Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response

Guo, Hongrui; Cui, Hengmin; Fang, Jing; Zuo, Zhicai; Deng, Junliang; Wang, Xun; Zhao, Ling; Chen, Kejie; Deng, Jie

doi:10.18632/aging.101108

Cited by 34 publications

(24 citation statements)

References 70 publications

(81 reference statements)

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“…In our previous studies, we have found that NiCl 2 induces inflammatory destruction in the kidney and liver of broiler chickens, by activating NF-κB pathway activation and upregulating the mRNA levels of IL-1β, -6, -8 and TNF-α [30, 31]. Here, we showed that NiCl 2 activated NF-κB pathway.…”

Section: Discussionmentioning

confidence: 61%

“…Total RNA was isolated from the treated BMDM and was reverse transcribed. QRT-PCR reactions were carried out as proposed by Guo et al [30]. QRT-PCR data were analyzed by the 2 −ΔΔCT method [40].…”

Section: Methodsmentioning

confidence: 99%

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Guo

Liu

Jian

et al. 2019

Aging

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Nickel (Ni), an environmental hazard, widely causes allergic contact hypersensitivity worldwide. Despite that Ni-stimulated pro-inflammatory response is vital in allergy, the underlying molecular mechanisms remain largely unclear. Here, we demonstrated that NiCl2 activated nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1β (IL-1β), -6, -8, -18, tumor necrosis factor-α (TNF-α) and interferon β (INF-β). We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1β. NiCl2 induced the accumulation of mitochondrial reactive oxygen species (mtROS) and the release of mitochondrial DNA (mtDNA), thus activating NLRP3 inflammasome pathway. Additionally, NiCl2-induced apoptosis was dependent on the generation of mtROS, and caspase-1 activation might also partly contribute to the apoptotic process. Altogether, abovementioned results indicate that NiCl2 induces inflammatory activation in BMDMs via NF-κB, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.

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“…BOK has a proapoptotic function in regulating ER stress-induced apoptosis. This links apoptotic sensing at the ER to apoptotic activity at the mitochondria [ 33 , 34 ]. In the second aspect, BCL2 has a crucial effect on autophagy.…”

Section: Discussionmentioning

confidence: 99%

Coherent apoptotic and autophagic activities involved in regression of chicken postovulatory follicles

Lin

Liu

et al. 2018

Aging

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After ovulation in mammals, rupture of mature follicles is reorganized into the corpus luteum that secrets progesterone (P4) to stimulate endometrial development. The situation in birds differs considerably. Beyond ovulation the ruptured avian follicle forms a postovulatory follicle (POF) that is not considered analogous to mammalian corpus luteum. The function and regression mechanisms of avian POFs remain poorly understood. Here we investigated the changes in apoptotic and autophagic activities that were involved during POF degradation. Results showed that the structure and secretory function of POF3 manifested the most apparent deterioration during whole processes of regression. A TUENL assay revealed that the granulosa layer maintained longer viability than the theca layer. Importantly, mitochondrial apoptosis and endoplasmic reticulum (ER) stress-associated genes and proteins reached their highest levels in the granulosa cells of POF3. Beclin1 was distributed mainly in theca cells and coupled with LC3β-II accumulation, Sequestosome-1 (p62) degradation and Beclin1 elevation confirmed that autophagic activity had increased dramatically in the theca layer of POFs. These results indicate that the apoptosis of the granulosa cells from POFs occurs by mitochondrial apoptosis and ER stress and that a coherence of Beclin1-induced autophagy and caspase-induced apoptosis results in regression of theca layers of avian POFs.

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“…DNA damaged cells accumulate at Gap1 (G1), DNA synthesis (s), or Gap2 / Mitosis (G2/M). Studies have shown that [68][69] Nickel chloride (NiCl2) induces G2 / M arrest of the liver. A large number of metal ions accumulated in the body can induce a series of pro-in ammatory reactions.…”

Section: Discussionmentioning

confidence: 99%

Study on Mechanical Property and Biocompatibility in Vitro of 3D Printing Tantalum- Niobium Alloy Implants.

Zhang

Yao

et al. 2021

Preprint

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tooth defects or deletions. Tantalum (Ta) has been widely used in the biomedical field, but its application in artificial dental implants is rarely reported. In this study, Tantalum-Niobium alloy (TaNb40) implant prepared by 3D printing—SLS was used as the research subject. Its mechanical properties in vitro and the biocompatibility by utilizing human Oral Mucosa Fibroblasts (hOMF) were studied. Results: The mechanical property test results were that the Tensile Strength, Yield Strength, Elongation, and Vickers hardness of TaNb40 implant was 548 ± 50MPa, 420 ± 30MPa, 40%, and 425HV, respectively, manifesting the two indicators met the requirements of dental metal implant, and had good mechanical properties of wear resistance and not easy to brittle fracture. The cytocompatibility test showed that TaNb40 did not inhibit cell proliferation and produce cell cycle arrest. The cytotoxicity grade was 1, there was almost no metal ion release in the culture medium, and the surface had fine cell early adhesion, which met the requirements of biomedical materials. Conclusion: The TaNb40 prepared by domestic 3D printing—SLS has excellent mechanical properties and cytocompatibility in vitro, which is expected to replace the Titanium metal implant prepared by the traditional casting method, having a leading significance for the formation of implants with independent intellectual property rights.

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“…Numbers in in vitro and in vivo studies have presented that Ni and Ni compounds can induce DNA damage [29,30,31,32,33]. We also found that DNA oxidative damage and cell cycle arrest can be induced by dietary nickel chloride (NiCl 2 ) in excess of 300 mg/kg in the thymus, the bursa of Fabricius, the kidney, and the liver of broiler chickens [34,35,36,37]. If the DNA repair system cannot repair the damaged DNA, and the damaged DNA is passed onto the daughter DNA, this causes genomic instability, which finally promotes cancer development [38,39,40,41].…”

Section: Introductionmentioning

confidence: 99%

Nickel Carcinogenesis Mechanism: DNA Damage

Guo

Liu

et al. 2019

IJMS

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Nickel (Ni) is known to be a major carcinogenic heavy metal. Occupational and environmental exposure to Ni has been implicated in human lung and nasal cancers. Currently, the molecular mechanisms of Ni carcinogenicity remain unclear, but studies have shown that Ni-caused DNA damage is an important carcinogenic mechanism. Therefore, we conducted a literature search of DNA damage associated with Ni exposure and summarized known Ni-caused DNA damage effects. In vitro and vivo studies demonstrated that Ni can induce DNA damage through direct DNA binding and reactive oxygen species (ROS) stimulation. Ni can also repress the DNA damage repair systems, including direct reversal, nucleotide repair (NER), base excision repair (BER), mismatch repair (MMR), homologous-recombination repair (HR), and nonhomologous end-joining (NHEJ) repair pathways. The repression of DNA repair is through direct enzyme inhibition and the downregulation of DNA repair molecule expression. Up to now, the exact mechanisms of DNA damage caused by Ni and Ni compounds remain unclear. Revealing the mechanisms of DNA damage from Ni exposure may contribute to the development of preventive strategies in Ni carcinogenicity.

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Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response

Cited by 34 publications

References 70 publications

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Coherent apoptotic and autophagic activities involved in regression of chicken postovulatory follicles

Study on Mechanical Property and Biocompatibility in Vitro of 3D Printing Tantalum- Niobium Alloy Implants.

Nickel Carcinogenesis Mechanism: DNA Damage

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