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Title: Ras oncogene and Hypoxia-inducible factor-1 alpha (Hif-1α) expression in the Amazon fish Colossoma macropomum (Cuvier, 1818) exposed to benzo(a)pyrene
Authors: Silva, Grazyelle Sebrenski da
Fé, Luciana Mara Lopes
Silva, Maria de Nazaré Paula da
Val, Vera Maria Fonseca Almeida e
Keywords: Benzo(a)pyrene
Corn Oil
Hypoxia Inducible Factor 1alpha
Animals Cell
Animals Experiment
Animals Tissue
Cell Membrane
Cell Vacuole
Colossoma Macropomum
Comet Assay
Concentration (parameters)
Controlled Study
Gene Expression
Gene Overexpression
Hif 1alpha Gene
Liver Cell Nucleus
Liver Parenchyma
Membrane Rupture
Oncogene Ras
Quantitative Analysis
Real-time Polymerase Chain Reaction
Issue Date: 2017
metadata.dc.publisher.journal: Genetics and Molecular Biology
metadata.dc.relation.ispartof: Volume 40, Número 2, Pags. 491-501
Abstract: Benzo[a]pyrene (B[a]P) is a petroleum derivative capable of inducing cancer in human and animals. In this work, under laboratory conditions, we analyzed the responses of Colossoma macropomum to B[a]P acute exposure through intraperitoneal injection of four different B[a]P concentrations (4, 8, 16 and 32 μmol/kg) or corn oil (control group). We analyzed expression of the ras oncogene and the Hypoxia-inducible factor-1 alpha (hif-1α) gene using quantitative real-time PCR. Additionally, liver histopathological changes and genotoxic effects were evaluated through the comet assay. Ras oncogene was overexpressed in fish exposed to 4, 8 of 16 μmol/kg B[a]P, showing 4.96, 7.10 and 6.78-fold increases, respectively. Overexpression also occurred in hif-1α in fish injected with 4 and 8 μmol/kg B[a]P, showing 8.82 and 4.64-fold increases, respectively. Histopathological damage in fish liver was classified as irreparable in fish exposed to 8, 16 and 32 μmol/kg μM B[a]P. The genotoxic damage increased in fish injected with 8 and 16 μmol/kg in comparison with the control group. Acute exposure of B[a]P was capable to interrupt the expression of ras oncogene and hif-1α, and increase DNA breaks due to tissue damage. © 2017, Sociedade Brasileira de Genética.
metadata.dc.identifier.doi: 10.1590/1678-4685-GMB-2016-0066
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