Water samples were collected at a fringing coral reef in overlying water, in bottom water between corals and in crevices under coral colonies, and analyzed for nutrient concentrations, bacterial numbers and production. We found decreasing bacterial densities from overlying water through bottom water into crevices (range 9 to 2 X 105 ml-l). Bacterial specific growth was enhanced in reef crevices (range 0.005 to 0.04 h-'). Although bactenal growth was enhanced, bacterial numbers were reduced, showing a transfer of bacterial biomass into the reef. The differences in bacterial numbers and grnwth between water types depended on water movement and bottom relief Nutrients were enhanced in reef crevices as a result of mineralization. Mineralization of bacterla removed by filterfeeders could contribute 11 and 21 '70 to the increase in N and P, respectively, in coral reef crevices.
Many studies have shown that narcosis or baseline toxicity of polycyclic aromatic hydrocarbons (PAHs) is strongly related to their lipophilicity. For azaarenes, such relationships have also been demonstrated, but for some compounds, deviations from these relationships have been observed, even for closely related compounds such as isomers. In the present study, the toxicity of four azaarene isomer pairs to the marine flagellate Dunaliella tertiolecta was determined. For quinoline, isoquinoline, acridine, phenanthridine, benz[a]acridine, and benz[c]acridine, the 72-h median effective concentrations for growth were 571, 464, 2.10, 14.7, 0.50, and 0.11 microM, respectively. For the five-ringed isomers dibenz[a,i]acridine and dibenz[c,h]acridine, no effects were observed at the highest concentration tested (0.1 and 0.005 microM, respectively). Growth inhibition by the two-, three-, and four-ringed isomer pairs to D. tertiolecta was well described by molecular volume and log Kow, indicating a narcotic mode of action. However, the toxicity of acridine and benz[c]acridine was much higher than that of their respective isomers, phenanthridine and benz[a]acridine, suggesting an additional specific mode of action. Based on the differences in energies between the highest occupied molecular orbital and the lowest unoccupied molecular orbital, acridine and benz[c]acridine are susceptible to ultraviolet (UV) radiation, in contrast to the other tested compounds. Because UV was present, it is therefore argued that the toxicity of both compounds was photoenhanced. Photoenhanced toxicity may increase the environmental hazard of azaarenes, indicating the importance of enlarging the present monitoring of PAHs with phototoxic N-heterocyclic PAHs and incorporating this mode of action in water-quality criteria.
UV radiation is absorbed by PAHs, structurally altering these compounds into a variety of oxygenated products. Until recently, only hazards of parental PAHs in the environment were investigated. This study aims to determine the fate and effects of azaarenes (N-heterocyclic PAHs) together with their photoproducts in marine environments. Photoreaction kinetics of eight azaarenes, ranging from two-ringed to five-ringed structures, were examined using two different light sources: one with an emission peak at 300 nm (UV−B) and the other with an emission peak at 350 nm (UV−A). Azaarenes degraded rapidly in the presence of short-waved light, UV−B being more effective than UV−A. Especially preexposure of azaarenes to UV−A radiation led to products toxic to the marine diatom Phaeodactylum tricornutum. Since UV−A constitutes a larger fraction of sunlight at the earth surface and in the water column, photolysis by UV−A may increase the toxic risk of aromatic compounds in the marine environment.
The present study seeks quantitative measures for photoenhanced toxicity under natural light regimes by comparing the effects of an aromatic compound under natural and laboratory light. To this purpose, the influence of light irradiance and spectral composition on the extent of photoenhanced toxicity of acridine, a three-ringed azaarene, to the marine diatom Phaeodactylum tricornutum was analyzed. Under laboratory light containing ultraviolet radiation (UV), the 72-h EC50 growth value for acridine was 1.55 microM. Under natural light, a 72-h EC50 value for acridine below the lowest test concentration (0.44 microM) was observed. Under both laboratory and natural light, the toxicity of acridine was equally enhanced by total UV (UV-A and UV-B) and UV-A radiation, while in the absence of UV no enhancement of toxicity was observed. Hence, the UV-A region of light was dominant in the photoenhanced toxicity of acridine to P. tricornutum, in accordance with its absorption spectrum in the UV-A region. Therefore, the total amount of UV radiation absorbed by aqueous acridine was calculated for each separate treatment. The amount of UV absorbed by acridine effectively described the effect of acridine on the growth of P. tricornutum in a dose-response-dependent manner. It is concluded that photoenhanced toxicity of aromatic compounds expressed as a function of the actually absorbed UV may circumvent some of the variability between studies using different concentrations of the phototoxic compounds and light sources. The UV quantity absorbed by these compounds allows a comparison with the absorption characteristics of natural waters and, thus, is a key parameter to determine the role of photoenhanced toxicity in water.
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