Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/87074
Type: Artigo de periódico
Title: Carotenoids Inhibit Lipid Peroxidation And Hemoglobin Oxidation, But Not The Depletion Of Glutathione Induced By Ros In Human Erythrocytes
Author: Chiste R.C.
Freitas M.
Mercadante A.Z.
Fernandes E.
Abstract: Aims Despite the presence of endogenous antioxidants in erythrocytes, these cells are highly susceptible to oxidative damage and some exogenous antioxidants, such as carotenoids, are able to inhibit the pro-oxidant effect provided by reactive oxygen species. In this study, we evaluated the potential of carotenoids usually detected in human blood plasma (β-carotene, zeaxanthin, lutein, β-cryptoxanthin and lycopene) to prevent the oxidative damage in erythrocytes. Main methods Human erythrocytes were subjected to induced oxidative damage and the following biomarkers of oxidative stress were monitored: lipid peroxidation [induced by tert-butyl hydroperoxide (tBHP) or by 2,2′-azobis (2-methylpropionamidine) dihydrochloride (AAPH)] and AAPH-induced oxidation of hemoglobin and depletion of glutathione. Key findings When tBHP was used to induce lipid peroxidation, lycopene was the most efficient carotenoid (IC50 = 2.2 ± 0.4 μM), while lutein was the most efficient (IC50 = 2.5 ± 0.7 μM) when peroxyl radicals (ROO) were generated by AAPH. In relation to the hemoglobin oxidation induced by AAPH, β-carotene and zeaxanthin were the most efficient antioxidants (IC50 = 2.9 ± 0.3 μM and 2.9 ± 0.1 μM, respectively). Surprisingly β-cryptoxanthin and lycopene did not inhibit hemoglobin oxidation or lipid peroxidation when induced by AAPH, even at the highest tested concentration (3 μM). Additionally, the tested carotenoids did not prevent ROO-mediated GSH depletion and GSSG formation probably due to the lack of interaction between carotenoids (apolar) and glutathione (polar). Significance Our study contributes with important insights that carotenoids may exert therapeutical potential to act as a natural antioxidant to prevent ROO-induced toxicity in human erythrocytes. © 2014 Elsevier Inc.
Editor: 
Rights: fechado
Identifier DOI: 10.1016/j.lfs.2014.01.059
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-84896732745&partnerID=40&md5=d4fd741700f03ea7de89bdb01d4a5f82
Date Issue: 2014
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.