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Indian Veterinary Research Institute (IVRI), India.
*Corresponding Author: ([email protected])
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Nickel is an emerging essential trace element. The essentiality of nickel is now generally
accepted, based on the various symptoms caused by nickel deficiency in different animals. It
is found in highest concentrations in lung, kidney and some hormone-producing tissues.
Alteration in nickel concentration affects the production and action of some hormones like
prolactin, adrenaline, noradrenaline and aldosterone. Within cells, nickel changes membrane
properties and influences oxidation/reduction systems. It has great affinity for cellular
structures like chromosomes and ion channels. This element is also important for proper
functioning of the immune system. In animals, nickel deficiency has been associated with
depressed growth, reduced reproductive rates and alterations in glucose and lipid metabolism
whereas nickel toxicity induces embryo-toxic, teratogenic and cancerogenic effects.
/ -0 )' : Nickel, trace element, deficiency, toxicity.
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Nickel (Ni) is an essential trace element for many species. In animals, nickel deficiency has
been associated with depressed growth, alterations in carbohydrate and lipid metabolism,
delayed gestation period, fewer offspring, anaemia, skin eruptions, reduced haemoglobin and
hematocrit values, hematopoiesis and alterations in the content of iron, copper, and zinc in
liver and reduced activity of several enzymes like hydrogenases, transaminases and αamylase2. The element is important for proper functioning of the immune system. This heavy
metal is a common sensitizing agent and is also reported to induce embryotoxic, teratogenic
and carcinogenic effects. It is also an important metal pollutant of considerable concern;
because its concentration is rapidly increasing in soils of different parts of the world1,
4&9
.
Most forage plants absorb most of the minerals and heavy metals from the soil and polluted
air. So, the uptake of mineral elements can provide significant information on plant forage
mineral concentrations23.
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Pure nickel is a hard silver-white metal with atomic number 28 and weight 58.69. In contrast
to the soluble nickel salts (chloride, nitrate, and sulphate), metallic nickel, nickel sulphides,
and nickel oxides are poorly water soluble. Nickel and its compounds have no characteristic
odour or taste. Nickel usually has two valence electrons, but oxidation states of +1, +3, or +4
may also exist. It occurs naturally in five isotopic forms: 58 (67.8%), 60 (26.2%), 61 (1.2%),
62 (3.7%), and 64 (1.2%).
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Nickel is ubiquitous in the biosphere and ranks 24th in crustal abundance of all elements. This
metal is found in all soil, drinking water and air. There is little evidence that nickel
compounds accumulate in the food chain. Nickel concentrations in air of remote areas are in
the range of 1–3 ng/m3, whereas concentrations in rural and urban air range from 5-35 ng/m3.
Its concentrations in groundwater depend on the soil use, pH, and depth of sampling.
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Of various heavy metals, Ni content of feed or food stuff varies with the site and species. Ni
levels in feed are generally in the range 0.01–0.1 mg/kg. It is fairly evenly distributed
throughout the various food groups but highest concentrations (1-10 mg nickel/kg fresh
weights) are found in roots and vegetables, cocoa and chocolate, soybeans, oatmeal, nuts and
almonds, bread and cereals food groups. Higher median levels of nickel (0.1–0.4 mg/kg) were
found in wholemeal products, whereas markedly higher levels (1–6 mg/kg) were found in
beans, seeds, nuts, and wheat bran. Even higher nickel levels (8–12 mg/kg) were found in
cacao. Diets based on animal origin and fats may be low in nickel16.
Ni concentrations in components used in diets for livestock were 1.4% of corn and 0.6% of
cotton seed hull. Concentrations of Ni in grasses are generally lower than those in soils but
legumes such as Alfalfa contain more Ni. In general, plant foods are higher in Ni than foods
of animal origin. It has been noticed that with diets very low in Ni, animals have failed to
grow, develop and reproduce normally.
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Nickel is a constituent part of all organs of vertebrates3. It is bound to a histidine complex,
albumin, and α-2- macroglobulin in serum. The highest nickel concentrations were found in
the kidneys and lungs, whereas nickel concentrations in the liver were low. Several reports
indicate that trans-placental transfer of nickel occurs in animals. Metal accumulation was not
detected in the blood, brain, hair, small intestine, liver, and testes of adult male rats fed 10 or
20 mg Ni/kg body weight (as NiCI2) for 14 days15.
