Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis

Yavuz Cakir, Zhen Yang, Cynthia A. Knight, Melissa Pompilius, David Westbrook, Shannon M. Bailey, Kent E Pinkerton, Scott W. Ballinger

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Environmental tobacco smoke (ETS) exposure and alcohol (EtOH) consumption often occur together, yet their combined effects on cardiovascular disease development are currently unclear. A shared feature between ETS and EtOH exposure is that both increase oxidative stress and dysfunction within mitochondria. The hypothesis of this study was that simultaneous EtOH and ETS exposure will significantly increase atherogenesis and mitochondrial damage compared to the individual effects of either factor (ETS or EtOH). To test this hypothesis, apoE-/- mice were exposed to EtOH and/or ETS singly or in combination for 4 weeks and compared to filtered air, nonalcohol controls. Atherosclerotic lesion formation (oil red O staining of whole aortas), mitochondrial DNA (mtDNA) damage, and oxidant stress were assessed in vascular tissues. Combined exposure to ETS and EtOH had the greatest impact on atherogenesis, mtDNA damage, and oxidant stress compared to filtered air controls, alcohol, or ETS-exposed animals alone. Because moderate EtOH consumption is commonly thought to be cardioprotective, these studies suggest that the potential influence of common cardiovascular disease risk factors, such as tobacco smoke exposure or hypercholesterolemia, on the cardiovascular effects of alcohol should be considered.

Original languageEnglish (US)
Pages (from-to)1279-1288
Number of pages10
JournalFree Radical Biology and Medicine
Volume43
Issue number9
DOIs
StatePublished - Nov 1 2007

Fingerprint

Tobacco
Mitochondrial DNA
Smoke
DNA Damage
Atherosclerosis
Alcohols
Oxidants
Cardiovascular Diseases
Air
Mitochondria
Oxidative stress
Environmental Exposure
Apolipoproteins E
Hypercholesterolemia
Alcohol Drinking
Blood Vessels
Aorta
Animals
Oxidative Stress
Tissue

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry

Cite this

Cakir, Y., Yang, Z., Knight, C. A., Pompilius, M., Westbrook, D., Bailey, S. M., ... Ballinger, S. W. (2007). Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis. Free Radical Biology and Medicine, 43(9), 1279-1288. https://doi.org/10.1016/j.freeradbiomed.2007.07.015

Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis. / Cakir, Yavuz; Yang, Zhen; Knight, Cynthia A.; Pompilius, Melissa; Westbrook, David; Bailey, Shannon M.; Pinkerton, Kent E; Ballinger, Scott W.

In: Free Radical Biology and Medicine, Vol. 43, No. 9, 01.11.2007, p. 1279-1288.

Research output: Contribution to journalArticle

Cakir, Y, Yang, Z, Knight, CA, Pompilius, M, Westbrook, D, Bailey, SM, Pinkerton, KE & Ballinger, SW 2007, 'Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis', Free Radical Biology and Medicine, vol. 43, no. 9, pp. 1279-1288. https://doi.org/10.1016/j.freeradbiomed.2007.07.015
Cakir Y, Yang Z, Knight CA, Pompilius M, Westbrook D, Bailey SM et al. Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis. Free Radical Biology and Medicine. 2007 Nov 1;43(9):1279-1288. https://doi.org/10.1016/j.freeradbiomed.2007.07.015
Cakir, Yavuz ; Yang, Zhen ; Knight, Cynthia A. ; Pompilius, Melissa ; Westbrook, David ; Bailey, Shannon M. ; Pinkerton, Kent E ; Ballinger, Scott W. / Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis. In: Free Radical Biology and Medicine. 2007 ; Vol. 43, No. 9. pp. 1279-1288.
@article{b264ccd29b334cb8af76623aef389a87,
title = "Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis",
abstract = "Environmental tobacco smoke (ETS) exposure and alcohol (EtOH) consumption often occur together, yet their combined effects on cardiovascular disease development are currently unclear. A shared feature between ETS and EtOH exposure is that both increase oxidative stress and dysfunction within mitochondria. The hypothesis of this study was that simultaneous EtOH and ETS exposure will significantly increase atherogenesis and mitochondrial damage compared to the individual effects of either factor (ETS or EtOH). To test this hypothesis, apoE-/- mice were exposed to EtOH and/or ETS singly or in combination for 4 weeks and compared to filtered air, nonalcohol controls. Atherosclerotic lesion formation (oil red O staining of whole aortas), mitochondrial DNA (mtDNA) damage, and oxidant stress were assessed in vascular tissues. Combined exposure to ETS and EtOH had the greatest impact on atherogenesis, mtDNA damage, and oxidant stress compared to filtered air controls, alcohol, or ETS-exposed animals alone. Because moderate EtOH consumption is commonly thought to be cardioprotective, these studies suggest that the potential influence of common cardiovascular disease risk factors, such as tobacco smoke exposure or hypercholesterolemia, on the cardiovascular effects of alcohol should be considered.",
author = "Yavuz Cakir and Zhen Yang and Knight, {Cynthia A.} and Melissa Pompilius and David Westbrook and Bailey, {Shannon M.} and Pinkerton, {Kent E} and Ballinger, {Scott W.}",
year = "2007",
month = "11",
day = "1",
doi = "10.1016/j.freeradbiomed.2007.07.015",
language = "English (US)",
volume = "43",
pages = "1279--1288",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

