Modeling food web structure and selenium biomagnification in Lake Macquarie, New South Wales, Australia, using stable carbon and nitrogen isotopes.

As a consequence of coal-fired power station operations, elevated selenium concentrations have been reported in the sediments and biota of Lake Macquarie (New South Wales, Australia). In the present study, an ecosystem-scale model has been applied to determine how selenium in a seagrass food web is processed from sediments and water through diet to predators, using stable isotopes (δ(13) C and δ(15) N) to establish the trophic position of organisms. Trophic position, habitat, and feeding zone were examined as possible factors influencing selenium bioaccumulation. Selenium concentrations ranged from 0.2 µg/g dry weight in macroalgae species to 12.9 µg/g in the carnivorous fish Gerres subfasciatus. A mean magnification factor of 1.39 per trophic level showed that selenium is biomagnifying in the seagrass food web. Habitat and feeding zone influenced selenium concentrations in invertebrates, whereas feeding zone was the only significant factor influencing selenium concentrations in fish. The sediment-water partitioning coefficient (Kd ) of 4180 showed that partitioning of selenium entering the lake to particulate organic material (POM) is occurring, and consequently availability to food webs from POM is high. Trophic transfer factors (invertebrate = 1.9; fish = 1.2) were similar to those reported for other water bodies, showing that input source is not the main determinant of the magnitude of selenium bioaccumulation in a food web, but rather the initial partitioning of selenium into bioavailable POM. Environ Toxicol Chem 2015;34:608-617. © 2014 SETAC.

Exposure-dose-response of Tellina deltoidalis to contaminated estuarine sediments 3. Selenium spiked sediments.

The metalloid selenium is an essential element which at slightly elevated concentrations is toxic and mutagenic. In Australia the burning of coal for power generation releases selenium into estuarine environments where it accumulates in sediments. The relationship between selenium exposure, dose and response was investigated in the deposit feeding, benthic, marine bivalve Tellina deltoidalis. Bivalves were exposed in microcosms for 28 days to individual selenium spiked sediments, 0, 5 and 20 µg/g dry mass. T. deltoidalis accumulated selenium from spiked sediment but not in proportion to the sediment selenium concentrations. The majority of recovered subcellular selenium was associated with the nuclei and cellular debris fraction, probably as protein bound selenium associated with plasma and selenium bound directly to cell walls. Selenium exposed organisms had increased biologically detoxified selenium burdens which were associated with both granule and metallothionein like protein fractions, indicating selenium detoxification. Half of the biologically active selenium was associated with the mitochondrial fraction with up to 4 fold increases in selenium in exposed organisms. Selenium exposed T. deltoidalis had significantly reduced GSH:GSSG ratios indicating a build-up of oxidised glutathione. Total antioxidant capacity of selenium exposed T. deltoidalis was significantly reduced which corresponded with increased lipid peroxidation, lysosomal destabilisation and micronuclei frequency. Clear exposure-dose-response relationships have been demonstrated for T. deltoidalis exposed to selenium spiked sediments, supporting its suitability for use in selenium toxicity tests using sub-lethal endpoints.

Exposure-dose-response of Anadara trapezia to metal contaminated estuarine sediments: 3. Selenium spiked sediments.

Selenium enters near shore marine environments from the activities of coal-fired power stations. Although selenium is an essential element, at elevated concentrations it can cause genotoxic damage. The relationship between selenium exposure dose and response was investigated in Anadara trapezia exposed to selenium spiked sediment (5 µg/g and 20 µg/g dry mass) for 56 days. A. trapezia reached an equilibrium selenium tissue concentration (2 µg/g and 10 µg/g respectively) by day 42. Gills had significantly more selenium than the hepatopancreas and haemolymph. Between 12 and 21% of accumulated selenium in the gill and hepatopancreas was detoxified and in the metal rich granule. Most of the biologically active selenium in both tissues was in the mitochondrial fraction. Glutathione peroxidase activity and mean total glutathione concentrations for selenium exposed organisms were not significantly different to controls. The ratio of reduced to oxidised glutathione and the total antioxidant capacity were significantly reduced in selenium exposed organisms compared to control organisms. Increased selenium exposure resulted in significant increases in lipid peroxidation, lysosomal destabilisation and an increased frequency of micronuclei. A significant exposure-dose-response relationship for A. trapezia exposed to selenium enriched sediments indicates that elevated sediment selenium concentrations can increased biologically active selenium burdens and cause impairment of cellular processes and cell integrity.