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Nickel has long been considered a non-essential element, but recent evidence has shown that
it is generally required in small amounts for normal plant growth and thus it has been
included among the micronutrients. It has also been shown to be essential for a wide variety
of animal species including chickens, rats, pigs, cows, sheep, and goats. The essential nature
of an element is established when: (1) it is present in living matter; (2) it is able to interact
with living systems; and (3) a deficiency results in a reduction of a biological function,
preventable or reversible by physiological amounts of the element. Since 1970, nickel has
been shown to meet all these 3 criteria and is known to be essential for proper functioning of
animals13&18.
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Nickel is poorly absorbed from diets and is eliminated mainly in the faeces. Some faecal
nickel may come from the bile. Limited studies suggest that typically less than 10% of
ingested nickel is absorbed. Absorbed nickel is rapidly cleared from serum and excreted in
urine. Intravenously injected nickel is also excreted mainly in the urine.
The mechanism for intestinal absorption of nickel is not clear. In perfused rat jejunum,
saturation of nickel uptake was observed at high concentrations of nickel chloride. Iron
deficiency increased intestinal nickel absorption
and
, indicating that nickel is
partially absorbed by the active transport system for iron absorption in the intestinal mucosal
cells. Active transport of iron is relatively specific for the divalent cation. Thus, when dietary
iron is absorbed as the divalent cation, competition probably occurs between it and the Ni2+
ion for the active transport system. Iron concentrations in rat tissues were increased by dietary
nickel exposure.
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1. Nickel functions either as a cofactor or structural component in specific
metalloenzymes or metalloproteins or as a bio-ligand cofactor facilitating the
intestinal absorption of the Fe3+.
2. A nickel-containing macroglobulin, nickeloplasmin, has been found in human and
rabbit serum but its function is unknown.
3. Methanogenic bacteria possess an enzyme called methyl-CoM reductase that contains
a low-molecular-weight yellow compound named factor F430. This is a nickel
porphynoid (nickel is coordinated with the tetrapyrrole nitrogen) of unique structure.
Like nickeloplasmin, the function of factor F430 is unknown.
4. Another nickel porphynoid natural product called tunichlorin was also identified16&18.
5. Presently, 9 nickel-containing enzymes are known: urease from several plants like
jack beans and microorganisms, Ni-Fe hydrogenase of nickel-requiring "Knallgas"
bacteria, carbon monoxide dehydrogenase from acetogenic bacteria, acetyl-CoA
decarbonilase/synthase,
methyl
coenzyme
M
reductase,
certain
superoxide
dismutases, some glyoxylases, acireductone dioxygenase, and methylene diurease.
Urease from and several species of plants is a nickel protein. These plant enzymes
can affect animals via the microbiological digestion of food in the rumen3&18.
6. Nickel is an essential nutrient for selected microorganisms where it participates in a
variety of cellular processes. Many microbes are capable of sensing cellular nickel
ion concentrations and taking up this nutrient via nickel-specific permeases or ATPbinding cassette-type transport systems. The metal ion is specifically incorporated
into nickel-dependent enzymes, often via complex assembly processes requiring
accessory proteins and additional non-protein components, in some cases
accompanied by nucleotide triphosphate hydrolysis.
7. Nickel, which is bound to ribonucleic acid, has a special affinity for bone and skin
and has been suggested to play an important role in pigmentation.
