The discovery of macrofauna associated with sulfide-emitting deep-sea hydrothermal vents has stimulated research on physiological adaptations to sulfide in aerobic marine organisms. However, sulfide also occurs in marine sediments so that adaptations to sulfide are likely to be a very common phenomenon in the marine environment. The adaptations to sulfide in metazoans from the two types of habitats are discussed in terms of physiological mechanisms with special emphasis on animals without symbiotic sulfur bacteria. The physiological mechanisms are grouped into a hierarchy of sulfide defenses. The ecological implications of sulfide tolerance are discussed in terms of animal distribution and the fauna is suggested divided into sulfide tolerant and sulfide non-tolerant species.

The ecophysiological differences of 4 sibling species of the Capitella capitata species complex from habitats with different sulfide concentrations were studied: Capitella sp. S (small) from a North Sea intertidal flat, living in the upper sediment layer containing low sulfide concentrations (up to 20 pm01 I"); Capltella sp. L (large), sympatric to Capitella sp. S, but living in deeper sediment layers with high sulfide concentrations (up to 350 pm01 1-'1; Capitella sp. M from the Mediterranean Sea from highly sulfid~c sed~rnents (up to 710 pm01 1.') close to shallow hydrothermal vents, and Capitella sp. I from eutrophicated coastal areas of the North Atlantic. Capitella sp. L, Capitella sp. M and Capjtella sp. I are significantly more tolerant to anoxia and 760 pm01 1.' sulfide than Capitella sp. S from the upper North Sea sedirnents. Respiration rates showed that only CapiteUa sp. S can be characterized as an oxyconformer. The oxygen consumption of Capitella sp. S becomes successively reduced with declining ambient oxygen tensions. The 3 other sibling species are all oxyregulators with different regulation abilities. At moderate oxygen concentrations the aerobic metabolism of Capitella sp. S is inhibited at low sulfide levels (30 pm01 I-'). Conversely, at moderate oxygen levels the anaerobic metabolism of Capitella sp. S is increased at 20 pm01 I-' sulfide. In contrast, even at sulfide concentrations of 130 pm01 l.', the aerobic metabolism of Capjtella sp L is not affected. The anaerobic metabolism of Capitolla sp. L is not increased at sulfide concentrations

a b s t r a c tOkadaic acid (OA), dinophysistoxins (DTX) and pectenotoxins (PTX) produced by the dinoflagellates Dinophysis spp. can accumulate in shellfish and cause diarrhetic shellfish poisoning upon human consumption. Shellfish toxicity is a result of algal abundance and toxicity as well as accumulation and depuration kinetics in mussels. We mass-cultured Dinophysis acuta containing OA, DTX-1b and PTX-2 and fed it to the blue mussel, Mytilus edulis under controlled laboratory conditions for a week to study toxin accumulation and transformation. Contents of OA and DTX-1b in mussels increased linearly with incubation time, and the net toxin accumulation was 66% and 71% for OA and DTX-1b, respectively. Large proportions (z50%) of both these toxins were transformed to fatty acid esters. Most PTX-2 was transformed to PTX-2 seco-acid and net accumulation was initially high, but decreased progressively throughout the experiment, likely due to esterification and loss of detectability. We also quantified depuration during the subsequent four days and found half-life times of 5e6 days for OA and DTX-1b. Measurements of dissolved toxins revealed that depuration was achieved through excreting rather than metabolizing toxins. This is the first study to construct a full mass balance of DSP toxins during both accumulation and depuration, and we demonstrate rapid toxin accumulation in mussels at realistic in situ levels of Dinophysis. Applying the observed accumulation and depuration kinetics, we model mussel toxicity, and demonstrate that a concentration of only 75 Dinophysis cells l À1 is enough to make 60 mm long mussels exceed the regulatory threshold for OA equivalents.

Sulfide oxidation activity was quantified for different tissues of the polychaetes Nereis diversicolor and N virens. Blood, intestinal wall and intestinal fluid of both species catalyzed sulfide oxidahon. N. dvers~color showed a sign~flcantly higher activity than did N. virens. Sulfide oxidation activity in the blood correlated with the concentration of 'brown pigment' N. diversicolor was more tolerant to long-term exposure to hypoxia and to hypoxia in the presence of sulfide than N. virens, and was twice as tolerant as N. virens to short-term exposure to high concentrations of sulfide. Results are discussed in terms of habitat preferences and competitive interactions.

The physiology of sulfide detoxification in the isopod Saduria (Mesidotea) entomon (L.) was studied in vitro as well as in vivo using a sulfide oxidation assay and high-performance liquid chromatography. S. entornon is unable to prevent hydrogen sulfide from entering its body. Hydrogen sulfide is transported by the blood to the hepatopancreas, where it is detoxified in the fluid portion by an 0,-dependent oxidation to ~~0~~-and ~0~~-(S0 or ~0 ,~-formation could not be demonstrated). An 0 2 -independent binding of sulfide, probably by iron, also occurs in the hepatopancreas. In addition, HIS is oxidized to Sz03'-in the muscle. This oxidation is suggested to be localized in the mitochondrial fraction of the muscle. Glutathione does not play an important role in the detoxification. This study supports the hypothesis that hydrogen sulfide is an important factor in the distribution of marine invertebrates in soft sediments.