Journal of Clinical Biochemistry and Nutrition
Online ISSN : 1880-5086
Print ISSN : 0912-0009
Original Articles
Dietary açai modulates ROS production by neutrophils and gene expression of liver antioxidant enzymes in rats
Joyce Ferreira da Costa GuerraCíntia Lopes de Brito MagalhãesDaniela Caldeira CostaMarcelo Eustáquio SilvaMaria Lúcia Pedrosa
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Volume 49 (2011) Issue 3 Pages 188-194

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Abstract

Açai (Euterpe oleracea Mart.) has recently emerged as a promising source of natural antioxidants. Because increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the development of diabetic complications and many health claims have been reported for açai, the present study was undertaken to evaluate the possible protective effects of açai on the production of reactive oxygen species by neutrophils and on the liver antioxidant defense system in control and streptozotocin-induced diabetic rats. Diet supplementation with 2% açai was found to increase mRNA levels for gamma-glutamylcysteine synthetase and glutathione peroxidase in liver tissue and to decrease reactive oxygen species production by neutrophils. Compared to control animals, diabetic rats exhibited lower levels of mRNA coding for Zn-superoxide dismutase, glutathione peroxidase and gamma-glutamylcysteine synthetase and higher levels of reactive oxygen species production by neutrophils, thiobarbituric acid-reactive substances and carbonyl proteins in hepatic tissues. Although açai supplementation was not effective in restore gene expression of antioxidant enzymes in diabetic rats, it showed a protective effect, decreasing thiobarbituric acid-reactive substances levels and increasing reduced glutathione content in the liver. These findings suggest that açai can modulate reactive oxygen species production by neutrophils and that it has a significant favorable effect on the liver antioxidant defense system under fisiological conditions of oxidative stress and partially revert deleterious effects of diabetes in the liver.

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© 2011 by The Editorial Secretariat of JCBN
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