Nickel ammonium sulfate hexahydrate (H8N2NiO8S2) is an exogenous inorganic compound with an average molecular weight of 286.90 g/mol. It exists as a solid at room temperature. Nickel ammonium sulfate hexahydrate belongs to the transition metal sulfates, a subclass of transition metal oxoanionic compounds within the inorganic compounds. This substance is released from or found in electrical and electronic equipment, specifically antennas, electric switches, and thin magnetic films.
The compound interacts with ten recorded protein targets. Nickel exhibits a high affinity for chromatin proteins, such as Histone H1.4 (H1-4) and Histone H2B type 1-C/E/F/G/I (H2BC4); the resulting complexing with heterochromatin can lead to DNA hypermethylation, condensation, gene silencing, and inhibition of histone acetylation, which disturb gene expression. Nickel also substitutes for iron in several proteins, which inhibits their activity. This occurs in alpha-ketoglutarate-dependent dioxygenases, including DNA oxidative demethylase ALKBH2 and Alpha-ketoglutarate-dependent dioxygenase alkB homolog 3 (ALKBH3), thereby inhibiting DNA repair. Similarly, nickel substitutes for iron in prolyl hydroxylases EGLN1, EGLN2, and EGLN3, which prevents their enzyme activity and causes hypoxia-mimic stress through the accumulation of hypoxia inducible factor 1 alpha. Furthermore, nickel inhibits the demethylation activity of jmjC domain-containing histone demethylation proteins (unnamed protein) by substituting for iron. Finally, nickel is known to substitute for other essential elements in calcineurin, specifically targeting the catalytic subunit alpha (PPP3CA) and subunits B type 1 (PPP3R1) and type 2 (PPP3R2).
belongs to the class of inorganic compounds known as transition metal sulfates. These are inorganic compounds in which the largest oxoanion is sulfate, and in which the heaviest atom not in an oxoanion is a transition metal.
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)
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. (4)
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)
