Copper sulfate-induced endoplasmic reticulum stress promotes hepatic apoptosis by activating CHOP, JNK and caspase-12 signaling pathways.
Animals
Apoptosis
/ drug effects
Caspase 12
/ metabolism
Copper Sulfate
/ toxicity
Dose-Response Relationship, Drug
Endoplasmic Reticulum Chaperone BiP
Endoplasmic Reticulum Stress
/ drug effects
JNK Mitogen-Activated Protein Kinases
/ metabolism
Liver
/ drug effects
Mice
Mice, Inbred ICR
Signal Transduction
Transcription Factor CHOP
/ metabolism
Apoptosis
CHOP signaling
Caspase-12 signaling
Copper
ER stress
JNK signaling
Mouse
Journal
Ecotoxicology and environmental safety
ISSN: 1090-2414
Titre abrégé: Ecotoxicol Environ Saf
Pays: Netherlands
ID NLM: 7805381
Informations de publication
Date de publication:
15 Mar 2020
15 Mar 2020
Historique:
received:
13
11
2019
revised:
16
01
2020
accepted:
21
01
2020
pubmed:
1
2
2020
medline:
6
5
2020
entrez:
1
2
2020
Statut:
ppublish
Résumé
Copper (Cu), a transition metal, is an essential trace element in human and animal nutrition at low concentration, but Cu has toxic effects on tissues and organs at high concentration. Endoplasmic reticulum (ER) is a toxicological target in Cu poison. Thus far, no studies have focused on the relationship among copper, endoplasmic reticulum (ER) stress and apoptosis in animal and human livers. In the present study, mice treated with copper sulfate (CuSO
Identifiants
pubmed: 32001424
pii: S0147-6513(20)30075-0
doi: 10.1016/j.ecoenv.2020.110236
pii:
doi:
Substances chimiques
Endoplasmic Reticulum Chaperone BiP
0
HSPA5 protein, human
0
Hspa5 protein, mouse
0
Transcription Factor CHOP
147336-12-7
JNK Mitogen-Activated Protein Kinases
EC 2.7.11.24
Caspase 12
EC 3.4.22.-
Copper Sulfate
LRX7AJ16DT
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110236Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that there are no conflicts of interest.