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Circulation. 2004;110:3715-3720
Published online before print November 29, 2004, doi: 10.1161/01.CIR.0000149747.82157.01
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(Circulation. 2004;110:3715-3720.)
© 2004 American Heart Association, Inc.


Vascular Medicine

Prenatal Environmental Tobacco Smoke Exposure Promotes Adult Atherogenesis and Mitochondrial Damage in Apolipoprotein E–/– Mice Fed a Chow Diet

Zhen Yang, MD; Cynthia A. Knight, BS; Madonna M. Mamerow, MS; Kasey Vickers, BS; Arthur Penn, PhD; Edward M. Postlethwait, PhD; Scott W. Ballinger, PhD

From the Division of Molecular and Cellular Pathology, Department of Pathology (Z.Y., C.A.K., K.V., S.W.B.), and Department of Environmental Health Sciences, School of Public Health (E.M.P.), University of Alabama at Birmingham; Department of Human Ecology, Division of Nutritional Sciences, University of Texas at Austin (M.M.M.); and School of Veterinary Medicine, Louisiana State University, Baton Rouge (A.P.).

Correspondence to Scott W. Ballinger, PhD, Division of Molecular and Cellular Pathology, VH G019F, 1530 3rd Ave S, Birmingham, AL 35294-0019. E-mail sballing{at}path.uab.edu

Received May 19, 2004; revision received August 12, 2004; accepted September 9, 2004.

Background— Environmental tobacco smoke (ETS) exposure is recognized as a cardiovascular disease risk factor; however, the impact of prenatal ETS exposure on adult atherogenesis has not been examined. We hypothesized that in utero ETS exposure promotes adult atherosclerotic lesion formation and mitochondrial damage.

Methods and Results— Atherosclerotic lesion formation, mitochondrial DNA damage, antioxidant activity, and oxidant load were determined in cardiovascular tissues from adult apolipoprotein E–/– mice exposed to either filtered air or ETS in utero and fed a standard chow diet (4.5% fat) from weaning until euthanasia. All parameters were significantly altered in male mice exposed in utero to ETS.

Conclusions— These data support the hypothesis that prenatal ETS exposure is sufficient to promote adult cardiovascular disease development.


Key Words: smoking • mitochondria • pregnancy • prenatal exposure delayed effects • atherosclerosis




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