1983 Biscayne Bay hydrocarbon study: final report

A two year, comprehensive, quantitative investigation was conducted to analyze and identify the spatial distribution of petrogenic and biogenic hydrocarbons in sediments, surface waters, fish and shellfish of Biscayne Bay, Florida. The goal for the first year of the project was to establish baseline information to support oil spill impact assessment and clean-up. One hundred fifty-five sediment and eleven biota samples were collected. The areas sampled included the Miami River, Intracoastal Waterway, tidal flats, access canals and environmentally sensitive shorelines. The second year of the study centered on areas exhibiting petroleum contamination. These areas included the Miami River, Little River, Goulds Canal, Black Creek and Military Canal. Surface and subsurface sediment, biota and surface water were collected. Sample collection, analyses, and data handling for the two year project were conducted so that all information was court-competent and scientifically accurate. Chain of custody was maintained for all samples. Total hydrocarbon content of surface sediments ranged from below detection limits to a high of 2663.44 pg/g. Several sample stations contained petroleum contamination. The majority of biota samples exhibited hydrocarbon concentrations and characteristics that indicated little, if any, petroleum contamination. Surface water samples ranged from 0.78 to 64.47 μg/L and several samples contained petroleum hydrocarbons. Our results indicate several areas of petroleum contamination. These areas are characterized by industrial complexes, port facilities, marinas, major boating routes and many of the major tributaries emptying into Biscayne Bay

Bradykinin and inositol 1,4,5-trisphosphate-stimulated calcium release from intracellular stores in cultured bovine endothelial cells

The relative importance of intracellular and extracellular Ca2+ in the release of endothelium-derived relaxing factor (EDRF) and the mechanisms involved in the release of intracellular Ca2+ were investigated in cultured bovine endothelial cells. The release of EDRF by bradykinin, determined by bioassay, was dose-dependent showing an EC50 of 4x10-10 M. The bradykinin-induced EDRF release from endothelial cells was maintained in the presence of extracellular Ca2+. However, in the absence of external Ca2+, bradykinin-induced EDRF release was both attenuated and transient. In cells loaded to isotopic equilibrium with45Ca, bradykinin increased the45Ca efflux into both calcium-containing and calcium-free solutions, with an EC50 for the increase in45Ca efflux induced by bradykinin of 1.3x10-9 M. The involvement of an intracellular Ca2+ store and the participation of a second messenger in its release were investigated in saponin-permeabilized endothelial cells. In saponin-permeabilized cells, ATP-sensitive calcium uptake was Ca2+,Mg2+-ATPase-dependent. The ATP-sensitive uptake of calcium at different free Ca2+ concentrations showed at least two compartments involved in the uptake of Ca2+. The45Ca uptake into the compartment with the lowest affinity and highest capacity could be inhibited by sodium azide, suggesting that this uptake was into mitochondria. The majority of the45Ca uptake into the azide-insensitive store could be released by inositol-1,4,5-trisphosphate (IP3). The IP3-induced release was not affected by apyrase or exogenous GTP. The EC50 for the release of Ca2+ by IP3 was 1.0 μM and was unaffected by an inhibitor of IP3 breakdown (2,3-diphosphoglyceric acid). The results suggest that the release of EDRF is dependent on extracellular Ca2+ influx and the release of intracellular Ca2+. The release of calcium from one of the high affinity intracellular Ca2+ stores is mediated by the intracellular second messenger, IP3

Role of calcium in the activation of endothelial cells

The involvement of calcium in the release of EDRF from cultured endothelial cells is reviewed. It is suggested that both intracellular and extracellular calcium can release EDRF depending not only on the experimental conditions but also on the agonist involved in the release. Calcium enters the cell, following receptor occupation, through a nonselective receptor-operated channel. Intracellular release of calcium following receptor occupation is probably via the production of inositol trisphosphate (IP3). It is suggested that the initial calcium signal for the release of endothelium-derived relaxant factor (EDRF) is of intracellular origin whereas the maintained release of EDRF is due to calcium entry from the extracellular space