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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens
Hongrui Guo1, Hengmin Cui1,2, Jing Fang1,2
1College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China.
Abstract:
Ni, a metal with industrial and commercial uses, poses a serious hazard to human and animal health. In the present study, we used flow cytometry, immunohistochemistry and qRT-PCR to investigate the mechanisms of NiCl2-induced apoptosis in kidney cells. After treating 280 broiler chickens with 0, 300, 600 or 900 mg/kg NiCl2 for 42 days, we found that two caspase-dependent pathways were involved in the induced renal tubular cell apoptosis. In the mitochondria-mediated caspase-dependent apoptotic pathway, cyt-c, HtrA2/Omi, Smac/Diablo, apaf-1, PARP, and caspase-9, 3, 6 and 7 were all increased, while. XIAP transcription was decreased. Concurrently, in the Fas-mediated caspase-dependent apoptotic pathway, Fas, FasL, caspase-8, caspase-10 and Bid levels were all increased. These results indicate that dietary NiCl2 at 300+ mg/kg induces renal tubular cell apoptosis in broiler chickens, involving both mitochondrial and Fas-mediated caspase-dependent apoptotic pathways. Our results provide novel insight into Ni and Ni-compound toxicology evaluated in vitro and in vivo.
Insights
Nickel chloride (NiCl2) exposure at 300+ mg/kg induces kidney cell apoptosis in broiler chickens. This occurs through both mitochondria-mediated and Fas-mediated caspase-dependent pathways, highlighting nickel toxicity mechanisms.
Area of Science:
- Toxicology
- Cell Biology
- Animal Health
Background:
- Nickel (Ni) is an industrially significant metal with known human and animal health risks.
- Understanding the specific mechanisms of nickel-induced cellular damage is crucial for risk assessment and mitigation.
Purpose of the Study:
- To investigate the molecular mechanisms underlying nickel chloride (NiCl2)-induced apoptosis in broiler chicken kidney cells.
- To elucidate the specific apoptotic pathways involved in NiCl2 toxicity.
Main Methods:
- Flow cytometry, immunohistochemistry, and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were employed.
- Broiler chickens were treated with varying doses of NiCl2 (0, 300, 600, 900 mg/kg) for 42 days.
Main Results:
- NiCl2 exposure significantly increased markers of apoptosis in renal tubular cells.
- The mitochondria-mediated pathway showed increased levels of cytochrome c, HtrA2/Omi, Smac/Diablo, apaf-1, PARP, and caspases (-9, -3, -6, -7), with decreased XIAP.
- The Fas-mediated pathway exhibited elevated levels of Fas, FasL, caspase-8, caspase-10, and Bid.
Conclusions:
- Dietary NiCl2 at concentrations of 300 mg/kg and above induces renal tubular cell apoptosis in broiler chickens.
- Apoptosis is mediated via both the mitochondria-dependent and Fas-dependent caspase pathways.
- These findings offer new insights into nickel and nickel compound toxicology in vivo.
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