8. Nickel supplementation alleviates bush sickness caused due to cobalt deficiency.
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Among animals, plants, and micro-organisms, nickel interacts with at least 13 essential
elements (Ca, Cr, Co, Cu, I, Fe, K, Mg, Mn, Mo, Na, P, and Zn). It has been suggested that
many pathogenic effects of nickel are due to the interference with the metabolism of essential
metals like Fe, Mn, Ca, Zn, or Mg12. Both nickel deficiency and toxicity tended to suppress
haematopoiesis and markedly altered femur and Iiver trace elements content in marginally
iron deficient rats. The alterations included elevated copper, iron and nickel, and depressed
calcium and manganese in femurs. High dietary nickel (5, 10, 20 or 50 mg/kg) stimulated
haematopoiesis and increased the iron content of marginally iron-adequate rats17. Dietary
nickel (0.3, 50, or 100 mg/kg diet) did not significantly influence Fe concentrations in plasma,
liver, kidney, femur and spleen of rats and did not alter Cu status. At the same time Zn
concentrations in femur were significantly decreased after feeding the diet with 100 mg/kg.
However, Zn in plasma, liver, kidney, and spleen was not affected. In calves nickel
supplementation reduced iron concentrations in lung, liver and muscle and manganese
concentration in muscle. In chickens, supplementation of nickel toxic diets (500 mg/kg) with
100 mg/kg of cobalt, iron, copper, and zinc did not alleviate the symptoms of nickel toxicity
or consistently affect tissue nickel accumulation. Nickel deficiency is accompanied by
reduced iron resorption and results in anaemia. It can disturb the incorporation of calcium into
skeleton leading to parakeratosis-like damage3. Severe iron deficiency was found to be more
detrimental to nickel-supplemented than to nickel-deficient rats, as growth was more severely
depressed and perinatal mortality was higher in nickel-supplemented rats. Like the synergistic
relationship, the antagonistic interaction between nickel and iron (this time as Fe2+) occurs
during absorption. The findings that nickel and cobalt form porphynoid natural products and
apparently occur in a rather constant ratio in some living organisms suggest that these two
elements have interrelated biological functions.
An antagonistic interaction between nickel and copper was found in rats. The findings
showed that if copper deprivation was not too severe, signs of copper deficiency in rats were
more severe with, than without, supplemental nickel (diet contained 16-20 ng/g.), and that
effect was greater when dietary nickel was 50 µg/g rather than 5 µg/g. Nickel
supplementation did not depress the level of copper in the liver or plasma of copper-deficient
rats, thus indicating that nickel probably exacerbated copper deficiency by a mechanism other
than interfering with copper absorption. The antagonism between copper and nickel was
probably due to the isomorphous replacement of copper by nickel at various functional sites.
At those sites nickel did not perform, or less efficiently performed, the functions of copper,
thus resulting in a more severe copper deficiency.
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Nickel was first shown to be essential for chicks fed on a highly purified diet under strict
environmental control conditions. Depigmentation of the skin, thickened legs, swollen hocks,
growth retardation and anaemia were reported in chicks given a basal diet providing only 215 µg Ni/kg and an additional 50µg Ni/kg alleviated all abnormalities.
Nickel was also found to improve growth and fertility in rats. The symptoms of deficiency
include growth retardation, impaired reproduction and anaemia. Feeding of Ni deficient diet
(13µg/kg diet) or a Ni adequate diet (1mg/kg) to rats indicated that Ni deficiency significantly
(p<0.05) lowered the concentration of T3 and T4 hormones. Optimum amount of Ni in the diet
is 25 mg/kg, which has a positive influence on bone strength characteristics and performance
of female broilers. Nickel deficiency causes a significant triacylglycerol accumulation in
liver, with greater concentrations of saturated fatty acids and polyunsaturated fatty acids than
nickel adequate rats. Moreover, nickel-deficient rats show lower activities of the lipogenic
enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malie
enzyme and fatty acid synthase than nickel-adequate rats.
Nickel deprivation in rats decreases spermatozoa motility and density in the epididymis,
epididymal transit time of spermatozoa, and testes sperm production rate. In addition the
weights of the seminal vesicles and prostate glands in these animals are also reduced22. Nickel
deprivation also affects distribution and proper functioning of other nutrients including
calcium, iron, zinc, and vitamin B12.
Body weight gain, haemoglobin, and plasma alkaline phosphatase were significantly reduced
in weanling rats exposed to nickel (as nickel acetate) at concentrations of 500 or 1000 mg/kg
in the diet (equivalent to 25 or 50 mg/kg of body weight per day) for 6 weeks compared with
controls. No effects were observed in rats exposed to 100 mg/kg in the diet (equivalent to 5
mg/kg of body weight per day).
