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Organisms, such as the mussel Geukensia demissa, that inhabit high-sulfide sediments have mechanisms that impede sulfide poisoning of aerobic respiration. Oxygen consumption rates (nO2) of excised ciliated gills from freshly collected G. demissa were stimulated 3-fold at sulfide concentrations between 200 and 500 μM and remained stimulated at 1000 μM. Maintenance of mussels in sulfide-free conditions resulted in less stimulation of gill nO2 at &lt;500 μM sulfide and inhibition between 500 and 1000 {mu}M sulfide. Gills of Mytilus galloprovincialis from a sulfide-free environment were inhibited by {ge}200 μM sulfide. These results indicate that sulfide stimulation of nO2 may be correlated to environmental exposure to sulfide. Serotonin, a neurohormonal stimulant of ciliary beating, further increased sulfide-stimulated nO2, possibly in support of energy demand. Sulfide-stimulated nO2 was negligible in boiled gills and was 61% inhibited by cyanide, implicating the participation of mitochondrial electron flux. Mitochondrial cytochromes c and oxidase oxidation/ reduction state changed little at &lt;500 μM sulfide, but reduction occurred at 500-2000 μM sulfide, suggesting that although cytochrome oxidation/reduction state may be regulated in the face of increased electron flux, regulation may fail at inhibitory sulfide levels. Sulfide-stimulated nO2 may represent a detoxification mechanism in G. demissa.

Sulfide-Stimulation of Oxygen Consumption Rate and Cytochrome Reduction in Gills of the Estuarine Mussel Geukensia demissa