T1 - Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis

AU - Cakir, Yavuz

AU - Yang, Zhen

AU - Knight, Cynthia A.

AU - Pompilius, Melissa

AU - Westbrook, David

AU - Bailey, Shannon M.

AU - Pinkerton, Kent E

AU - Ballinger, Scott W.

PY - 2007/11/1

Y1 - 2007/11/1

N2 - Environmental tobacco smoke (ETS) exposure and alcohol (EtOH) consumption often occur together, yet their combined effects on cardiovascular disease development are currently unclear. A shared feature between ETS and EtOH exposure is that both increase oxidative stress and dysfunction within mitochondria. The hypothesis of this study was that simultaneous EtOH and ETS exposure will significantly increase atherogenesis and mitochondrial damage compared to the individual effects of either factor (ETS or EtOH). To test this hypothesis, apoE-/- mice were exposed to EtOH and/or ETS singly or in combination for 4 weeks and compared to filtered air, nonalcohol controls. Atherosclerotic lesion formation (oil red O staining of whole aortas), mitochondrial DNA (mtDNA) damage, and oxidant stress were assessed in vascular tissues. Combined exposure to ETS and EtOH had the greatest impact on atherogenesis, mtDNA damage, and oxidant stress compared to filtered air controls, alcohol, or ETS-exposed animals alone. Because moderate EtOH consumption is commonly thought to be cardioprotective, these studies suggest that the potential influence of common cardiovascular disease risk factors, such as tobacco smoke exposure or hypercholesterolemia, on the cardiovascular effects of alcohol should be considered.

AB - Environmental tobacco smoke (ETS) exposure and alcohol (EtOH) consumption often occur together, yet their combined effects on cardiovascular disease development are currently unclear. A shared feature between ETS and EtOH exposure is that both increase oxidative stress and dysfunction within mitochondria. The hypothesis of this study was that simultaneous EtOH and ETS exposure will significantly increase atherogenesis and mitochondrial damage compared to the individual effects of either factor (ETS or EtOH). To test this hypothesis, apoE-/- mice were exposed to EtOH and/or ETS singly or in combination for 4 weeks and compared to filtered air, nonalcohol controls. Atherosclerotic lesion formation (oil red O staining of whole aortas), mitochondrial DNA (mtDNA) damage, and oxidant stress were assessed in vascular tissues. Combined exposure to ETS and EtOH had the greatest impact on atherogenesis, mtDNA damage, and oxidant stress compared to filtered air controls, alcohol, or ETS-exposed animals alone. Because moderate EtOH consumption is commonly thought to be cardioprotective, these studies suggest that the potential influence of common cardiovascular disease risk factors, such as tobacco smoke exposure or hypercholesterolemia, on the cardiovascular effects of alcohol should be considered.

UR - http://www.scopus.com/inward/record.url?scp=34548792321&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548792321&partnerID=8YFLogxK

U2 - 10.1016/j.freeradbiomed.2007.07.015

DO - 10.1016/j.freeradbiomed.2007.07.015

M3 - Article

C2 - 17893041

AN - SCOPUS:34548792321

VL - 43

SP - 1279

EP - 1288

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

IS - 9

ER -