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International Journal of Oral Science Feb 2022Various engine-driven NiTi endodontic files have been indispensable and efficient tools in cleaning and shaping of root canals for practitioners. In this review, we... (Review)
Review
Various engine-driven NiTi endodontic files have been indispensable and efficient tools in cleaning and shaping of root canals for practitioners. In this review, we introduce the relative terms and conceptions of NiTi file, including crystal phase composition, the design of the cutting part, types of separation. This review also analysis the main improvement and evolution of different generations of engine-driven nickel-titanium instruments in the past 20 years in the geometric design, manufacturing surface treatment such as electropolishing, thermal treatment, metallurgy. And the variety of motion modes of NiTi files to improve resistance to torsional failure were also discussed. Continuous advancements by the designers, provide better balance between shaping efficiency and resistance to of NiTi systems. In clinical practice an appropriate system should be selected based on the anatomy of the root canal, instrument characteristics, and operators' experience.
Topics: Dental Alloys; Dental Instruments; Equipment Design; Nickel; Root Canal Preparation; Titanium
PubMed: 35181648
DOI: 10.1038/s41368-021-00154-0 -
Metal Ions in Life Sciences 2013This review focuses on the impact of nickel on human health. In particular, the dual nature of nickel as an essential as well as toxic element in nature is described,... (Review)
Review
This review focuses on the impact of nickel on human health. In particular, the dual nature of nickel as an essential as well as toxic element in nature is described, and the main forms of nickel that can come in contact with living systems from natural sources and anthropogenic activities are discussed. Concomitantly, the main routes of nickel uptake and transport in humans are covered, and the potential dangers that nickel exposure can represent for health are described. In particular, the insurgence of nickel-derived allergies, nickel-induced carcinogenesis as well as infectious diseases caused by human pathogens that rely on nickel-based enzymes to colonize the host are reviewed at different levels, from their macroscopic aspects on human health to the molecular mechanisms underlying these points. Finally, the importance of nickel as a beneficial element for human health, especially being essential for microorganisms that colonize the human guts, is examined.
Topics: Cell Transformation, Neoplastic; Humans; Hypersensitivity; Intestinal Mucosa; Intestines; Nickel
PubMed: 24470096
DOI: 10.1007/978-94-007-7500-8_10 -
Protein Science : a Publication of the... May 2020Nickel enzymes, present in archaea, bacteria, plants, and primitive eukaryotes are divided into redox and nonredox enzymes and play key functions in diverse metabolic... (Review)
Review
Nickel enzymes, present in archaea, bacteria, plants, and primitive eukaryotes are divided into redox and nonredox enzymes and play key functions in diverse metabolic processes, such as energy metabolism and virulence. They catalyze various reactions by using active sites of diverse complexities, such as mononuclear nickel in Ni-superoxide dismutase, glyoxylase I and acireductone dioxygenase, dinuclear nickel in urease, heteronuclear metalloclusters in [NiFe]-carbon monoxide dehydrogenase, acetyl-CoA decarbonylase/synthase and [NiFe]-hydrogenase, and even more complex cofactors in methyl-CoM reductase and lactate racemase. The presence of metalloenzymes in a cell necessitates a tight regulation of metal homeostasis, in order to maintain the appropriate intracellular concentration of nickel while avoiding its toxicity. As well, the biosynthesis and insertion of nickel active sites often require specific and elaborated maturation pathways, allowing the correct metal to be delivered and incorporated into the target enzyme. In this review, the phylogenetic distribution of nickel enzymes will be briefly described. Their tridimensional structures as well as the complexity of their active sites will be discussed. In view of the latest findings on these enzymes, a special focus will be put on the biosynthesis of their active sites and nickel activation of apo-enzymes.
Topics: Biocatalysis; Catalytic Domain; Dioxygenases; Enzymes; Hydrogenase; Lactoylglutathione Lyase; Nickel; Protein Conformation; Superoxide Dismutase; Urease
PubMed: 32022353
DOI: 10.1002/pro.3836 -
The Journal of Biological Chemistry Jul 2009Of the eight known nickel enzymes, all but glyoxylase I catalyze the use and/or production of gases central to the global carbon, nitrogen, and oxygen cycles. Nickel... (Review)
Review
Of the eight known nickel enzymes, all but glyoxylase I catalyze the use and/or production of gases central to the global carbon, nitrogen, and oxygen cycles. Nickel appears to have been selected for its plasticity in coordination and redox chemistry and is able to cycle through three redox states (1+, 2+, 3+) and to catalyze reactions spanning approximately 1.5 V. This minireview focuses on the catalytic mechanisms of nickel enzymes, with an emphasis on the role(s) of the metal center. The metal centers vary from mononuclear to complex metal clusters and catalyze simple hydrolytic to multistep redox reactions.
Topics: Acetate-CoA Ligase; Biochemistry; Carbon; Catalysis; Enzymes; Hydrogenase; Hydrolysis; Metals; Models, Molecular; Molecular Conformation; Nickel; Nitrogen; Oxidation-Reduction; Oxygen; Urease
PubMed: 19363030
DOI: 10.1074/jbc.R900020200 -
Journal of the American Chemical Society Apr 2018We describe the development of an arenophile-mediated, nickel-catalyzed dearomative trans-1,2-carboamination protocol. A range of readily available aromatic compounds...
We describe the development of an arenophile-mediated, nickel-catalyzed dearomative trans-1,2-carboamination protocol. A range of readily available aromatic compounds was converted to the corresponding dienes using Grignard reagents as nucleophiles. This strategy provided products with exclusive trans-selectivity and high enantioselectivity was observed in case of benzene and naphthalene. The utility of this methodology was showcased by controlled and stereoselective preparation of small, functionalized molecules.
