The effect of α-Tocopherol on monocyte proatherogenic activity

Ishwarlal Jialal, Sridevi Devaraj, Nalini Kaul

Research output: Contribution to journalArticle

84 Citations (Scopus)

Abstract

Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. α-Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 iu/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1β and TNF-α release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor κB. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F2-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.

Original languageEnglish (US)
JournalJournal of Nutrition
Volume131
Issue number2
StatePublished - 2001
Externally publishedYes

Fingerprint

Tocopherols
tocopherols
monocytes
Monocytes
Atherosclerosis
tumor necrosis factors
interleukin-1
atherosclerosis
Interleukin-1
Lipids
adhesion
lipid peroxidation
Tumor Necrosis Factor-alpha
F2-Isoprostanes
Integrin alpha4beta1
Arachidonate 5-Lipoxygenase
atherogenesis
protein kinase C
lipoxygenase
endothelium

Keywords

  • α-tocopherol
  • Antioxidant
  • Inflammation
  • Monocytes
  • Vitamin E

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Jialal, I., Devaraj, S., & Kaul, N. (2001). The effect of α-Tocopherol on monocyte proatherogenic activity. Journal of Nutrition, 131(2).

The effect of α-Tocopherol on monocyte proatherogenic activity. / Jialal, Ishwarlal; Devaraj, Sridevi; Kaul, Nalini.

In: Journal of Nutrition, Vol. 131, No. 2, 2001.

Research output: Contribution to journalArticle

Jialal, I, Devaraj, S & Kaul, N 2001, 'The effect of α-Tocopherol on monocyte proatherogenic activity', Journal of Nutrition, vol. 131, no. 2.
Jialal, Ishwarlal ; Devaraj, Sridevi ; Kaul, Nalini. / The effect of α-Tocopherol on monocyte proatherogenic activity. In: Journal of Nutrition. 2001 ; Vol. 131, No. 2.
@article{98c3f3c5703749179e650c9df723d4a7,
title = "The effect of α-Tocopherol on monocyte proatherogenic activity",
abstract = "Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. α-Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 iu/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1β and TNF-α release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor κB. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F2-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.",
keywords = "α-tocopherol, Antioxidant, Inflammation, Monocytes, Vitamin E",
author = "Ishwarlal Jialal and Sridevi Devaraj and Nalini Kaul",
year = "2001",
language = "English (US)",
volume = "131",
journal = "Journal of Nutrition",
issn = "0022-3166",
publisher = "American Society for Nutrition",
number = "2",

}

TY - JOUR

T1 - The effect of α-Tocopherol on monocyte proatherogenic activity

AU - Jialal, Ishwarlal

AU - Devaraj, Sridevi

AU - Kaul, Nalini

PY - 2001

Y1 - 2001

N2 - Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. α-Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 iu/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1β and TNF-α release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor κB. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F2-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.

AB - Atherosclerosis is the leading cause of morbidity and mortality in Westernized populations. The monocyte is a crucial cell in the genesis of the atherosclerotic lesion and is present during all stages of atherosclerosis. α-Tocopherol (AT) is the most active component of the vitamin E family and is the principal and most potent lipid-soluble antioxidant in plasma and LDL. With regard to monocyte function, AT supplementation (1200 iu/d) has been shown to decrease release of reactive oxygen species, lipid oxidation, release of cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and decrease adhesion of monocytes to human endothelium. The mechanism of inhibition of superoxide and lipid oxidation by monocytes appears to be via inhibition of protein kinase C (PKC), the decrease in IL-1β and TNF-α release by inhibition of 5-lipoxygenase and the inhibition of monocyte-endothelial cell adhesion via decrease in adhesion molecules on monocytes, CD11b and VLA-4 and by decreasing DNA-binding activity of nuclear transcription factor κB. Thus, in addition to the decrease in oxidative stress resulting from AT supplementation, as evidenced by decreased F2-isoprostanes and LDL oxidizability, AT is anti-inflammatory and exerts beneficial antiatherogenic effects on cells crucial in atherogenesis such as monocytes.

KW - α-tocopherol

KW - Antioxidant

KW - Inflammation

KW - Monocytes

KW - Vitamin E

UR - http://www.scopus.com/inward/record.url?scp=0035150318&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035150318&partnerID=8YFLogxK

M3 - Article

VL - 131

JO - Journal of Nutrition

JF - Journal of Nutrition

SN - 0022-3166

IS - 2

ER -