Hypoxia-induced autoxidation of haemoglobin in the benthic invertebrates Arenicola marina (Polychaeta) and Astarte borealis (Bivalvia) and the possible effects of sulphide

Haemoglobin autoxidation and the simultaneous liberation of H2O2 was studied in the blood of the lugworm, Arenicola marina, and the haemolymph of the clam, Astarte borealis, under normoxia, hypoxia, and hypoxia with 200 μmol·l−1 sulphide. In both species Hb autoxidation and hydrogen peroxide liberation into the respiratory fluid increased under hypoxia. Even higher hydrogen peroxide levels were measured under sulphidic hypoxia conditions. Under normoxia and hypoxia, autoxidation of the respiratory pigment seems to be a major source of H2O2 in blood and haemolymph. Whereas the body fluids of both species lack the hydrogen peroxide scavenger catalase, they contain considerable amounts of the antioxidant enzymes glutathione reductase (Astarte borealis only) and superoxide-dismutase (SOD). SOD activity in Arenicola marina blood was unaffected by sulphide in vivo and in vitro, while haemolymph SOD activity was significantly reduced during sulphide treatment in Astarte borealis. Catalase activity in the gills of Astarte borealis and the chloragog storage tissue of Arenicola marina were reduced by prolonged hypoxia, while the SOD activities in the tissues were unaffected. A possible involvement of H2O2, partly deriving from autoxidation of respiratory pigments, in H2S oxidation in invertebrate body fluids is discussed.