Molecular mechanisms of selenocystine protective effects against methylmercury-induced cell damage in human HepG2 cells

Methylmercury (MeHg) has been recognized as a very toxic contaminant present in certain foodstuffs that adversely affects health and impairs the normal function of different organs. Experimental studies have shown that selenocompounds play an important role as cellular detoxificant and protective agents against the harmful effects of mercury. The present study examined the potential preventive activities of organic selenocompounds, focused on selenocystine (SeCys), against MeHg-induced toxicity in human HepG2 cells. Combined treatment of SeCys and MeHg protected HepG2 cells against MeHg-induced cell damage, showing this selenocompound a more relevant effect than those of selenium methylselenocysteine and selenium methionine. Co-treatment with SeCys exerted a protective effect against MeHg by restraining ROS generation and glutathione decrease, and through the modulation of antioxidant enzymes activities. In addition, SeCys delayed MeHg-induced apoptosis and prevented extracellular regulated kinases (ERKs) deactivation, as well as p38 and c-Jun N-terminal kinase (JNK) stimulations in comparison to MeHg-treated cells. ERK, JNK and p38 involvement on the protective effect of SeCys against MeHg-induced cell damage was confirmed by using selective inhibitors. All these results indicate that SeCys protects against MeHg-induced cell damage by modulating the redox status and key proteins related to cell stress and survival/proliferation pathways. 2013 Elsevier Ltd. All rights reserved.

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Bibliographic Details
Main Authors: Cordero Herrera, Isabel, Cuello, Susana, Goya, Luis, Madrid, Yolanda, Bravo, Laura, Cámara, Carmen, Ramos, Sonia
Other Authors: Ministerio de Ciencia e Innovación (España)
Format: artículo biblioteca
Language:English
Published: Elsevier 2013
Subjects:Selenocystine, Cell death, HepG2 cells, Antioxidant and detoxificant defences, Methylmercury,
Online Access:http://hdl.handle.net/10261/88116
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/100012818
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