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Effects of Hg(II) Exposure on MAPK Phosphorylation and Antioxidant System in D. melanogaster
Author(s) -
Paula M. T.,
Zemolin A. P.,
Vargas A. P.,
Golombieski R. M.,
Loreto E. L. S.,
Saidelles A. P.,
Picoloto R. S.,
Flores E. M. M.,
Pereira A. B.,
Rocha J. B. T.,
Merritt T. J. S.,
Franco J. L.,
Posser T.
Publication year - 2014
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21788
Subject(s) - acetylcholinesterase , antioxidant , drosophila melanogaster , glutathione , kinase , superoxide dismutase , p38 mitogen activated protein kinases , mapk/erk pathway , toxicity , phosphorylation , chemistry , protein kinase a , biochemistry , biology , toxicology , enzyme , gene , organic chemistry
The heavy metal mercury is a known toxin, but while the mechanisms involved in mercury toxicity have been well demonstrated in vertebrates, little is known about toxicological effects of this metal in invertebrates. Here, we present the results of our study investigating the effects associated with exposure of fruit fly Drosophila melanogaster to inorganic mercury (HgCl 2 ). We quantify survival and locomotor performance as well as a variety of biochemical parameters including antioxidant status, MAPK phosphorylation and gene expression following mercury treatment. Our results demonstrate that exposure to Hg(II) through diet induced mortality and affected locomotor performance as evaluated by negative geotaxis, in D. melanogaster . We also saw a significant impact on the antioxidant system including an inhibition of acetylcholinesterase (Ache), glutathione S‐transferase (GST) and superoxide dismutase (SOD) activities. We found no significant alteration in the levels of mRNA of antioxidant enzymes or NRF‐2 transcriptional factor, but did detect a significant up regulation of the HSP83 gene. Mercury exposure also induced the phosphorylation of JNK and ERK, without altering p38 MAPK and the concentration of these kinases. In parallel, Hg(II) induced PARP cleavage in a 89 kDa fragment, suggesting the triggering of apoptotic cell death in response to the treatment. Taken together, this data clarifies and extends our understanding of the molecular mechanisms mediating Hg(II) toxicity in an invertebrate model. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 621–630, 2014.