ABSTRACT
From the early 1950s until the late 1970s, Augusta Bay (Sicily, Italy) served as a major European (petro) chemical hub. It thereafter began a progressive decline as several crude oil refining and industrial plants closed due to the transfer of production cycles to other sites around the globe. As a result of the rapid and relatively uncontrolled post-WWII development of the site, several environmental studies identified significant contamination in sediments around the southernmost sector of the bay. The pollution was mainly due to barium (Ba) and mercury (Hg), attributable to the former chlor-alkali plant (1958-2003), and polychlorobiphenyls (PCBs) and hexachlorobenzene (HCB). The present study focuses on understanding the broad legacy of pollution across the whole harbour by systematically analysing 10 sediment cores collected in 2008 for contaminant concentration profiles of Hg, Ba, PCBs, HCB and grain-size variations. Pre-industrial environmental geochemical background conditions were identified using data from the deeper parts of cores. The results show that contamination has affected the entire harbour area to varying degrees, and this has allowed identifying contamination transfer, based on decreasing concentrations and related depths in the sediment cores from the southernmost sector to the central and northern area. A recent finding by the current researchers is that the construction of the dam/breakwater in the early 1960s, that largely coincided with the start of industrial inputs, led to the trapping of fine terrestrial sediment inside the harbour, particularly in the central and northern area. This trapped sediment provides a granulometric time marker in those cores. The presence of highly contaminated sediments inside the harbour represents a significant future liability unless remedial action is applied to remove the worst of the polluted sediment.
ABSTRACT
Extracellular nucleotides and nucleosides have emerged as important elements regulating tissue homeostasis. Acting through specific receptors, have the ability to control gene expression patterns to direct cellular fate. We observed that SKOV-3 cells express the ectonucleotidases: ectonucleotide pyrophosphatase 1 (ENPP1), ecto-5'-nucleotidase (NT5E), and liver alkaline phosphatase (ALPL). Strikingly, in pulse and chase experiments supplemented with ATP, SKOV-3 cells exhibited low catabolic efficiency in the conversion of ADP into AMP, but they were efficient in converting AMP into adenosine. Since these cells release ATP, we proposed that the conversion of ADP into AMP is a regulatory node associated with the migratory ability and the mesenchymal characteristics shown by SKOV-3 cells under basal conditions. The landscape of gene expression profiles of SKOV-3 cell cultures treated with apyrase or adenosine demonstrated similarities (e.g., decrease FGF16 transcript) and differences (e.g., the negative regulation of Wnt 2, and 10B by adenosine). Thus, in SKOV-3 we analyzed the migratory ability and the expression of epithelium to mesenchymal transition (EMT) markers in response to apyrase. Apyrase-treatment favored the epithelial-like phenotype, as revealed by the re-location of E-cadherin to the cell to cell junctions. Pharmacological approaches strongly suggested that the effect of Apyrase involved the accumulation of extracellular adenosine; this notion was strengthened when the incubation of the SKOV-3 cell with α,ß-methylene ADP (CD73 inhibitor) or adenosine deaminase was sufficient to abolish the effect of apyrase on cell migration. Overall, adenosine signaling is a fine tune mechanism in the control of cell phenotype in cancer. J. Cell. Biochem. 118: 4468-4478, 2017. © 2017 Wiley Periodicals, Inc.
