Nickel (Ni) is an essential nutrient for higher animals. Although a number
of cellular effects of nickel have been documented, a deficiency disease has
not been described in man. Nickel is found in highest concentrations in lung,
kidney and some hormone-producing tissues.
Although nickel-specific enzymes have yet to be identified in higher animals,
nickel can activate or inhibit a number of enzymes that usually contain other
elements. The production or action of some hormones (prolactin, adrenaline,
noradrenaline, aldosterone) responds to changes in nickel concentration. Within
cells, nickel alters membrane properties and influences oxidation/reduction
systems. Nickel has great affinity for cellular structures such as chromosomes
and ion channels, but its influence on them at normal tissue concentrations
is not known.
Deficiencies: It is difficult to induce a deficiency because the
requirement is low and nickel comes from a variety of sources. Feeding a low
nickel diet has reduced the growth of several species of animals. At the cellular
level structures become disorganized and membrane properties change. Nickel
deficiency has been linked to low blood glucose levels, abnormal bone growth,
poor absorption of ferric iron, and altered metabolism of calcium, vitamin
B-12 and energy nutrients.
Diet recommendations: Based on animal experiments, the human requirement
for nickel probably does not exceed 100 µg/day. Nickel content of Western
self-selected and institutional diets ranges from 60 to 260 µg/day. Adequacy
of the lower intakes may depend on the bio availability of nickel (the nickel
compounds ingested and foods consumed with them).
Food sources: Rich food sources of nickel include oatmeal, dried
beans and peas, nuts, and chocolate. The apparent absorption from test meals
is about 1%. Up to 27% is absorbed from water but the daily intake of water
provides only 1-2 µg Ni. Absorption is influenced by the amount fed, the acidity
of the gut, and the presence of various binding agents (as phytate) or competing
substances. In particular, the levels of other minerals such as iron, magnesium,
zinc and calcium may alter nickel absorption from the gut.
Toxicity: Toxicity has occurred in workers exposed to nickel dust
or nickel carbonyl formed in refining. Increased risk of nasal and lung cancers
was linked to occupational nickel exposure before current workplace safety
standards were set. Environmental sources of lower levels of nickel include
tobacco, dental or orthopedic implants, stainless steel kitchen utensils and
inexpensive jewelry. Repeated exposures may lead to asthma and contact dermatitis,
symptoms of which may worsen if the diet is high in nickel. The oral toxic
dose is about 1000 times the amount consumed in food. Different chemical forms
vary widely in toxicity. Excessive nickel in tissues is pro-oxidant (damaging
chromosomes and other cell components) and alters hormone and enzyme activities,
movement of ions through membranes, and immune function. These effects can
change glucose tolerance, blood pressure, response to stress, growth rate,
bone development and resistance to infection. Under some conditions, large
amounts of nickel may precipitate magnesium deficiency or cause accumulation
of iron or zinc.
Recent research: Additional information is needed to establish more
precisely an intake/exposure range that is both adequate and safe, and to
account for other factors that affect the need and tolerance for nickel.
For further information:
Kenney, M.A., & McCoy, H. (1992) A review of bio interactions of Ni and
Mg. I. Enzyme, endocrine, transport, and skeletal systems. Magnes. Res. 5:
Nielsen, F.H. (1991) Nutritional requirements for boron, silicon, vanadium,
nickel, and arsenic: current knowledge and speculation. FASEB J. 5: 2661-2667
Sigel, H. & Sigel, A., eds. (1988) Metal Ions in Biological Systems, vol.
23. Nickel and Its Role in Biology. Marcel Dekker, New York, NY.
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