Article
In vivo interaction between mercury compounds and selenium: effects on thioredoxin reductase and glutathione peroxidase
Free Radical Biology & Medicine
— 2012 — Elsevier
Key information
Authors:
Published in
February 2012
Abstract
Mercury compounds exert toxic effects via interaction with many vital enzymes involved in antioxidant reg- ulation, such as selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (GPx). Selenium supplementation can reactivate the mercury-inhibited TrxR and recover the cell viability in vitro. To gain an insight on how selenium supplementation affects mercury toxicity in vertebrates, we investigated the ef- fects of selenium on the mercury accumulation and TrxR and GPx activities in a fish model. Juvenile zebra- seabreams were exposed either to methylmercury (MeHg) or inorganic mercury (Hg2+) in the presence or absence of sodium selenite (Se) for 28 days followed by 14 days of depuration. Mercury accumulation was found to be 10-fold higher under MeHg exposure than under Hg2+ exposure. Selenium supplementation caused a half decrease of the accumulation of MeHg but did not influence Hg2+ accumulation. Exposure to both mercurials led to a decrease of the activity of TrxR (b50% of control) in all organs. Se supplementation coincident with Hg2+ exposure protected the thioredoxin system in fish liver. However, supplementation of Se during the depuration phase had no effects. The activity of GPx was only affected in the brain of fishes upon the exposure to MeHg and coexposure to MeHg and Se. Selenium supplementation has a limited capac- ity to prevent mercury effects in brain and kidney. These results demonstrate that Se supplementation plays a protective role in a tissue-specific manner and also highlight the importance of TrxR as a main target for mer- curials in vivo.
Publication details
Authors in the community:
João Alfredo Vieira Canário
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Publisher
Elsevier
Title of the publication container
Free Radical Biology & Medicine
First page or article number
781
Last page
793
Volume
52
Issue
4
Fields of Science and Technology (FOS)
biological-sciences - Biological sciences
Publication language (ISO code)
eng - English
Rights type:
Restricted access