Chronic copper treatment prevents the liver critical balance transcription response induced by acetaminophen
Author
dc.contributor.author
Latorre, Mauricio
Author
dc.contributor.author
Burkhead, Jason L.
Author
dc.contributor.author
Hodar, Christian
Author
dc.contributor.author
Arredondo, Miguel
Author
dc.contributor.author
González, Mauricio
Author
dc.contributor.author
Araya, Magdalena
Admission date
dc.date.accessioned
2019-10-15T12:25:29Z
Available date
dc.date.available
2019-10-15T12:25:29Z
Publication date
dc.date.issued
2019
Cita de ítem
dc.identifier.citation
Journal of Trace Elements in Medicine and Biology, Volumen 53,
Identifier
dc.identifier.issn
18783252
Identifier
dc.identifier.issn
0946672X
Identifier
dc.identifier.other
10.1016/j.jtemb.2019.02.007
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/171699
Abstract
dc.description.abstract
The independent toxic effects of copper and acetaminophen are among the most studied topics in liver toxicity. Here, in an animal model of Cebus capucinus chronically exposed to high dietary copper, we assessed clinical and global transcriptional adaptations of the liver induced by a single high dose of acetaminophen. The experiment conditions were chosen to resemble a close to human real-life situation of exposure to both toxic stimuli. The clinical parameters and histological analyses indicated that chronic copper administration does not induce liver damage and may have a protective effect in acetaminophen challenge. Acetaminophen administration in previously non-exposed animals induced down-regulation of a complex network of gene regulators, highlighting the putative participation of the families of gene regulators HNF, FOX, PPAR and NRF controlling this process. This gene response was not observed in animals that previously received chronic oral copper, suggesting that this m