Copper exposure induces mitochondrial dysfunction and hepatotoxicity via the induction of oxidative stress and PERK/ATF4 -mediated endoplasmic reticulum stress

Copper is an essential trace element, and excessive exposure could result in hepatoxicity, however, the underlying molecular mechanisms remain incompletely understood. The present study is aimed to investigate the molecular mechanisms of copper sulfate (CuSO4) exposure-induced hepatoxicity both in v...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Environmental pollution (1987) 2024-07, Vol.352, p.124145-124145, Article 124145
Hauptverfasser:	Li, Meng, Tang, Shusheng, Velkov, Tony, Shen, Jianzhong, Dai, Chongshan
Format:	Artikel
Sprache:	eng
Schlagworte:	acetylcysteine Activating Transcription Factor 4 - genetics Activating Transcription Factor 4 - metabolism Animals antioxidants Apoptosis Apoptosis - drug effects biomarkers calcium caspases Cell Survival - drug effects cell viability Chemical and Drug Induced Liver Injury - metabolism Copper - toxicity Copper sulfate Copper Sulfate - toxicity cytotoxicity dose response eIF-2 Kinase - genetics eIF-2 Kinase - metabolism endoplasmic reticulum Endoplasmic Reticulum Chaperone BiP endoplasmic reticulum stress Endoplasmic Reticulum Stress - drug effects ER stress Hep G2 Cells Hepatotoxicity histopathology Humans Liver - drug effects Liver - metabolism liver function Male Mice Mice, Inbred C57BL mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial dysfunction oxidative stress Oxidative Stress - drug effects pollution protein synthesis Reactive Oxygen Species - metabolism trace elements ultrastructure
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Schreiben Sie den ersten Kommentar!