Related Experiment Video
Updated: Mar 12, 2026
High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC
Published on: May 10, 2016
Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response
Hongrui Guo1, Hengmin Cui1,2, Jing Fang1,2
1College of Veterinary Medicine, Sichuan Agricultural University Ya'an 625014, China.
Abstract:
Up to now, the precise mechanism of Ni toxicology is still indistinct. Our aim was to test the apoptosis, cell cycle arrest and inflammatory response mechanism induced by NiCl2 in the liver of broiler chickens. NiCl2 significantly increased hepatic apoptosis. NiCl2 activated mitochondria-mediated apoptotic pathway by decreasing Bcl-2, Bcl-xL, Mcl-1, and increasing Bax, Bak, caspase-3, caspase-9 and PARP mRNA expression. In the Fas-mediated apoptotic pathway, mRNA expression levels of Fas, FasL, caspase-8 were increased. Also,NiCl2 induced ER stress apoptotic pathway by increasing GRP78 and GRP94 mRNA expressions. The ER stress was activated through PERK, IRE1 and ATF6 pathways, which were characterized by increasing eIF2α, ATF4, IRE1, XBP1 and ATF6 mRNA expressions. And, NiCl2 arrested G2/M phase cell cycle by increasing p53, p21 and decreasing cdc2, cyclin B mRNA expressions. Simultaneously, NiCl2 increased TNF-α, IL-1β, IL-6, IL-8 mRNA expressions through NF-κB activation. In conclusion, NiCl2 induces apoptosis through mitochondria, Fas and ER stress-mediated apoptotic pathways and causes cell cycle G2/M phase arrest via p53-dependent pathway and generates inflammatory response by activating NF-κB pathway.
Insights
Nickel chloride (NiCl2) exposure in broiler chickens induces liver cell death through apoptosis and ER stress, arrests cell cycle progression, and triggers inflammation via NF-κB activation.
Area of Science:
- Toxicology
- Cell Biology
- Immunology
Background:
- The precise mechanisms of nickel (Ni) toxicology remain unclear.
- Understanding Ni-induced cellular damage is crucial for animal health and food safety.
Purpose of the Study:
- To investigate the mechanisms of apoptosis, cell cycle arrest, and inflammatory responses induced by nickel chloride (NiCl2) in broiler chicken livers.
Main Methods:
- Analysis of mRNA expression levels related to apoptosis (mitochondrial, Fas, ER stress pathways), cell cycle regulation, and inflammatory markers (TNF-α, IL-1β, IL-6, IL-8).
- Assessment of key proteins and signaling pathways including Bcl-2 family, caspases, PARP, ER stress markers (GRP78, GRP94), cell cycle regulators (p53, p21, cdc2, cyclin B), and NF-κB.
Main Results:
- NiCl2 significantly increased hepatic apoptosis via mitochondria-mediated (Bax, Bak, caspase-3, -9, PARP), Fas-mediated (Fas, FasL, caspase-8), and ER stress pathways (GRP78, GRP94).
- NiCl2 induced G2/M phase cell cycle arrest by upregulating p53 and p21 while downregulating cdc2 and cyclin B.
- NiCl2 elevated pro-inflammatory cytokine mRNA expression (TNF-α, IL-1β, IL-6, IL-8) through NF-κB activation.
Conclusions:
- NiCl2 induces apoptosis through multiple pathways: mitochondrial, Fas, and ER stress.
- NiCl2 causes G2/M cell cycle arrest via a p53-dependent mechanism.
- NiCl2 triggers inflammatory responses by activating the NF-κB pathway.
More Related Videos
09:32Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
Published on: October 17, 2025
08:23Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line
Published on: August 9, 2014
Related Concept Videos
01:24Drug Toxicity: Dose-Dependent Reactions
01:28Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
01:31The Intrinsic Apoptotic Pathway