Rats (25 per sex per dose) were exposed to nickel (as nickel sulphate) in the diet at doses of 0,
100, 1000, or 2500 mg/kg (equivalent to 0, 5, 50, and 125 mg/kg of body weight per day) for
2 years. Growth was depressed in rats at 1000 and 2500 mg/kg of diet, but there were
indications that decreased food consumption might explain the decreased body weight gains,
particularly at 2500 mg/kg of diet.
Intra-peritoneal administration of nickel nitrate (12 mg of nickel per kg of body weight) to
male mice resulted in reduced fertilizing capacity of spermatozoa; no effects were seen at 8
mg of nickel per kg body weight.
Nickel salts affect the T-cell system and suppress the activity of natural killer (NK) cells in
rats and mice. Mitogen-dependent lymphocyte stimulation was inhibited and in spleens of
mice exposed to nickel. Dose-related decreased spleen proliferative response to
lipopolysaccharide was observed in mice exposed to nickel sulphate in drinking-water for 180
days. At the lowest dose (44 mg of nickel per kg of body weight per day), decreased thymus
weight was observed, but there was no nickel-induced immunosuppression NK cell activity or
response to T-cell mitogens.
Nickel can induce various effects on the immune system, depending on dose,
physicochemical form of the compound and route of exposure. Thymic weights were
decreased in mice exposed to 1.8 mg Ni/m3 (Ni3S2) 6 hr/day, 5 days per week for 65 days10.
Single intramuscular injections of NiCI2in mice (18.3 mg/kg) and rats (20 mg/kg) cause a
significant involution of thymus. Natural killer (NK) cell activity was significantly suppressed
in rats injected intramuscularly with 10, 15, or 20 mg/kg NiCI2. Exposure to 1.8 mg Ni/m3
Ni3S2 as well as a single intramuscular injection of 18.3 mgt kg NiCl2 has been also reported
to lower the activity of spleen NK cells in mice. At higher concentrations, NiCI2 induces a
significant decrease in NK cell activity in rats and monkeys5. On the other hand, exposure to
Ni3S2 or NiS04.6H20 has been shown to have no effect on the NK cell activity of mouse
spleen cells. NiO and Ni3S2 exposure results in decreased alveolar macrophage phagocytic
activity in mice. Intra-tracheal NiCI2 exposure of rats decreased the number of antibody
forming cells in lung associated lymph nodes and spleen. A significant suppression of the
primary antibody response to the T-cell dependent antigen sheep red blood cells has been
reported following a single injection of 18.3 mg/kg NiCl2 in mice. No alterations in the
response of animals immunized with the T-cell independent antigen polyvinylpyrrolidone
have been observed. No significant differences between control and Ni-treated rats (single
intramuscular injection NiCI2 at doses ranging from 10 to 20mg/kg) in the primary antibody
response to sheep red blood cells have been detected.
Significant reduction in
mitogen-stimulated response of lymphocytes from NiCI2-
treated mice (24 h following a single I/M injection of 18.3 or 36.6 mg/kg) have been observed
for the T-cell mitogen phytohemagglutinin and concanavalin A, and the B- and T-cell
mitogen pokeweed mitogen but not the B-cell mitogen lipopolysaccharide. On the other hand,
in Fischer 344 rats receiving a single intramuscular injection of NiCl2 at doses ranging from
10 to 20 mg/kg, the Iympho-proliferative responses of splenocytes to the T cell mitogens
concanavalin A, phytohemagglutinin, the T and B mitogen pokeweed mitogen and the B cell
mitogen
mitogen have not been found to differ significantly from
controls.
It has been suggested that nickel may contribute to the progression of target organ and/or
inflammatory character, such as diabetes and myocarditis11. Nickel is a strong biological
sensitizer and consequently may induce a delayed hypersensitivity reaction (type IV immune
response) 14. In some cases the immunosuppressive effects of nickel (especially NiCI2) were
reported to be transient with responses returning to normal within a few days.
