Hg(2+) and Cu(2+) interfere with agonist-mediated Ca(2+) signaling in isolated Mytilus digestive gland cells

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The effects of mercury and copper on agonist-mediated Ca-signaling were investigated in isolated cells from the marine mussel: Mytilus galloprovincialis Lam., by single cell fluorescence microscopy. In isolated digestive gland cells, short-term exposure (10 min) to both Hg2+, a highly toxic metal and Cu2+, essential metal, in the nano-low mu M range caused a sustained increase in cytosolic [Ca2+]. The effect of mercury on resting [Ca2+] was stronger than that of copper. The Hg-induced elevation in [Ca2+] seemed to be mainly due to an increased influx through Verapamil-sensitive Ca-channels, whereas the effect of Cu2+ was related to a release from thapsigargin-sensitive intracellular stores. Agonists, such as epidermal growth factor (EGF), bradykinin (BK) and ATP, evoked Ca2+ transients in isolated digestive gland cells through different mechanisms similar to those observed in mammalian cells, demonstrating the presence of common pathways of Ca-mediated cell signaling in both invertebrates and vertebrates. The agonist-mediated Ca2+ response was affected by exposure to Hg2+ and Cu2+ in a concentration dependent manner: both metals significantly reduced the amplitude of the Ca2+ spikes elicited by BK and ATP and decreased the percentage of EGF-responsive cells. The effects of Hg2+ and Cu2+ were apparently independent of their different type of interaction with the mechanisms involved in Ca2+ homeostasis. The results clearly demonstrate that, in marine invertebrate cells, short-term exposure to heavy metal concentrations comparable to environmental exposure levels results in alterations of intracellular Ca2+ homeostasis which compromise the cell response to extracellular stimuli involving Ca-mediated signaling. The mechanisms of heavy metal interference with Ca-homeostasis and signaling are discussed. (C) 2000 Elsevier Science B.V. All rights reserved.

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