Little is known of the antioxidant role of selenium (Se) in aquatic invertebrates. We investigated the effects of Se on mercury-induced DNA damage in haemocytes from Mytilus edulis using alkaline single cell gel electrophoresis, that is, the Comet assay. The basal percentage tail DNA value for mussel haemocytes was 9.8+/-0.2% (mean+/-S.E.M., n=70). Exposing mussels to Hg(2+) (nominal concentration 20 microgL(-1)) for three days led to an increase in tail DNA to 61.1+/-1.8% (n=10). With added Se (as selenite, nominal concentration 4 microgL(-1)), Hg-induced DNA damage was reduced to 39.5+/-3.1% (n=10). Se pre-exposure also provided some protection against Hg-induced DNA damage (% tail DNA=51.0+/-2.9%, n=10). Basal glutathione peroxidase (GPx) activity in cell-free haemolymph was 93.7+/-3.5 nmol min(-1)mg(-1) (mean+/-S.E.M., n=70). Increases in GPx activity were seen when Se was added during and/or after exposure to Hg. For example, a 3-4-fold increase was seen after three days exposure to Hg in the presence of added Se. Interestingly GPx activity doubled after three days in the presence of added Se alone, but was unchanged after exposure to HgCl(2) alone. These results suggest that the availability of Se in the natural environment could affect the antioxidant status of mussels, and consequently could affect levels of DNA damage.
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http://dx.doi.org/10.1016/j.aquatox.2007.05.009 | DOI Listing |
J Occup Health
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Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
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Department of Biology, Hamilton College, Clinton, NY, USA.
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Section on DNA Repair, Laboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
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Department of Veterinary Medicine, University of Teramo, Via Renato Balzarini 1, 64100, Teramo, Italy.
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European Research Institute for the Biology of Ageing, University Medical Center Groningen, Groningen, Netherlands.
While the effect of amplification-induced oncogene expression in cancer is known, the impact of copy-number gains on "bystander" genes is less understood. We create a comprehensive map of dosage compensation in cancer by integrating expression and copy number profiles from over 8000 tumors in The Cancer Genome Atlas and cell lines from the Cancer Cell Line Encyclopedia. Additionally, we analyze 17 cancer open reading frame screens to identify genes toxic to cancer cells when overexpressed.
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