Molecular mechanisms of nickel induced neurotoxicity and chemoprevention

Song, Xin; Kenston, Samuel Selorm Fiati; Kong, Lu; Zhao, Jinshun

doi:10.1016/j.tox.2017.10.006

Cited by 84 publications

(47 citation statements)

References 114 publications

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“…We demonstrate that Ni exposure increased LPO and NO levels, accompanied by a significant decrease in SOD and CAT activities in the hippocampus in male and female rats. These results are in agreement with several recent studies showing an increase in LPO levels with a significant decrease in SOD and CAT activities in the brain rats following Ni administration, suggesting an elevation of oxidative stress [56,74]. …”

Section: Discussionsupporting

confidence: 93%

Effect of Chronic Administration of Nickel on Affective and Cognitive Behavior in Male and Female Rats: Possible Implication of Oxidative Stress Pathway

et al. 2018

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Nickel (Ni) toxicity has been reported to produce biochemical and behavioral dysfunction. The present study was undertaken to examine whether Ni chronic administration can induce alterations of affective and cognitive behavior and oxidative stress in male and female rats. Twenty-four rats, for each gender, divided into control and three test groups (n = 6), were injected intraperitoneally with saline (0.9% NaCl) or NiCl2 (0.25 mg/kg, 0.5 mg/kg and 1 mg/kg) for 8 weeks. After treatment period, animals were tested in the open-field, elevated plus maze tests for anxiety-like behavior, and forced swimming test for depression-like behavior. The Morris Water Maze was used to evaluate the spatial learning and memory. The hippocampus of each animal was taken for biochemical examination. The results showed that Ni administration dose dependently increased anxiety-like behavior in both tests. A significant increase in depression-like symptoms was also exhibited by Ni treated rats. In the Morris Water Maze test, the spatial learning and memory were significantly impaired just in males treated with 1 mg/kg of Ni. With regard to biochemical analysis, activity of catalase (CAT) and superoxide dismutase (SOD) were significantly decreased, while the levels of nitric oxide (NO) and lipid peroxidation (LPO) in the hippocampus were significantly increased in the Ni-treated groups. Consequently, chronic Ni administration induced behavioral and biochemical dysfunctions.

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Section: Discussionsupporting

confidence: 93%

Effect of Chronic Administration of Nickel on Affective and Cognitive Behavior in Male and Female Rats: Possible Implication of Oxidative Stress Pathway

et al. 2018

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“…The high spread of products containing this metal unavoidably leads to pollution of the environment by nickel and its secondary products at all stages of manufacturing, recycling and disposal. Even though no existing evidence denotes the nutritional value of Ni in humans, it has been recognized as an essential nutrient for some microorganisms, plants, and animal species [2]. Enzymes or cofactors containing nickel are not known in higher organisms, but nickel-based enzymes are well known in the Archaea, bacteria, algae, primitive eukaryotes and plants [3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

“…Nickel-induced mitochondrial damage can occur, due to impairment of mitochondrial membrane potential, reduction of mitochondrial ATP concentration and destruction of mitochondrial DNA. According to Song and collaborators [2], the use of antioxidant molecules, such as L-carnitine, taurine and melatonin, molecules that stimulate and amplify antioxidant enzyme activity, can prevent nickel-induced neurotoxicity and carcinogenicity [18,19]. Mitochondrial dysfunctions can interfere with electron respiratory chain and can increase ROS.…”

Section: Introductionmentioning

confidence: 99%

Nickel: Human Health and Environmental Toxicology

Genchi

Carocci

Lauria

et al. 2020

IJERPH

877

383

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Nickel is a transition element extensively distributed in the environment, air, water, and soil. It may derive from natural sources and anthropogenic activity. Although nickel is ubiquitous in the environment, its functional role as a trace element for animals and human beings has not been yet recognized. Environmental pollution from nickel may be due to industry, the use of liquid and solid fuels, as well as municipal and industrial waste. Nickel contact can cause a variety of side effects on human health, such as allergy, cardiovascular and kidney diseases, lung fibrosis, lung and nasal cancer. Although the molecular mechanisms of nickel-induced toxicity are not yet clear, mitochondrial dysfunctions and oxidative stress are thought to have a primary and crucial role in the toxicity of this metal. Recently, researchers, trying to characterize the capability of nickel to induce cancer, have found out that epigenetic alterations induced by nickel exposure can perturb the genome. The purpose of this review is to describe the chemical features of nickel in human beings and the mechanisms of its toxicity. Furthermore, the attention is focused on strategies to remove nickel from the environment, such as phytoremediation and phytomining.

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“…Additionally, mitochondria are considered to be the main sites producing ROS. Mitochondrial dysfunction can interfere with electron transferring and further amplifying more ROS generation [32]. In our previous study, we detected the nickel-induced intracellular ROS production, including nonspecific intracellular esterase, superoxide anions, hydrogen peroxide, or hydroxyl radical while using various ROS-sensitive probes.…”

Section: Discussionmentioning

confidence: 99%

Metformin Mitigates Nickel-Elicited Angiopoietin-Like Protein 4 Expression via HIF-1α for Lung Tumorigenesis

Kang

Hsu

et al. 2020

IJMS

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Nickel (Ni), which is a carcinogenic workplace hazard, increases the risk of lung cancer. Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional cytokine that is involved in both angiogenesis and metastasis, but its role in lung cancer is still not clear. In this study, we assessed the role of ANGPTL4 in lung carcinogenesis under nickel exposure and investigated the effects of the antidiabetic drug metformin on ANGPTL4 expression and lung cancer chemoprevention. Our results showed that ANGPTL4 is increased in NiCl2-treated lung cells in a dose- and time-course manner. The expression of ANGPTL4 and HIF-1α induced by NiCl2 were significantly repressed after metformin treatment. The downregulation of HIF-1α expression by ROS savenger and HIF-1α inhibitor or knockdown by lentiviral shRNA infection diminished NiCl2-activated ANGPTL4 expression. Chromatin immunoprecipitation and the luciferase assay revealed that NiCl2-induced HIF-1α hypoxia response element interactions activate ANGPTL4 expression, which is then inhibited by metformin. In conclusion, the increased presence of ANGPTL4 due to HIF-1α accumulation that is caused by nickel in lung cells may be one mechanism by which nickel exposure contributes to lung cancer progression. Additionally, metformin has the ability to prevent NiCl2-induced ANGPTL4 through inhibiting HIF-1α expression and its binding activity. These results provide evidence that metformin in oncology therapeutics could be a beneficial chemopreventive agent.

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Molecular mechanisms of nickel induced neurotoxicity and chemoprevention

Cited by 84 publications

References 114 publications

Effect of Chronic Administration of Nickel on Affective and Cognitive Behavior in Male and Female Rats: Possible Implication of Oxidative Stress Pathway

Effect of Chronic Administration of Nickel on Affective and Cognitive Behavior in Male and Female Rats: Possible Implication of Oxidative Stress Pathway

Nickel: Human Health and Environmental Toxicology

Metformin Mitigates Nickel-Elicited Angiopoietin-Like Protein 4 Expression via HIF-1α for Lung Tumorigenesis

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