Evidence for the involvement of hydroxyl radicals in nickel mediated enhancement of lipid peroxidation: Implications for nickel carcinogenesis

Athar, Mohammad; Hasan, Syed Kazim; Srivastava, R.C.

doi:10.1016/s0006-291x(87)80208-5

Cited by 78 publications

(32 citation statements)

References 15 publications

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“…As reported by Athar et al [4], Ni(I1) ions could trigger peroxidation damage of lipids by lowering glutathione peroxidase activity. Moreover, our results show that, when chelated with peptides containing the glycylglycyl-L-histidine sequence, Ni(I1) ions could also peroxidize lipids either through hydrogen peroxide disproportionation and hydroxyl radical production or directly by reaction with the lipid hydroperoxides.…”

Section: Discussionmentioning

confidence: 57%

“…In vivo, the carcinogenic and toxic activities of nickel are thought to result in depletion of glutathione peroxidase [4]: increased levels of reduced glutathione may indirectly help to generate free radicals by reducing ferric ions to ferrous ions. On the contrary, in spin trapping EPR studies of isolated systems, Inoue and Kawanishi [6] have reported the formation of significant amounts of hydroxyl radical adducts and superoxide adducts with glycylglycyl-lhistidine, triglycine, tetraglycine and pentaglycine but not with glycyl-L-histidine or glycylglycine.…”

Section: Methodsmentioning

confidence: 99%

“…In vivo, nickel like iron was reported to increase lipid peroxidative damage [3,4]. The peroxidative potential of iron is generally related to its ability to generate, in situ, reactive oxygen species through reactions commonly referred to as Haber-Weiss and Fenton chemistry [5] and summarized as follows:…”

Section: Introductionmentioning

confidence: 99%

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Nickel (II) as a temporary catalyst for hydroxyl radical generation

Torreilles

Guérin

1990

FEBS Letters

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Many in vivo studies show peroxidative damage during nickel toxicity, suggesting the generation of oxygen-activated species. Using the murexide (5,Snitrilodibarbituric acid ammonium salt) bleaching technique, we attempted to spectroscopically determine whether there are any histidylpeptides-Ni (II) complexes able to catalyze a nickel-dependent reduction of hydrogen peroxide leading to free oxygen radical production, We show that peptides containing the glycyl-glycyl-L-histidyl sequence trigger nickel-dependent production of oxygen radicals which can damage proteins, cause a rapid loss of tryptophan and a significant production of bityrosine and also induce peroxidation of polyunsaturated fatty acids. During the reaction, the histidine residue in the peptide is selectively damaged and breakdown of the peptide switches off hydroxyl-radical production.

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Section: Discussionmentioning

confidence: 57%

Section: Methodsmentioning

confidence: 99%

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Nickel (II) as a temporary catalyst for hydroxyl radical generation

Torreilles

Guérin

1990

FEBS Letters

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“…75 The administration of nickel to rats results in enhanced lipid peroxidation, decreased glutathione peroxidase activity, and increased tissue iron levels. 92 The carcinogenicity of nickel compounds may be related to enhanced production of reactive oxygen species, presumably through the formation of oxidative tissue damage including damage to DNA. It is possible that the nickel-induced accumulation of iron may be directly responsible for the formation of reactive oxygen species and the subsequent enhancement of lipid peroxidation.…”

Section: Nickelmentioning

confidence: 99%

Oxidative mechanisms in the toxicity of metal ions

Stohs

Bagchi

1995

Free Radical Biology and Medicine

3,691

2,001

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The role of reactive oxygen species, with the subsequent oxidative deterioration of biological macromolecules in the toxicities associated with transition metal ions, is reviewed. Recent studies have shown that metals, including iron, copper, chromium, and vanadium undergo redox cycling, while cadmium, mercury, and nickel, as well as lead, deplete glutathione and protein-bound sulfhydryl groups, resulting in the production of reactive oxygen species as superoxide ion, hydrogen peroxide, and hydroxyl radical. As a consequence, enhanced lipid peroxidation, DNA damage, and altered calcium and sulfhydryl homeostasis occur. Fenton-like reactions may be commonly associated with most membranous fractions including mitochondria, microsomes, and peroxisomes. Phagocytic cells may be another important source of reactive oxygen species in response to metal ions. Furthermore, various studies have suggested that the ability to generate reactive oxygen species by redox cycling quinones and related compounds may require metal ions. Recent studies have suggested that metal ions may enhance the production of tumor necrosis factor alpha (TNFc0 and activate protein kinase C, as well as induce the production of stress proteins, Thus, some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics. Specific differences in the toxicities of metal ions may be related to differences in solubilities, absorbability, transport, chemical reactivity, and the complexes that are formed within the body. This review summarizes current studies that have been conducted with transition metal ions as well as lead, regarding the production of reactive oxygen species and oxidative tissue damage.

