Sulfide as an environmental factor and toxicant: tolerance and adaptations in aquatic organisms
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This review brings together a large number of independent and seemingly unrelated studies in various disciplines under four major topics: (1) sulfide as an environmental factor in aquatic habitats; (2) sulfide as a toxicant; (3) sulfide tolerance of aquatic organisms; and (4) adaptations limiting sulfide toxicity. Sulfide is widely distributed in the aquatic environment, but has been largely overlooked as an environmental factor for aquatic organisms. Sulfide at nanomoiar to millimolar concentrations adversely affects cytochrome c oxidase, various other enzymes, oxygen transport proteins, cellular structures, and consequently the physiological functions of organisms. These toxic effects are well documented in the biomedical literature, and also occur in the aquatic organisms that have been studied. Sulfide tolerance varies widely among protozoans, sediment meiofauna, polychaetes, bivalves, crustaceans, marine and freshwater fishes, and aquatic plants, often in correlation with the relative sulfide levels in the respective habitats. Aquatic organisms have evolved various adaptations against sulfide toxicity, possibly several acting in concert. Most animals are able to avoid and escape from sulfide, but cannot exclude sulfide from the body. No sulfide-resistant cytochrome c oxidase has been demonstrated, and most animals are capable of some degree of anaerobic meabolism. Various invertebrates have entered into symbiotic associations with sulfide-oxidizing bacteria. Some of these invertebrates immobilize and transport sulfide by means of sulfide-binding proteins or persulfides in the blood. Detoxication of sulfide occurs by methylation, non-specific oxidation, and enzymatic oxidation by mitochondria. Oxidative detoxication of sulfide to thiosulfate by mitochondria is common to several major taxa (protozoan, mollusk, teleosts, mammal), and is effective at low micromolar sulfide concentrations. Among organisms lacking sulfide-oxidizing bacterial symbionts, the mitochondria may thus provide the chief defense against environmental sulfide, and may allow the whole organism to tolerate sulfide concentrations 2–3 orders of magnitude greater than would inhibit cytochrome c oxidase.
CitationBagarinao, T. (1992). Sulfide as an environmental factor and toxicant: tolerance and adaptations in aquatic organisms.
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Conference paperSM Aypa - In TU Bagarinao & EEC Flores (Eds.), Towards sustainable aquaculture in Southeast Asia and Japan: Proceedings of the Seminar-Workshop on Aquaculture Development in Southeast Asia, Iloilo City, Philippines, 26-28 July, 1994, 1995 - SEAFDEC Aquaculture DepartmentAquaculture is regarded as the most promising source of protein food in the years ahead. Milkfish and Nile tilapia are the major fishes now produced but groupers, sea bass, rabbitfish, red snappers, carps, and catfishes are grown by some farmers. The tiger shrimp is still the most important cultured crustacean, but white shrimps and mudcrabs also have great potential. Oysters and mussels are produced in considerable amounts. Mariculture of the seaweed Eucheuma is now a well established industry, and the pond culture of Gracilaria for agar extraction is beginning to take off.
Resistance of two Nile tilapia, Oreochromis niloticus (L.) strains exposed to a mixture of zinc, cadmium and inorganic mercury MLA Cuvin-Aralar - In CL Marte, GF Quinitio & AC Emata (Eds.), Proceedings of the Seminar-Workshop on Breeding and Seed Production of Cultured Finfishes in the Philippines, Tigbauan, Iloilo, Philippines, 4-5 May 1993, 1996 - SEAFDEC Aquaculture DepartmentTwo strains of one month-old Oreochromis niloticus namely CLSU (obtained from Central Luzon State University, Philippines) and NIFI (from National Inland Fisheries Institute, Thailand) were exposed to a sublethal mixture of 1.0 mg L-1 Zn, 0.1 mg L-1 Cd, and 0.01 mg L-1 Hg for two months in aquaria. Another set served as control with only BFS tapwater in the aquaria. At the end of the exposure period the fish were grown for another 2 months in net cages in Laguna de Bay. During the exposure (aquarium) and grow-out (lake) phases, the uptake and elimination of the metals were determined by AAS. Accumulation of the metals peaked at 13.9 µg g-1 Hg, 78.5 µg g-1 Cd, and 1447.0 µg g-1 Zn for NIFI and 14.2 µg g-1 Hg, 82.4 µg g-1 Cd, and 1591.3 µg g-1 Zn for CLSU lost 94.9% Hg, 98.76% Cd, and 89.99% Zn after two months in the lake. After the grow-out period, 2 females and 1 male of each strain were stocked in replicate polyethylene tanks. Time to first spawning, spawning frequency, fry production, and fry survival (after 30 days) were monitored. Results showed no significant effect of treatment and strain with respect to time to first spawning, spawning frequency, and mean fry survival. There was also no significant difference between the treatment and strain in mean fry production when dam weight was used as a covariate in the analysis. The results suggest that both strains of O. niloticus are resistant to long-term exposure to the metals. In addition, the elimination of the metals during the grow-out phase may have also diminished their effect on the breeders of the two strains.
Sulphide tolerance and adaptation in the California killifish, Fundulus parvipinnis, a salt marsh resident Hydrogen sulphide is a toxicant naturally produced in hypoxic marine sediments, hydrocarbon and brine seeps and hydrothermal vents. The California killifish, a salt marsh resident, is remarkably tolerant of sulphide. The 50% lethal concentration is 700 μM total sulphide in 96 h, and 5 mM in 8 h (determined in flow-through, oxygenated sea water). Killifish exposed to sulphide produce thiosulphate which accumulates in the blood. The cytochrome c oxidase (a major site of toxicity) of the killifish is 50% inhibited by <1 μM sulphide. Killifish liver mitochondria are poisoned by 50–75 μM sulphide but can oxidize 10–20 μM sulphide to thiosulphate. Sulphide causes sulphhaemoglobin formation (and impairment of oxygen transport) at 1–5 mM in vitro and to a small extent at 2 mM in vivo. Killifish blood neither catalyses sulphide oxidation significantly nor binds sulphide at environmental (low) sulphide concentrations. Exposure to 200 μM and 700 μM sulphide over several days causes significant increases in lactate concentrations, indicating shift to anaerobic glycolysis. However, individuals with the most lactate die. In terms of diffusible H2S, the killifish can withstand concentrations two to three orders of magnitude greater than would poison cytochrome c oxidase. The high sulphide tolerance of the killifish, particularly of concentrations typical of salt marshes, can be explained chiefly by mitochondrial sulphide oxidation. Sulphide tolerance and mitochondrial sulphide oxidation in the killifish have a constitutive basis, i.e. do not diminish in fish held in the laboratory in sulphide-free water for 1–2 months, and are improved by prior acclimation.