Nickel tetracarbonyl Ni(CO)4 is an organometallic compound of nickel. Its volatility at room temperature and toxicity have earned the compound the nickname liquid death. This pale-yellow liquid is the principal carbonyl of nickel. It is an intermediate in the Mond process for the purification of nickel and a reagent in organometallic chemistry. Nickel carbonyl is one of the most toxic substances encountered in industrial processes.Nickel is a chemical compound with the atomic number 28. It is found abundantly in nature in laterite ore minerals, such as limonite, garnierite, and pentlandite. Nickel has a biological role and is found in certain enzymes, including urease, hydrogenase, methylcoenzyme M reductase, and carbon monoxide dehydrogenase. (2, 3, 7)
belongs to the class of inorganic compounds known as miscellaneous mixed metal/non-metals. These are inorganic compounds containing non-metal as well as metal atoms but not belonging to afore mentioned classes.
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. (3, 1)
Metabolism
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. (3)
Toxicity Values
LC50: 35 ppm over 30 minutes (Inhalation, Mouse) (8)
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. (3)
Symptoms
Symptoms of nickel poisoning include headache, nausea, vomiting, dizziness, irritability, and difficulty sleeping, followed by chest pains, sweating, rapid heart beat, and a dry cough. Nickel tetracarbonyl poisoning is characterized by a two-stage illness. The first consists of headaches and chest pain lasting a few hours, usually followed by a short remission. The second phase is a chemical pneumonitis which starts after typically 16 hours with symptoms of cough, breathlessness and extreme fatigue. These reach greatest severity after four days, possibly resulting in death from cardiorespiratory or renal failure. Convalescence is often extremely protracted, often complicated by exhaustion, depression and dyspnea on exertion. (4, 7)
Treatment
Excess exposure to nickel is usually handled by preventing further exposure and symptomatic treatment. Nickel poisoning may also be treated using chelation therapy with sodium diethyldithiocarbamate. (4)