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“…Nickel compounds such as nickel subsulfide (Ni 3 S 2 ) are potent carcinogens, but soluble nickel salts such as nickel chloride (NiCl 2 ) exert weaker effects. The molecular mechanisms involved in the cytotoxicity and carcinogenicity of nickel compounds are not fully understood, but nickel might be associated with the intracellular production of reactive oxygen species (ROS), including superoxide, H 2 O 2 , singlet oxygen, and hydroxyl radicals (4)(5)(6)(7)(8). Nickel also increases lipid peroxide (LPO) levels, resulting in the generation of peroxyl radicals, lipid hydroperoxides, and alkoxyl radicals (9)(10)(11).…”

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confidence: 99%

Identification of Two Nickel Ion-Induced Genes, NCI16 and Pc GST1 , in Paramecium caudatum

et al. 2014

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dHere, we describe the isolation of two nickel-induced genes in Paramecium caudatum, NCI16 and PcGST1, by subtractive hybridization. NCI16 encoded a predicted four-transmembrane domain protein (ϳ16 kDa) of unknown function, and PcGST1 encoded glutathione S-transferase (GST; ϳ25 kDa) with GST and glutathione peroxidase (GPx) activities. Exposing cells to cobalt chloride also caused the moderate upregulation of NCI16 and PcGST1 mRNAs. Both nickel sulfate and cobalt chloride dose dependently induced NCI16 and PcGST1 mRNAs, but with different profiles. Nickel treatment caused a continuous increase in PcGST1 and NCI16 mRNA levels for up to 3 and 6 days, respectively, and a notable increase in H 2 O 2 concentrations in P. caudatum. NCI16 expression was significantly enhanced by incubating cells with H 2 O 2 , implying that NCI16 induction in the presence of nickel ions is caused by reactive oxygen species (ROS). On the other hand, PcGST1 was highly induced by the antioxidant tertbutylhydroquinone (tBHQ) but not by H 2 O 2 , suggesting that different mechanisms mediate the induction of NCI16 and PcGST1. We introduced a luciferase reporter vector with an ϳ0.42-kb putative PcGST1 promoter into cells and then exposed the transformants to nickel sulfate. This resulted in significant luciferase upregulation, indicating that the putative PcGST1 promoter contains a nickel-responsive element. Our nickel-inducible system also may be applicable to the efficient expression of proteins that are toxic to host cells or require temporal control. N ickel is used extensively for electroplating metals, alloys such as cupronickel, and rechargeable batteries. Occupational exposure to nickel occurs in industrial workers, in particular those involved in mining, smelting, and refining, the production of steel and other metals, and electronic devices (1). Nickel compounds are released into the environment from power plants that burn oil, trash incinerators, wastewater from nickel mines, and industries that manufacture nickel products for industrial and consumer use. Nickel has toxic and carcinogenic effects on most microorganisms and animals and is considered to impose an industrial health hazard (2, 3). Nickel compounds such as nickel subsulfide (Ni 3 S 2 ) are potent carcinogens, but soluble nickel salts such as nickel chloride (NiCl 2 ) exert weaker effects. The molecular mechanisms involved in the cytotoxicity and carcinogenicity of nickel compounds are not fully understood, but nickel might be associated with the intracellular production of reactive oxygen species (ROS), including superoxide, H 2 O 2 , singlet oxygen, and hydroxyl radicals (4-8). Nickel also increases lipid peroxide (LPO) levels, resulting in the generation of peroxyl radicals, lipid hydroperoxides, and alkoxyl radicals (9-11). Carcinogenesis related to nickel is explained by several types of DNA damage, such as cleavage, depurination, cross-linking, and DNA base damage caused by ROS (12). Nickel inhibits processes in the DNA repair system, such as DNA ligation and DNA p...

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Evidence for the involvement of hydroxyl radicals in nickel mediated enhancement of lipid peroxidation: Implications for nickel carcinogenesis

Cited by 78 publications

References 15 publications

Nickel (II) as a temporary catalyst for hydroxyl radical generation

Nickel (II) as a temporary catalyst for hydroxyl radical generation

Oxidative mechanisms in the toxicity of metal ions

Identification of Two Nickel Ion-Induced Genes, NCI16 and Pc GST1 , in Paramecium caudatum

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