NDLI: Diphenyl diselenide improves the antioxidant response via activation of the Nrf-2 pathway in macrophage cells.

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Diphenyl diselenide improves the antioxidant response via activation of the Nrf-2 pathway in macrophage cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mancini, Gianni Raniel Straliotto, Marcos da Rocha, João Batista Texeira de Bem, Andreza Fabro
Description	Author Affiliation: Mancini G ( Universidade Federal de Santa Catarina (Centro de Ciências Biológicas), Departamento de Bioquimica, Brasil. Electronic address: gianni.mancini@gmail.com.); Raniel Straliotto M ( Universidade Federal de Santa Catarina (Centro de Ciências Biológicas), Departamento de Bioquimica, Brasil.); da Rocha JB ( Universidade Federal de Santa Maria (Centro de Ciências Biológicas), Departamento de Bioquímica, Brasil.); de Bem AF ( Universidade Federal de Santa Catarina (Centro de Ciências Biológicas), Departamento de Bioquimica, Brasil.)
Abstract	Diphenyl diselenide [(PhSe)2] is an organoselenium compound that can mimic endogenous antioxidant enzymes, such as glutathione peroxidase (GPx), or be metabolized by thioredoxin reductase to form selenol intermediate, which can copy the function of the antioxidant selenoenzymes. This compound has shown potential role in preventing atherosclerosis and other oxidative stress-related diseases. The understanding of the underlying mechanism by which (PhSe)2 modulates the glutathione-related antioxidant defenses is a relevant question. Therefore, we tested its ability to promote the nuclear translocation of the nuclear factor (erythroid 2-like)-related factor 2 (Nrf-2), increasing the expression of enzymes related to the antioxidant system, such as heme oxygenase 1 (HO-1) and peroxiredoxin 1 (Prx-1), in addition to the main enzyme in the glutathione synthesis - gamma glutamylcysteine synthetase (?-GCS) - in murine J774 macrophage cells. (PhSe)2 (1µM) was able to promote nuclear translocation and increased the expression of the Nrf-2 factor in the nucleus in a time-dependent manner (1-24hours). In addition, this compound significantly increased the expression of HO-1 and Prx-1 at 24hours and GPx-1 after the first hour. Furthermore, (PhSe)2 was able to enhance GSH levels in a time-dependent manner, as well as GPx and GGCS activities. The increase in GPx and GGCS activities was dependent on the activation of PI3K, JNK, and p38MAPKs signaling pathways that may activate the Nrf2 factor. Altogether, these results show that (PhSe)2 improved the antioxidant defense by increasing the expression of HO-1 and Prx-1 and the synthesis of GSH as a consequence of the activation and nuclear translocation of Nrf-2 factor.
File Format	HTM / HTML
ISSN	08915849
Issue Number	Suppl 1
Journal	Free Radical Biology and Medicine
Volume Number	75
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2014-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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