Hepatic toxicity of nickel chloride in mice

Gathwan, Khalid H.; Al-Karkhi, Isam Hussain T.; Al-Mulla, Emad A. Jaffar

doi:10.1007/s11164-012-0780-x

Cited by 23 publications

(14 citation statements)

References 14 publications

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“…Previous studies have shown that Ni exposure caused liver injuries and dysfunction [7, 43]. The present investigation, the decrease of serum ALB, GLB, TP contents and increase of serum AST, ALT, ALP, GGT activities and TBIL contents demonstrate that excessive NiCl 2 induces hepatic damage.…”

Section: Discussionsupporting

confidence: 68%

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

Guo

Cui

Fang

et al. 2016

Aging

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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.

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Section: Discussionsupporting

confidence: 68%

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

Guo

Cui

Fang

et al. 2016

Aging

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“…Also, our findings are in agreement with the the results of Ma et al and Hossain et al [ 41 , 42 ] who demonstrate that nickel nanowires (Ni NWs) induce apoptosis in Hela cells and human pancreatic adenocarcinoma cells. Also, Gathwan et al [ 43 ] have reported that NiCl 2 can cause apoptotis in liver of male mice.…”

Section: Discussionmentioning

confidence: 99%

Modulation of the PI3K/Akt Pathway and Bcl-2 Family Proteins Involved in Chicken’s Tubular Apoptosis Induced by Nickel Chloride (NiCl2)

Guo

Cui

Peng

et al. 2015

IJMS

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Exposure of people and animals to environments highly polluted with nickel (Ni) can cause pathologic effects. Ni compounds can induce apoptosis, but the mechanism and the pathway of Ni compounds-induced apoptosis are unclear. We evaluated the alterations of apoptosis, mitochondrial membrane potential (MMP), phosphoinositide-3-kinase (PI3K)/serine-threonine kinase (Akt) pathway, and Bcl-2 family proteins induced by nickel chloride (NiCl2) in the kidneys of broiler chickens, using flow cytometry, terminal deoxynucleotidyl transferase 2ʹ-deoxyuridine 5ʹ-triphosphate dUTP nick end-labeling (TUNEL), immunohistochemstry and quantitative real-time polymerase chain reaction (qRT-PCR). We found that dietary NiCl2 in excess of 300 mg/kg resulted in a significant increase in apoptosis, which was associated with decrease in MMP, and increase in apoptosis inducing factor (AIF) and endonuclease G (EndoG) protein and mRNA expression. Concurrently, NiCl2 inhibited the PI3K/Akt pathway, which was characterized by decreasing PI3K, Akt1 and Akt2 mRNA expression levels. NiCl2 also reduced the protein and mRNA expression of anti-apoptotic Bcl-2 and Bcl-xL and increased the protein and mRNA expression of pro-apoptotic Bax and Bak. These results show that NiCl2 causes mitochondrial-mediated apoptosis by disruption of MMP and increased expression of AIF and EndoG mRNA and protein, and that the underlying mechanism of MMP loss involves the Bcl-2 family proteins modulation and PI3K/Akt pathway inhibition.

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“…Nickel can be found naturally in soil, groundwater and surface water, and is used in the coating of stainless steel and alloy products. Nickel can be toxic to mammals and can lead to heart and liver disorders (Gathwan et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

Karabağlar Polyesi̇nde Yeralti Suyu Metal-Metaloi̇t İçeri̇ği̇ni̇n Jeoi̇stati̇sti̇ksel Yöntemlerle Değerlendi̇ri̇lmesi̇ (Muğla, Türki̇ye)

Kurtuluş

Sağır

Avșar

2016

Maden Tetkik Ve Arama Dergisi

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In this research, heavy metals (Ti, Cr, Mn, Fe, Co, Ni, Cu, Zn, Mo, Cd, Ba, Pb) and a metalloid (As) sampled from 84 wells used for drinking water and irrigation in Karabaglar Karstic Polje (Muğla, Turkey) were analyzed. The results were evaluated by different statistical methods in order to investigate the interaction between elements. Ti, Mn, Fe, Zn, Mo and Pb were detected in many wells. According to findings, the strongest correlation is between As and Cu (R=0.832). As-Ni (R=0.789) and Cu-Ni (R=0.776) are the other strong correlations. The relationship between these elements were also shown by Cluster Analysis (CA). With respect to CA, the closest proximity distance matrix are found for these three elements. Also, elements examined composed 3 main clusters in dendrogram created from CA result matrix. These clusters match up with the findings of Principal Component Analysis (PCA) too. PCA gathers all elements up in 3 components: As, Cu and Ni at the first component; Mo and Cd at the second; Cr and Ba at the third. The accumulation of the elements studied were investigated by Kruskal-Wallis and Mann-Whitney U tests. According to the results, the least and the most common elements are Cu and Ba, respectively. The differences in the amount of all elements except Ni and Mo were statistically significant (p<0.05). In addition, both the amount of the elements and some water quality parameters were compared with EPA (U. S. Environmental Protection Agency) and Turkish inland water quality classes and no hazardous situation has been found.

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Hepatic toxicity of nickel chloride in mice

Cited by 23 publications

References 14 publications

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

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

Modulation of the PI3K/Akt Pathway and Bcl-2 Family Proteins Involved in Chicken’s Tubular Apoptosis Induced by Nickel Chloride (NiCl2)

Karabağlar Polyesi̇nde Yeralti Suyu Metal-Metaloi̇t İçeri̇ği̇ni̇n Jeoi̇stati̇sti̇ksel Yöntemlerle Değerlendi̇ri̇lmesi̇ (Muğla, Türki̇ye)

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