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First published online October 21, 2005
Journal of Experimental Biology 208, 4109-4122 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01867

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Mitochondrial depolarization following hydrogen sulfide exposure in erythrocytes from a sulfide-tolerant marine invertebrate

David Julian^1,2,*, Kelly L. April¹, Shiven Patel¹, Jenny R. Stein¹ and Stephanie E. Wohlgemuth¹

¹ Department of Zoology, University of Florida, Gainesville, FL 32611-8525, USA
² Mount Desert Island Biological Laboratory, Bar Harbor, ME 24533, USA

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

Accepted 25 August 2005

Sulfide-tolerant marine invertebrates employ a variety of mechanisms to detoxify sulfide once it has entered their bodies, but their integumentary, respiratory epithelium and circulatory cells may still be exposed to toxic sulfide concentrations. To investigate whether sulfide exposure is toxic to mitochondria of a sulfide-tolerant invertebrate, we used the fluorescent dyes JC-1 and TMRM to determine the effect of sulfide exposure on mitochondrial depolarization in erythrocytes from the annelid Glycera dibranchiata. In erythrocytes exposed to 0.11-1.9 mmol l^-1 sulfide for 1 h, the dyes showed fluorescence changes consistent with sulfide-induced mitochondrial depolarization. At the highest sulfide concentration, the extent of depolarization was equivalent to that caused by the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP). Even when induced by as little as 0.3 mmol l^-1 sulfide, the depolarization was not reversible over a subsequent 5 h recovery period. The mechanism of toxicity was likely not via inhibition of cytochrome c oxidase (COX), since other COX inhibitors and other mitochondrial electron transport chain inhibitors did not produce similar effects. Furthermore, pharmacological inhibition of the mitochondrial permeability transition pore failed to prevent sulfide-induced depolarization. Finally, increased oxidation of the free radical indicators H₂DCFDA and MitoSOX^TM in erythrocytes exposed to sulfide suggests that sulfide oxidation increased oxidative stress and superoxide production, respectively. Together, these results indicate that sulfide exposure causes mitochondrial depolarization in cells of a sulfide-tolerant annelid, and that this effect, which differs from the actions of other COX inhibitors, may be via increased free radical damage.

Key words: hydrogen sulfide, Glycera dibranchiata, mitochondria, coelomocyte, free radical

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