Nitric oxide and bcl-2 mediated the apoptosis induced by nickel(II) in human T hybridoma cells

Guan, Fuqin; Zhang, Dongmei; Wang, Xinchang; Chen, Junhui

doi:10.1016/j.taap.2007.01.029

Cited by 29 publications

(21 citation statements)

References 45 publications

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“…In the study of Guan, it has been demonstrated that the generation of NO was stimulated by Ni [77]. Generally, NO is produced at the cellular level from arginine and oxygen.…”

Section: Discussionmentioning

confidence: 99%

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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“…In the study of Guan, it has been demonstrated that the generation of NO was stimulated by Ni [77]. Generally, NO is produced at the cellular level from arginine and oxygen.…”

Section: Discussionmentioning

confidence: 99%

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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“…In contrast, over expression of Bad and Bax promotes initiation of apoptosis. It was reported that apoptotic effects in Hep3B and Jurkat cells induced by Ni may involve downregulation of Bcl-2 expression (Kang et al, 2004;Guan et al, 2007). Thus, Bcl-2 was selected as one candidate involved in Ni-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Nickel(II)-Induced Oxidative Stress, Apoptosis, G2/M Arrest, and Genotoxicity in Normal Rat Kidney Cells

Chen¹,

Lin

Chang

et al. 2010

Journal of Toxicology and Environmental Health, Part A

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In order to elucidate the effects of nickel (Ni) on oxidative stress, apoptosis, and genotoxicity in renal cells, the levels of intracellular oxidants, lipid peroxidation, apoptotic proteins, and DNA damage were measured in normal rat kidney (NRK) cells after nickel chloride (NiCl(2)) treatment. NiCl(2) appeared to increase the formation of the fluorescent oxidized compound (dichlorofluorescein, DCF) and levels of thiobarbituric acid-reactive substances (TBARS). In flow cytometric analysis, a rise in cell proportion in sub-G1 phase occurred in a concentration-dependent manner. After Ni treatment, there was reduced expression of Bcl-2 and Bcl-xL proteins, while induced Bad and Bax proteins expression was higher. Single-strand DNA breakage induced by Ni in NRK cells was determined by comet assay. Significant increase DNA damage score (arbitrary units) was noted in a concentration-related manner after treatment with Ni. Induction of intracellular oxidants by Ni was accompanied by an increasing frequency of DNA strand breakage. Our data indicate that Ni-induced oxidative stress and genotoxicity in NRK cells may involve reactive oxygen intermediates, and that Bcl family-mediated signaling pathway may be involved in positive regulation of Ni-induced renal cytotoxicity.

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“…The cytotoxic effects of nickel involved significant morphological changes and chromosomal condensation [178]. Indication of apoptotic cell death by nickel was mediated by reduction of Bcl-2 expression.…”

Section: Apoptosismentioning

confidence: 99%

Metals and apoptosis: Recent developments

Rana

2008

Journal of Trace Elements in Medicine and Biology

332

175

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Nitric oxide and bcl-2 mediated the apoptosis induced by nickel(II) in human T hybridoma cells

Cited by 29 publications

References 45 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(II)-Induced Oxidative Stress, Apoptosis, G2/M Arrest, and Genotoxicity in Normal Rat Kidney Cells

Metals and apoptosis: Recent developments

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