Mariana Gonzalez

Polybrominated diphenyl ethers and organochlorine compound levels in brown trout (Salmo trutta) from Andean Patagonia, Argentina

Polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), DDTs and endosulfan residues were analyzed in muscle, liver, gonads, gills and stomach content of brown trout (Salmo trutta) from the Andean Patagonia. PBDEs, PCBs and DDTs levels were positively correlated with lipid content, while less hydrophobic endosulfans showed a poor correlation. Endosulfan levels were about 99.9% of total contaminant (highest levels in liver 500×10(3)ng g(-1) lipid weight), with α-/β-isomers ratio >1 in all organs. These results are in agreement to the current-use of the technical endosulfan and also suggest acute exposure to this insecticide. Conversely, DDT/DDE ratio reflects fish exposure to old DDT sources, showing a DDE predominance. Gills had the highest levels of DDTs, PCBs and PBDEs, indicating they represent the main uptake pathway for such hydrophobic compounds from water column. PCBs showed the lowest levels in all organs and the PBDEs/PCBs ratios >1 agree with worldwide trends. PBDEs levels in gonads, gills, liver and muscle exceeded 80 ng g(-1) (lipid weight) and were higher than other values reported in the Southern Hemisphere. BDE-47 was the predominant congener, suggesting higher bioaccumulation potential and possible brown trout metabolism of higher congeners. Since there is no point source of PBDEs in the region and residues were dominated by lower brominated congeners, atmospheric transport could be the main source of these compounds. This first report of PBDEs levels in fish from Argentina contributes to the knowledge about environmental trends of these persistent organic pollutants (POPs) in remote areas such as the Andean Patagonia.

CAMKIIγ, HSP70 and HSP90 transcripts are differentially expressed in chronic myeloid leukemia cells from patients with resistant mutated disease.

Abstract Patients with chronic myeloid leukemia (CML) can develop disease resistance to tyrosine kinase inhibitor (TKI) therapy, which is mainly attributable to the presence of point mutations in the tyrosine kinase domain of BCR–ABL1. In order to examine suitable markers to monitor treatment efficacy, we investigated transcript expression profiles of genes known to be involved in myeloid cell proliferation, such as CAMKIIγ and KI67, and in protein stability and ultimately cell survival under physiological and stress conditions, such as heat shock proteins HSP70 and HSP90. We studied 101 patients with CML in different stages of disease and with different responses to TKI treatment. The results of quantitative real-time polymerase chain reaction (qPCR) analyses showed that the expression levels of CAMKIIγ, KI67, HSP70 and HSP90 genes were up-regulated at diagnosis, and in cases with signs of treatment resistance both in chronic and advanced phases (accelerated and blastic phases) with respect to chronic phase in remission and healthy donors. When only 56 resistant cases, 31 with mutations (MT) and 25 without mutations (WT), in the BCR–ABL1 tyrosine kinase domain were considered, the transcript expression profile showed an unexpected significant increase in CAMKIIγ and HSP70, and a significant decrease in HSP90 in MT versus WT cases. This differential transcript expression prompted us to design an expression score, log(CAMKIIγ × HSP70/HSP90), which can be used to provide rapid screening to discriminate the presence or absence of mutations in resistant cells and to monitor TKI treatment efficacy in patients with CML.