The aim of this research was to generate data on the mechanisms of toxicity of copper [Cu (4-12 µg/L)] and nickel [Ni (33-40 µg/L)] during continuous sublethal exposure in seawater (32 ppt, 15 °C) in a sensitive test organism (Strongylocentrotus purpuratus) at its most sensitive life stage (developing embryo). Whole-body ions [calcium (Ca), sodium (Na), potassium (K), and magnesium (Mg)], metal burdens, Ca uptake, and Ca ATPase activity were measured every 12 h during the first 72-84 h of development. Ionoregulatory disruption was clearly an important mechanism of toxicity for both metals and occurred with minimal metal bioaccumulation. Most noteworthy was a significant disruption of Ca homeostasis, which was evident from an inhibition of unidirectional Ca uptake rates, whole-body Ca accumulation, and Ca ATPase activity intermittently during 72-84 h of development. At various times, Cu- and Ni-exposed embryos also displayed lower levels of K and increased levels of Na suggesting inhibition of Na/K ATPase activity. Greater levels of Mg during initial stages of development in Cu-exposed embryos were also observed and were considered a possible compensatory mechanism for disruptions to Ca homeostasis because both of these ions are important constituents of the developing spicule. Notably, most of these effects occurred during the initial stages of development but were reversed by 72-84 h. We therefore propose that it is of value to study the toxic impacts of contaminants periodically during development before the traditional end point of 48-72 h.
|Number of pages||12|
|Journal||Archives of Environmental Contamination and Toxicology|
|State||Published - Oct 1 2014|
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