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Biometals. 2006 Jun;19(3):237-44.

Cytochrome c oxydase subunit I gene is up-regulated by cadmium in freshwater and marine bivalves.

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Laboratoire d'Ecophysiologie et d'Ecotoxicologie des Systèmes Aquatiques (LEESA), Université Bordeaux1/UMR CNRS 5805, Place du Dr. Peyneau, 33120 Arcachon, France.


Inhibition of the mitochondrial electron transfer chain and induction of reactive oxygen species (ROS) production are one of the roots of cadmium (Cd) toxicity. To appreciate the impact of Cd on mitochondria, we focused on the expression of CoxI gene which encodes the subunit I of the Cytochrome c oxidase (complex IV of the respiratory chain). CoxI gene expression was studied by real-time quantitative PCR in three species: two freshwater bivalves (Corbicula fluminea and Dreissena polymorpha) and one marine bivalve (diploid or triploid Crassostrea gigas). Bivalves were exposed for 10 or 14 days to 0.13 microM Cd(2+) and 15.3 microM Zn(2+) in controlled laboratory conditions. We demonstrate that in the three mollusk species CoxI gene was up-regulated by Cd. Zinc (Zn), which is known to have antioxidant properties, had no effect on CoxI gene expression. In the presence of Cd and Zn, CoxI gene inducibility was lower than after a single Cd exposure, in each species; result that could not be fully explained by a decreased Cd accumulation. CoxI gene induction by Cd was 4.8-fold higher in triploid oysters than in diploid ones, indicating a possible influence of triploidy on animal responses to Cd contamination.

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