Santanalarsson8015

When salinity, temperature and pressure were set to seawater conditions, the values for interfacial tension between crude oil and water were below 1.0 mN m-1. Taken together, these results demonstrate that it is possible to obtain a nontoxic crude rhamnolipid product, with high productivity, to replace petroleum-based surfactants in oil spill cleanups and other environmental applications.In this research, the toxicological effect of untreated wastewater from of ethyl alcohol industry was evaluated on the zebrafish (Danio rerio) under experimental conditions. Fish were treated with zero, half, one and two percent of sewage effluent for 21 days. Toxic effects were monitored in liver by determining biochemical indicators, oxidative stress biomarkers, and the expression of genes involved in the detoxification. Results showed that Sod1, Gstp-1a, Gpx1a gene expressions were significantly increased in the hepatocytes after 21 days at 2.0% sewage exposure. Scutellarin mouse Sewage exposure also significantly increased Gsr, Ces2 and Cyp1a, Mt1 and Mt2 gene expression in the hepatocytes of zebrafish as compared to the reference group (P less then 0.01). Total cellular antioxidants, malondialdehyde (MDA) levels, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) activities in fish exposed to 1 and 2% of sewage were significantly higher than the control group (P less then 0.01), whereas alanine aminotransferase (ALT) was only increased in fish exposed to 2% sewage (P less then 0.01). A significant decrease in gamma-glutamyl-transferase (GGT) activity in fish exposed to 2% effluent was found (P less then 0.01). Catalase (CAT) activity was increased in zebrafish exposed to all concentrations of effluent. The transcriptional analysis of the detoxification-related genes and the changes in the biochemical indicators evidenced that drainage of sewage effluents from the ethyl alcohol company is a serious threat to the health of aquatic animals in the Khorram-Rood River. These results will contribute to further study on the impact of sewage effluents of the alcohol industry on aquatic organisms.Geochemical studies of 174 sediment cores collected by the MAREANO mapping program in Norwegian waters of the North Atlantic Ocean give new sets of values of background concentrations (BCs) for polycyclic aromatic hydrocarbons (PAHs) for the studied regions. The study is based on deep core sediment samples representing background levels of PAHs. The samples selected were only from the deeper parts of undisturbed sediment cores with low, stable concentrations of petrogenic and pyrogenic PAHs, with low variation for individual PAH compounds between the samples within the same core, and from below the parts of the cores dated with 210Pb to approximately the last 100-150 years. The results show that the main part of the studied area has BCs different from those previously established by OSPAR Commission (OSPAR) for the North-East Atlantic. Another area in central Barents Sea has a separate set of BCs of pyrogenic PAHs, apparently due to the influence from marginal ice zone mechanisms. A third area with its own set of BCs has been established for north-western Barents Sea off the coast of Svalbard, due to high natural contents of PAHs in this area. BCs for several PAHs not included in the present OSPAR list are also provided.The molecular characterization of secondary organic aerosol (SOA) is based mainly on LC-MS analyses of particulate matter (PM) samples collected with aerosol samplers. Several studies have analyzed atmospheric waters, including rain and cloud water, for the presence of SOA components, however, no separation techniques were used making identification of the individual components in these complex mixtures impossible. We have applied our improved UHPLC-HR-MS methodology to analyze atmospheric precipitates (hailstone, rain and snow), as well as SOA collected with high-volume samplers. We achieved sensitivity levels and separation efficiencies that were sufficient for molecular-level identification of individual compounds. Tracing commonly known SOA markers such as organosulfates (OS), C4-C6 dicarboxylic acids and terpenoic acids revealed that the chromatographic profiles for both atmospheric precipitate and PM samples were very similar, with both giving similar component ratios, especially for OS. We also demonstrated that SOA markers can be detected directly from raw rain samples. Our results show that LC-MS techniques are suitable for the convenient analysis of atmospheric precipitates containing SOA markers at the molecular level. It complements traditional SOA analyses and provides additional sampling opportunities which will no doubt allow for better elucidation of chemical transformations of volatile organic compounds in the atmosphere.Arsenic is a naturally occurring environmental toxicant. Chronic exposure to arsenic is linked with neurological damage. Although the mechanisms remain to be elucidated, it is currently believed that neural cell apoptosis is one of the underlying mechanisms of arsenic-induced neurotoxicity. Calreticulin (CRT) is a quality control chaperone located in the lumen of the endoplasmic reticulum (ER), which participates in many signaling pathways including apoptosis. However, the role of CRT in apoptosis is controversial. Whether CRT plays a role in arsenite-induced apoptosis and the relationship between CRT and ER stress-mediated apoptosis have not been mentioned before. In this study, we found that CRT expression as well as the cell apoptosis levels increased in a dose dependent manner upon arsenite exposure in HT-22 cells, a mouse hippocampal neural cell line. In addition, arsenite exposure resulted in the up-regulation of ER stress indicator GRP78 and ER stress-related proteins including p-PERK, ATF4, CHOP, calpain2 and cleaved caspases-12, accompanied by the down-regulation of Bcl-2 and up-regulation of Bax and cleaved caspase-3. Silence of CRT remarkably alleviated arsenite-induced apoptosis and reversed the expression of the proteins above. Our findings confirmed the role of CRT in the induction of apoptosis upon arsenite exposure and suggested that CRT mediated the intrinsic apoptotic cell death including both mitochondria-dependent (PERK/ATF4/CHOP/Bcl-2) and independent (calpain2/caspases-12) pathways initiated by ER stress, which we believed to be a previously undocumented property of arsenite-induced apoptosis.