Effects of sulfide exposure history and hemolymph thiosulfate on oxygen-consumption rates and regulation in the hydrothermal vent crab Bythograea thermydron

Abstract

The hydrothermal vent crab Bythograea thermydron is exposed to high environmental concentrations of sulfide and low levels of oxygen for extended periods of time. It has previously been shown that hydrogen sulfide is oxidized to the relatively non-toxic thiosulfate (S2O 3 2− ), which accumulates in the hemolymph. Hemolymph thiosulfate levels in freshly captured crabs vary significantly among crabs from different hydrothermal vent sites as well as between crabs from different microhabitats within the same site. Hemolymph thiosulfate concentrations were not significantly different between crabs captured at the same site 6 mo apart. Hemolymph thiosulfate concentrations ranged from 66 μmol 1−1 in a crab captured at a site with relatively low sulfide venting, to 3206 μmol 1−1 in an individual that was netted from an active “smoker” vent with much higher sulfide exposure. The differences in hemolymph thiosulfate between sites and the stability of hemolymph thiosulfate in crabs captured at the same site at different times suggest that sulfide exposure is significantly different between sites and that this exposure may not vary significantly over the course of a few months. B. thermydron experimentally exposed to sulfide had high levels of thiosulfate in their hemolymph and increased abilities to regulate oxygen consumption in conditions of low oxygen. This enhancement of regulatory abilities suggests that the previously demonstrated increased hemocyaninoxygen (Hc−O2) affinity due to elevated thiosulfate may be adaptive in vivo. Average oxygen-consumption rates were much higher in crabs experimentally exposed to sulfide than in unexposed crabs. Crabs injected with isosmotic thiosulfate did not have increased oxygen-consumption rates as did the sulfide-exposed individuals, but did show a similar reduction in Pc (the critical partial pressure of oxygen at which crabs can no longer regulate oxygen consumption). This suggests that it is the sulfide exposure and/or detoxification rather than the elimination of thiosulfate that causes the increase in metabolic rate. Thiosulfate diffuses into dead crabs and into live crabs exposed to 15 mmol S2O 3 2- l−1, indicating substantial permeability, and yet live crabs are able to eliminate thiosulfate when incubated in sea water containing 1.5 mmol S2O 3 2- l−1, suggesting a process that has an active component.