive cell death by both apoptosis and necrosis, with necrosis dominating at higher oxidant doses. In contrast, HOSCN is consumed more slowly, with cell death occurring only by apoptosis. Exposure of HCAEC to HOCl and HOSCN induces changes in mitochondrial membrane permeability, which, in the case of HOSCN, is associated with mitochondrial release of proapoptotic factors, including cytochrome c, apoptosis-inducing factor, and endonuclease G. With each oxidant, apoptosis appears to be caspase-independent, with the inactivation of caspases 3/7 observed, and pretreatment of the cells with the caspase inhibitor Z-VAD-fmk having no effect on the extent of cell death. Loss of cellular thiols, depletion of glutathione, and the inactivation of thiol-dependent enzymes, including glyceraldehyde-3-phosphate dehydrogenase, were seen with both oxidants, though to a much greater extent with HOCl. The ability of myeloperoxidase-derived oxidants to induce endothelial cell apoptosis may contribute to the formation of unstable lesions in atherosclerosis. The results with HOSCN may be particularly significant for smokers, who have elevated plasma levels of SCN(-), the precursor of this oxidant.

AB - In the immune response, hypohalous acids are generated by activated leukocytes via the release of myeloperoxidase and the formation of H2O2. Although these oxidants have important bactericidal properties, they have also been implicated in causing tissue damage in inflammatory diseases, including atherosclerosis. Hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN) are the major oxidants formed by myeloperoxidase under physiological conditions, with the ratio of these oxidants dependent on diet and smoking status. HOCl is highly reactive and causes marked cellular damage, but few data are available on the effects of HOSCN on mammalian cells. In this study, we have compared the actions of HOCl and HOSCN on human coronary artery endothelial cells (HCAEC). HOCl reacts rapidly with the cells, resulting in extensive cell death by both apoptosis and necrosis, with necrosis dominating at higher oxidant doses. In contrast, HOSCN is consumed more slowly, with cell death occurring only by apoptosis. Exposure of HCAEC to HOCl and HOSCN induces changes in mitochondrial membrane permeability, which, in the case of HOSCN, is associated with mitochondrial release of proapoptotic factors, including cytochrome c, apoptosis-inducing factor, and endonuclease G. With each oxidant, apoptosis appears to be caspase-independent, with the inactivation of caspases 3/7 observed, and pretreatment of the cells with the caspase inhibitor Z-VAD-fmk having no effect on the extent of cell death. Loss of cellular thiols, depletion of glutathione, and the inactivation of thiol-dependent enzymes, including glyceraldehyde-3-phosphate dehydrogenase, were seen with both oxidants, though to a much greater extent with HOCl. The ability of myeloperoxidase-derived oxidants to induce endothelial cell apoptosis may contribute to the formation of unstable lesions in atherosclerosis. The results with HOSCN may be particularly significant for smokers, who have elevated plasma levels of SCN(-), the precursor of this oxidant.

KW - Amino Acid Chloromethyl Ketones

KW - Apoptosis

KW - Apoptosis Inducing Factor

KW - Atherosclerosis

KW - Caspase 3

KW - Caspase 7

KW - Caspase Inhibitors

KW - Cell Line

KW - Cell Survival

KW - Coronary Vessels

KW - Cytochromes c

KW - Endodeoxyribonucleases

KW - Endothelial Cells

KW - Glutathione

KW - Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)

KW - Humans

KW - Hydrogen Peroxide

KW - Hypochlorous Acid

KW - Mitochondrial Membranes

KW - Necrosis

KW - Oxidation-Reduction

KW - Permeability

KW - Peroxidase

KW - Sulfhydryl Compounds

KW - Thiocyanates

U2 - 10.1016/j.freeradbiomed.2013.10.007

DO - 10.1016/j.freeradbiomed.2013.10.007

M3 - Journal article

C2 - 24120969

VL - 65

SP - 1352

EP - 1362

JO - Free Radical Biology & Medicine

JF - Free Radical Biology & Medicine

SN - 0891-5849

ER -

ID: 128974109