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First published online August 23, 2004
Journal of Experimental Biology 207, 3369-3380 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01152

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Cadmium-induced apoptosis in oyster hemocytes involves disturbance of cellular energy balance but no mitochondrial permeability transition

I. M. Sokolova^1,,*, S. Evans² and F. M. Hughes^1,

¹ Biology Department, University of North Carolina at Charlotte, 9201 University City Boulevard, Charlotte, NC 28223, USA
² Johnson C. Smith University, 100 Beatties Ford Road, Charlotte, NC 28216, USA

^* Author for correspondence (e-mail: insokolo{at}uncc.edu)

Accepted 18 June 2004

Exposure to environmentally prevalent heavy metals such as cadmium can have detrimental effects on a variety of commercially and ecologically important species such as oysters. Since Cd²⁺ is known to induce apoptosis in immune cells of vertebrates, we have investigated the effects of this metal on isolated oyster hemocytes, the main cellular immune defense in mollusks. Enhanced apoptosis of these cells could conceivably create immunosuppressed conditions in these organisms and result in reduced disease resistance and increased opportunistic infection, resulting in decline of their populations. Cd²⁺ exposure induced apoptosis in oyster hemocytes in a dose-dependent manner in the range of 10-100 µmol l^-1, as indicated by the translocation of phosphatidylserine to the outer leaflet of the plasma membrane. At higher concentrations (200-1000 µmol l^-1), there was no further increase in apoptosis but a significant increase in the level of necrosis. In stark contrast to vertebrate immune cells, there was no decrease in the mitochondrial membrane potential or activation of caspases in response to Cd²⁺ in the apoptotic range. Surprisingly, Cd²⁺ exposure in this range did cause a significant decrease in intracellular ATP levels, indicating a severe disturbance of energy metabolism. Similarly, Cd²⁺ exposure of isolated mitochondria resulted in partial uncoupling of mitochondria but no difference in mitochondrial membrane potential. The results demonstrate that the important environmental pollutant Cd²⁺ induces apoptosis in oyster immune cells and does so through a mitochondria/caspase-independent pathway, suggesting that a novel, perhaps ancient, apoptotic pathway is active in these cells. Furthermore, it appears that the observed decrease in ATP production during apoptosis is not due to the loss of the mitochondrial proton-motive force but is more likely to be due to inhibition of the F₀/F₁-ATPase and/or mitochondrial ADP/ATP or substrate transport.

Key words: cadmium, heavy metal, apoptosis, necrosis, oyster, hemocyte, Crassostrea virginica

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