Topics: Amination; Catalysis; Molecular Structure; Nickel; Stereoisomerism
PubMed: 29544244
DOI: 10.1021/jacs.8b01726 -
International Journal of Molecular... Sep 2019Nickel (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.... (Review)
Review
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.
Topics: Animals; Carcinogenesis; DNA Breaks, Double-Stranded; DNA Damage; DNA Mismatch Repair; DNA Repair; Humans; Nickel; Reactive Oxygen Species
PubMed: 31546657
DOI: 10.3390/ijms20194690 -
Biochemistry Oct 2012Nickel is an essential metal for a number of bacterial species that have developed systems for acquiring, delivering, and incorporating the metal into target enzymes and... (Review)
Review
Nickel is an essential metal for a number of bacterial species that have developed systems for acquiring, delivering, and incorporating the metal into target enzymes and controlling the levels of nickel in cells to prevent toxic effects. As with other transition metals, these trafficking systems must be able to distinguish between the desired metal and other transition metal ions with similar physical and chemical properties. Because there are few enzymes (targets) that require nickel for activity (e.g., Escherichia coli transports nickel for hydrogenases made under anaerobic conditions, and Helicobacter pylori requires nickel for hydrogenase and urease that are essential for acid viability), the "traffic pattern" for nickel is relatively simple, and nickel trafficking therefore presents an opportunity to examine a system for the mechanisms that are used to distinguish nickel from other metals. In this review, we describe the details known for examples of uptake permeases, metallochaperones and proteins involved in metallocenter assembly, and nickel metalloregulators. We also illustrate a variety of mechanisms, including molecular recognition in the case of NikA protein and examples of allosteric regulation for HypA, NikR, and RcnR, employed to generate specific biological responses to nickel ions.
Topics: Bacteria; Bacterial Proteins; Biological Transport; Gene Expression Regulation, Bacterial; Nickel
PubMed: 22970729
DOI: 10.1021/bi300981m -
Biochemical Society Transactions Aug 2022The nickel-pincer nucleotide (NPN) coenzyme, a substituted pyridinium mononucleotide that tri-coordinates nickel, was first identified covalently attached to a lysine...
The nickel-pincer nucleotide (NPN) coenzyme, a substituted pyridinium mononucleotide that tri-coordinates nickel, was first identified covalently attached to a lysine residue in the LarA protein of lactate racemase. Starting from nicotinic acid adenine dinucleotide, LarB carboxylates C5 of the pyridinium ring and hydrolyzes the phosphoanhydride, LarE converts the C3 and C5 carboxylates to thiocarboxylates, and LarC incorporates nickel to form a C-Ni and two S-Ni bonds, during the biosynthesis of this cofactor. LarB uses a novel carboxylation mechanism involving the transient formation of a cysteinyl-pyridinium adduct. Depending on the source of the enzyme, LarEs either catalyze a sacrificial sulfur transfer from a cysteinyl side chain resulting in the formation of dehydroalanine or they utilize a [4Fe-4S] cluster bound by three cysteine residues to accept and transfer a non-core sulfide atom. LarC is a CTP-dependent enzyme that cytidinylylates its substrate, adds nickel, then hydrolyzes the product to release NPN and CMP. Homologs of the four lar genes are widely distributed in microorganisms, with some species containing multiple copies of larA whereas others lack this gene, consistent with the cofactor serving other functions. Several LarA-like proteins were shown to catalyze racemase or epimerase activities using 2-hydroxyacid substrates other than lactic acid. Thus, lactate racemase is the founding member of a large family of NPN-containing enzymes.
Topics: Coenzymes; Lactobacillus plantarum; Nickel; Nucleotides; Sulfur
PubMed: 35960008
DOI: 10.1042/BST20220490 -
Reviews on Environmental Health 2011Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the... (Review)
Review
Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil- and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel can also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart, and testes can also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.
Topics: Animals; Carcinogens, Environmental; Chromosome Aberrations; DNA Damage; Environmental Exposure; Epigenesis, Genetic; Gene Expression Regulation; Humans; Nickel
PubMed: 21905451
DOI: 10.1515/reveh.2011.012 -
Ecotoxicology and Environmental Safety Feb 2022As one of the main environmental pollutants and occupational hazards, nickel has been reported to have mutagenic, carcinogenic, and teratogenic properties, as well as...
As one of the main environmental pollutants and occupational hazards, nickel has been reported to have mutagenic, carcinogenic, and teratogenic properties, as well as reproductive toxicity. However, how nickel affects human reproduction is still unclear. In this study, the toxicity of nickel on human sperm and the underlying mechanisms were evaluated in vitro. We found that NiCl (10, 50, and 250 μM) impaired sperm total motility and progressive motility in a dose- and time-dependent manner. In addition, sperm hyperactivation and the ability of human sperm to penetrate a viscous medium were found to be compromised after nickel exposure. Mechanically, NiCl significantly inhibited the basal intracellular Ca signaling. Besides, reactive oxygen species (ROS), superoxide, and malondialdehyde levels were increased in human sperm after exposure to different concentrations of NiCl. Consistently, eliminating excess ROS by N-acetyl-L-cysteine or tocopherol significantly alleviated nickel-impaired sperm motility. Taken together, these results revealed that nickel could compromise sperm functions by interfering with Ca signaling and inducing excessive oxidative stress. These findings suggest that, in the high and occupational nickel exposure environments, the contribution of nickel toxicity to the males who wish to preserve their fertility is worthy of careful evaluation.
Topics: Humans; Male; Nickel; Reactive Oxygen Species; Reproduction; Sperm Motility; Spermatozoa
PubMed: 35026585
DOI: 10.1016/j.ecoenv.2022.113181