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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 359879, 9 pages
http://dx.doi.org/10.1155/2012/359879
Research Article

Biomarkers of Adverse Response to Mercury: Histopathology versus Thioredoxin Reductase Activity

1Research Institute for Medicines and Pharmaceutical Sciences (iMed.UL), Faculty of Pharmacy, University of Lisbon, Avenue Professor Gama Pinto, 1649-003 Lisbon, Portugal
2Marine Environment and Biodiversity Unit, Institute for Sea and Atmospheric Research (IPIMAR/IPMA), Avenue Brasília, 1440-006 Lisbon, Portugal
3Aquaculture Unit, Institute for Sea and Atmospheric Research (IPIMAR/IPMA), Avenue Brasília, 1440-006 Lisbon, Portugal
4Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 17177 Stockholm, Sweden

Received 20 April 2012; Accepted 25 May 2012

Academic Editor: João B.T. Rocha

Copyright © 2012 Vasco Branco et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Exposure to mercury is normally assessed by measuring its accumulation in hair, blood or urine. Currently, the biomarkers of effect that have been proposed for mercurials, such as coproporphyrines or oxidative stress markers, are not sensitive enough and lack specificity. Selenium and selenoproteins are important targets for mercury and thioredoxin reductase (TrxR) in particular was shown to be very sensitive to mercury compounds both in vitro and in vivo. In this study we looked into the relation between the inhibition of thioredoxin reductase (TrxR) activity and histopathological changes caused by exposure to mercurials. Juvenile zeabra-seabreams were exposed to Hg2+ or MeHg for 28 days and histopathological changes were analyzed in the liver and kidney as well as TrxR activity. Both mercurials caused histopathological changes in liver and kidney, albeit Hg2+ caused more extensive and severe lesions. Likewise, both mercurials decreased TrxR activity, being Hg2+ a stronger inhibitor. Co-exposure to Hg2+ and Se fully prevented TrxR inhibition in the liver and reduced the severity of lesions in the organ. These results show that upon exposure to mercurials, histopathological alterations correlate with the level of TrxR activity and point to the potential use of this enzyme as a biomarker of mercury toxicity.