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Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oestrogens in the modulation of adaptive response to stress

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Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oestrogens in the modulation of adaptive response to stress

Abstract

There is increasing evidence that reactive oxygen species (ROS) are not only toxic but play an important role in cellular signalling and in the regulation of gene expression. We, here, discuss two examples of improved adaptive response to an altered cellular redox state. First, differences in longevity between males and females may be explained by a higher expression of antioxidant enzymes in females resulting in a lower yield of mitochondrial ROS. Oestrogens are made responsible for these phenomena. Oestradiol induces glutathione peroxidase-1 and MnSOD by processes requiring the cell surface oestrogen receptor (ER) and the activation of pathways usually involved in oxidative stress response. Second, oxygen radicals produced during moderate exercise as performed during training up-regulate the expression of antioxidant enzymes in muscle cells. An increased level of these enzymes might prevent oxidative damage during exhaustive exercise and should, therefore, not be prevented by antioxidants. The relevance of these findings is discussed in the context with observations made in transgenic animals overexpressing MnSOD or catalase.
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Title
Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oestrogens in the modulation of adaptive response to stress
Author(s)
Vina, Jose; Borras, Consuelo; Gomez-Cabrera, Mari-Carmen; Orr, William C.
Journal
Free Radical Research , Volume 40 (2) Informa Healthcare – Jan 1, 2006
Publisher
Informa UK Ltd
Copyright
© 2006 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted
Subject
Original
ISSN
1071-5762
eISSN
1029-2470
D.O.I.
10.1080/10715760500405778
Publisher site
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