Nickel-induced oxidative stress and apoptosis in Carassius auratus liver by JNK pathway

Zheng, Gui‐Hong; Liu, Chan-Min; Sun, Junqiang; Zhao-jun, Feng; Cheng, Chen

doi:10.1016/j.aquatox.2013.12.015

Cited by 73 publications

(37 citation statements)

References 37 publications

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“…In our previous studies, TUNEL and histopathological results showed that NiCl 2 induces apoptosis in the kidney [20, 21], thymus, spleen and cecal tonsil [17, 25, 36]. Our results are consist with those of Zheng, et al [37] who showed that NiSO 4 induces JNK-mediated oxidative stress and apoptosis in Carassius auratus liver. Ni compounds can increase apoptosis in HepG2 cells [38], normal rat kidney cells [39], and human neutrophils and lymphocytes [40, 41].…”

Section: Discussionsupporting

confidence: 89%

“…NiNPs and Ni fine particles reportedly increase caspase-3, 6 and 9 protein levels and activation in JB8 and A431 cells [33, 48]. Nickel ferrite nanoparticles increase caspase-3 and caspase-9 activation and expression in HepG2 and MFC-7 cells [49], and NiSO 4 increases hepatic caspase-3 activity in Carassius auratus [37]. Patel, et al [50] suggested that NiCl 2 increases caspae-3 and caspase-7 protein levels in human lung epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

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Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

et al. 2016

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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.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

et al. 2016

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“…GSH contents are decreased in the bursa of NiCl 2 -treated broilers, which is in agreement with the previous study [43]. NiSO 4 can decrease the GSH levels and activities of SOD and GSH-Px in Carassius auratus liver [44]. Nickel nanoparticles (Ni NPs) induce oxidative stress as evidenced by depletion of GSH and increase of ROS and lipid peroxidation (LPO) in human lung epithelial A549 cells and in A431 cells [45,46].…”

Section: Discussionsupporting

confidence: 85%

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

Yin¹,

Guo²,

Cui

et al. 2015

Biol Trace Elem Res

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The purpose of this study was to investigate the histopathological lesions, oxidative damage, changes of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) contents in the bursa of Fabricius and serum immunoglobulins (IgG, IgM, IgA) induced by dietary nickel chloride (NiCl2). Two hundred and eighty-one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Lesions were observed in the NiCl2-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae. Concurrently, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxyl radical and glutathione (GSH) contents were significantly (p < 0.05 or p < 0.01) decreased, while malondialdehyde (MDA) contents were increased in the NiCl2-treated groups. The serum IgG, IgM, and bursa IgG and IgM contents were significantly (p < 0.05 or p < 0.01) lower in the NiCl2-treated groups than those in the control group. The above-mentioned results show that dietary NiCl2 in excess of 300 mg/kg can cause histopathological lesions via oxidative damage, which finally impairs the function of the bursa of Fabricius and reduces IgG and IgM contents of the serum and the bursa of Fabricius. The study is aimed to provide helpful materials for studies on Ni- or Ni compounds-induced B cell toxicity in both human and other animals in the future.

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“…But majority of the studies supported the general hypothesis that ERK activation delivers a survival signal and inhibition of ERK signaling leads to increased sensitivity of some cell lines to cisplatin. 16,31,32 Although more often associated with survival, a pro-apoptotic function for the ERK pathway has also been suggested in several other model systems. 21,22 In our study, however, we provided evidence that activation of ERK is important for the inducting cisplatin-induced apoptosis in MKN-28 cells.…”

Section: Discussionmentioning

confidence: 99%

MAPK/ERK Activation Sensitizes MKN-28 Cells to Cisplatin-Induced Apoptosis

Zhang¹,

Liang²,

Zhang³

et al. 2015

Cancer Stud Mol Med Open J

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Cisplatin as a highly potent cytotoxic agent was widely used in the chemotherapy of gastric cancer. It kills cancer cells by inducing apoptosis. The Extracellular signal-regulated kinase (ERK) signaling pathway plays an important role in proliferation and survival. However, its roles in apoptosis vary. This study focused on the role of ERK in cisplatin-induced apoptosis in a stomach cancer cell line, MKN-28 cells. We found that cisplatin treatment substantially activated ERK, which was prevented by MEK inhibitor U0126. Transient transfection of MKN-28 cells with Constitutively Active-MEK1 (CA-MEK1) elevated cisplatin-induced apoptosis comparing with Dominant Negative-MEK1 (DN-MEK1). Cisplatin-induced ERK activation up-regulates pro-apoptotic gene BAK, whereas down-regulates anti-apoptotic gene BCL-2. Knocking down BCL-2 with siRNA sensitizes MKN-28 cells to the toxicity of cisplatin. These results suggested that (1) ERK activation is required for the cisplatin-induced apoptosis in MKN-28 cells; and (2) ERK mediates apoptosis by BCL-2.

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Nickel-induced oxidative stress and apoptosis in Carassius auratus liver by JNK pathway

Cited by 73 publications

References 37 publications

Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

MAPK/ERK Activation Sensitizes MKN-28 Cells to Cisplatin-Induced Apoptosis

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