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Utilize este identificador para citar ou criar um link para este item: http://acervodigital.unesp.br/handle/11449/18157
Título: 
Ventricular Remodeling Induced by Tissue Vitamin A Deficiency in Rats
Autor(es): 
Instituição: 
Universidade Estadual Paulista (UNESP)
ISSN: 
1015-8987
Resumo: 
Background/Aims: Experimental studies suggest that vitamin A plays a role in regulating cardiac structure and function. We tested the hypothesis that cardiac vitamin A deficiency is associated with adverse myocardial remodeling in young adult rats. Methods: Two groups of young female rats, control (C - n = 29) and tissue vitamin A deficient (RVA - n = 31), were subjected to transthoracic echocardiography exam, isolated rat heart study and biochemical study. Results: The RVA rats showed a reduced total vitamin A concentration in both the liver and heart [vitamin A in heart, mu mol/kg (C = 0.95 +/- 0.44 and RVA = 0.24 +/- 0.16, p = 0.01)] with the same serum retinol levels (C = 0.73 +/- 0.29 mu mol/L e RVA = 0.62 +/- 0.17 mu mol/L, p = 0.34). The RVA rats showed higher left ventricular diameters and reduced systolic function. The RVA rats also demonstrated increased lipid hydroperoxide/total antioxidant capacity ratio and cardiac levels of IFN-gamma and TNF-alpha but not of metalloproteinase (MMP)-2 and -9 activity. on the other hand, the RVA rats had decreased levels of beta-hydroxyacylcoenzyme A dehydrogenase and lactate dehydrogenase. Conclusions: Tissue vitamin A deficiency stimulated cardiac remodeling and ventricular dysfunction. Additionally, the data support the involvement of oxidative stress, energy metabolism, and cytokine production in this remodeling process. Copyright (C) 2010 S. Karger AG, Basel
Data de publicação: 
1-Jan-2010
Citação: 
Cellular Physiology and Biochemistry. Basel: Karger, v. 26, n. 3, p. 395-402, 2010.
Duração: 
395-402
Publicador: 
Karger
Palavras-chaves: 
  • Inflammation
  • Oxidative stress
  • Energetic metabolism
  • Vitamin A
  • Remodeling
Fonte: 
http://dx.doi.org/10.1159/000320563
Endereço permanente: 
Direitos de acesso: 
Acesso aberto
Tipo: 
outro
Fonte completa:
http://repositorio.unesp.br/handle/11449/18157
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