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ToxSci Advance Access published online on December 30, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfj080
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received August 22, 2005
Accepted December 16, 2005

Systems Toxicology

Beta-Carotene Supplementation Attenuates Cardiac Remodeling Induced by One-Month Tobacco-Smoke Exposure in Rats

Leonardo A. M. Zornoff MD, PhD 1 *, Luiz S. Matsubara MD, PhD 1, Beatriz B. Matsubara MD, PhD 1, Marina P. Okoshi MD, PhD 1, Katashi Okoshi MD, PhD 1, Maeli Dal Pai-Silva PhD 2, Robson F. Carvalho PhD 2, Antonio C. Cicogna MD, PhD 1, Carlos R. Padovani PhD 3, Ethel L. Novelli PhD 4, Rosangela Novo 1, Álvaro O. Campana MD, PhD 1, and Sergio A. R. Paiva MD, PhD 1

1 Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista (UNESP), Botucatu, Brazil
2 Departamento de Morfologia, Instituto de Biociências, Universidade Estadual Paulista (UNESP), Botucatu, Brazil
3 Departamento de Bioestatística, Instituto de Biociências, Universidade Estadual Paulista (UNESP), Botucatu, Brazil
4 Departamento de Bioquímica, Instituto de Biociências, Universidade Estadual Paulista (UNESP), Botucatu, Brazil

* To whom correspondence should be addressed.
Leonardo A. M. Zornoff, E-mail: lzornoff{at}fmb.unesp.br


  Abstract

Objective: The objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC).

Research Methods and Procedures: Rats were allocated into: Air (control, n=13); Air+BC (n=11); ETS (n=11); and BC+ETS (n=9). In Air+BC and BC+ETS, 500 mg of BC were added to the diet. After 3 months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-morten. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables.

Results: ETS presented smaller cardiac output (0.087 ± 0.001 vs. 0.105 ± 0.004 L/min; P=0.007), higher left ventricular diastolic diameter (19.6 ± 0.5 vs. 18.0 ± 0.5 mm/kg; p=0.024), higher left ventricular (2.02 ± 0.05 vs. 1.70 ± 0.03 g/kg; P<0.001) and atrium (0.24 ± 0.01 vs. 0.19 ± 0.01 g/kg; P=0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 ± 0.1 vs. 4.84 ± 0.1 nmol/g tissue; P=0.031) than Air. However, considering those variables, there were no differences between Air and BC+ETS (0.099 ± 0.004 L/min; 19.0 ± 0.5 mm/kg; 1.83 ± 0.04 g/kg; 0.19 ± 0.01 g/kg; 4.88 ± 0.1 nmol/g tissue, respectively; P>0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC+ETS, most fibers showed normal morphological aspects.

Conclusion: One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.

Keywords: beta-carotene; smoking; cardiac function; hypertrophy; ventricular dilation.
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