Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and _2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, wherease unabsorbed nickel is excreted in the faeces. (L41)
Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. (L41, A40)
Evaluation: There is sufficient evidence in humans for the carcinogenicity of nickel sulfate, and of the combinations of nickel sulfides and oxides encountered in the nickel refining industry. There is inadequate evidence in humans for the carcinogenicity of metallic nickel and nickel alloys. There is sufficient evidence in experimental animals for the carcinogenicity of metallic nickel, nickel monoxides, nickel hydroxides and crystalline nickel sulfides. There is limited evidence in experimental animals for the carcinogenicity of nickel alloys, nickelocene, nickel carbonyl, nickel salts, nickel arsenides, nickel antimonide, nickel selenides and nickel telluride. There is inadequate evidence in experimental animals for the carcinogenicity of nickel trioxide, amorphous nickel sulfide and nickel titanate. The Working Group made the overall evaluation on nickel compounds as a group on the basis of the combined results of epidemiological studies, carcinogenicity studies in experimental animals, and several types of other relevant data, supported by the underlying concept that nickel compounds can generate nickel ions at critical sites in their target cells. Overall evaluation: Nickel compounds are carcinogenic to humans (Group 1). Metallic nickel is possibly carcinogenic to humans (Group 2B). /Nickel compounds/
The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. (L41)
Direct reaction of meta powders with several sodium dithiocarbamates
作者：T. Tetsumi、M. Sumi、M. Tanaka、T. Shono
DOI：10.1016/s0277-5387(00)84424-1
日期：1986.1
Copper and nickel powders react directly with sodium dithiocarbamates in organic solvents and produce the corresponding metal complexes. The rate constants have been estimated spectrohotometrically. The effects of organic solvents and substituents of the carbamates on the relative reactivity were studied. The results show that copper powder reacts in chloroform more readily than any other system examined
Synthesis of Transition Metal Arsenides and Arsenic Metal Sulfides and Their Role in the Dearsenation of Shale Oils
作者：G.H. Singhal、L.D. Brown、D.F. Ryan
DOI：10.1006/jssc.1994.1095
日期：1994.4
upgrading shale oil is the presence of inherent arsenic, which is known to poison downstream catalysts. Highly dispersed transitionmetalsulfides formed in situ from the decomposition of dithiocarbamate (DTC) complexes of transitionmetals show excellent potential as dearsenation agents. We have studied the reaction of these sulfides with various arsenic compositions, and characterized the metal arsenides
页岩油升级的主要问题之一是固有砷的存在，已知该砷会毒害下游催化剂。高度分散的形成过渡金属硫化物原位从二硫代氨基甲酸的分解器（DTC）的过渡金属配合物表现出优异的电势作为dearsenation剂。我们已经研究了这些硫化物与各种砷成分的反应，并表征了形成的金属砷化物和砷金属硫化物以及其形成的难易程度。因此，双（丁基二硫代氨基甲酸酯）Ni（NiBuDTC）与模型化合物的反应非常容易，得到NiAs，NiAsS和NiAs 2- x S x。通常，硫化物的脱砷效果遵循Ni> Mo⪢Co的顺序，而硫化铁则完全无效。根据这些结果，使用Ni BuDTC和具有73 ppm固有砷的页岩油在高压釜（以及固定床流通装置）中进行测试。在最佳条件下，脱砷率可降至1 ppm以下。
Structural Organization of Nickel(II), Zinc(II), and Copper(II) Complexes with Diisobutyldithiocarbamate: EPR, 13C and 15N CP/MAS NMR, and X-Ray Diffraction Studies
作者：A. V. Ivanov、E. V. Korneeva、A. V. Gerasimenko、W. Forsling
DOI：10.1007/s11173-005-0157-4
日期：2005.10
amate were studied by EPR and 13C and 15N CP/MAS NMR spectroscopy and X-raydiffraction analysis. According to the EPR data, copper(II) forms mononuclear [63/65CuS2CNR2}2] and heterobinuclear complexes [63/65CuZnS2CNR2}4] under magnetic dilution conditions. The isomeric forms of nickel(II) and zinc(II) diisobutyldithiocarbamates were detected by 13C and 15N NMR spectroscopy. The crystalline zinc(II)
通过EPR和13 C和15 N CP / MAS NMR光谱学和X射线衍射分析研究了镍（II），锌（II）和铜（II）与二丁基和二异丁基二硫代氨基甲酸酯的配合物的结构和光谱性质。根据EPR数据，铜（II）在磁稀释条件下形成单核[ 63/65 Cu S 2 CNR 2 } 2 ]和异双核络合物[ 63/65 CuZn S 2 CNR 2 } 4 ]。在13 C和15 C下检测到二异丁基二硫代氨基甲酸镍（II）和锌（II）的异构体形式N NMR光谱。结晶锌（II）二异丁基二被发现具有以交替单核独特的结构组织[锌S 2 CN（ 我 -C 4 ħ 9）2 } 2 ]和双核分子形式[锌2 S 2 CN（ 我 - C 4 H 9）2 } 4 ]的比例为1：1。
