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Egl-9 family hypoxia-inducible factor (egln), an oxygen-sensing enzyme family, has been thoroughly characterized in mammals and certain fishes, but there is few research on its involvement in reproductive development and hypoxic stress in rainbow trout. In this study, we investigated the gene structure, physicochemical properties, and evolutionary connection of the egln gene family. The expression profile of egln gene family and their regulatory mechanism were explored using bioinformatics analysis and hypoxia treatment experiments. Five egln genes were discovered in the rainbow trout genome in this investigation (egln1, egln2a, egln2b, egln3a, and egln3b). Domain prediction revealed that all egln proteins have p4hc conserved domains, and phylogenetic analysis revealed that rainbow trout egln2 and egln3 were closely related to Atlantic salmon. The results of real-time quantitative PCR (RT-qPCR) showed that egln genes were generally expressed in all detected tissues, and higher in the ovary, testis, and brain in normoxia. Under hypoxia, the expression level of eglns was significantly down-regulated in most tissues except the liver. Our research contributes to future research on the functional properties of egln genes, as well as the evolution of teleosts and the impact of hypoxia on biological immunity. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of arsenic trioxide (As(2)O(3)) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells., Methods: Human multidrug-resistant leukemia cell line K562/ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 cells were determined using flow cytometry., Results: Zero point five to 20 micromol/L As(2)O(3) inhibited the proliferation of K562/ADM cells, and K562/ADM cells were more sensitive to As(2)O(3) than the parental K562 cells. As(2)O(3)-induced apoptosis of K562/ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As(2)O(3) significantly inhibited the P-gp expression of K562/ADM cells, and synergistically enhanced the sensitivity of the drug-resistant cells to adriamycin., Conclusions: As(2)O(3) induces growth-inhibition and apoptosis, down-regulates P-gp expression and exerts a synergistic effect in combination with adriamycin in multidrug-resistant leukemia cells.