Nickel deficient pigs had slower growth rate, delayed sexual maturity and higher piglet
mortality than control receiving 10ppm Ni. They further observed that Ni deficient animals
exhibited signs of Zn deficiency and low zinc status of the body.
Nickel-depleted pups have higher concentrations of triacylglycerols and phospholipids in
serum. Most of these alterations in lipid metabolism are similar to those obtained in iron
deficient animals. Because nickel deficiency also slightly compromised iron status, it has
been suggested that at least some of the observed alterations are due to moderate iron
deficiency.
In another study, dogs (three per sex per dose) were exposed to 0, 100, 1000, or 2500 mg of
nickel per kg of diet (equivalent to 0, 2.5, 25, and 62.5 mg/kg of body weight per day) for a
period of 2 years. In the 2500 mg/kg of diet group, decreased weight gain and food
consumption, higher kidney to body weight and liver to body weight ratios and histological
changes in the lung were observed.
Goats fed a low Ni diet (100ppb) had higher abortion rate, decreased conception rate, along
with a decreased viability of female goats and their offspring. Further studies revealed
lowered milk production, skin and skeletal lesions, abortion and lower testicular weights in
goats fed a low Ni diet. Urease produced by bacteria has been found to be Ni dependent.
Nickel has also been shown to be required by methanogenic bacteria and for hydrogenase
production in certain bacteria. Supplementation of diets containing 0.26-0.85 mg Ni/kg DM
with 5mg Ni (NiCl3) have increased ruminal urease, growth rate and feed conversion
efficiency of lambs. Supplementation of a similar basal diet has increased urease activity
without affecting growth19, urea utilization and N retention in lambs. Rumen microorganisms
involved with methanogenesis and sulphate reduction may require Ni. Ni supplementation has
also frequently altered patterns of VFA production in the rumen, but the changes have been
inconsistent.
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Nickel salts exert their toxic action mainly by gastrointestinal irritation and not by inherent
toxicity. The relative non-toxicity of nickel is apparently related to its low absorption by the
intestinal mucosa. Nickel also has little tendency to accumulate in tissues during lifetime
exposure. Large oral doses of nickel salts are necessary to overcome the homeostatic control
of nickel. Generally, 250 µg or more of nickel per gram of diet is required to produce signs of
nickel toxicity in rats, mice, chicks, rabbits, and monkeys. Thus, the ratio of the minimum
toxic dose and the minimum dietary requirement for chicks and rats is approximately 5,000.
This metal is not a cumulative toxin in animals. A lot of animal studies have been performed
in order to study the toxic potential of nickel and its compounds. Thus, groups of F344/N rats
and B6C3Fl mice were exposed to aerosols of nickel sulphate hexahydrate (NiS04.6H20) or
nickel subsulfide (NiS2) 6hr/day for 12 days. Two male rats and all mice exposed to 10.0 mg
Ni3S as well as all mice exposed to 7 mg NiS04.6H20/m3 or greater and 10 rats exposed to 15
mg NiS04.6H20/m3 or greater died before the end of the experiment. Histopathological
changes were seen in tissues of rats and mice exposed to as low as 3.5 mg NiS04.6H2O/m3.
Lesions related to NiS04.6H20 exposure occurred in lung, nose, and bronchial and mediastinal
lymph nodes. Lesions in rats and mice related to inhalation of Ni3S2 were found in the nasal
epithelium, lung, and bronchial lymph nodes. The most extensive lesions were observed in
the lung and included necrotizing pneumonia. Emphysema developed in rats exposed to 5.0 or
10.0 mg Ni3S, while fibrosis developed in mice exposed to 5.0 mg Ni3S. No mortality was
reported in female B6C3Fl mice given free access to the nickel sulphate in the drinking water
at 1, 5 or 10 gIl for 180 days. Decreases in body and organ weights were observed in mice
treated with 10 g/l nickel sulphate. The primary toxic effects of this compound were
expressed in the myeloid system. Dose-related decreases in bone-marrow cells as well as in
granulocyte-macrophage and pluripotent stem-cell proliferative responses were detected.
Mortality and anemia were observed in chickens receiving 1.1 g/kg nickel. Mallard
ducklings were fed nickel sulphate diet from day one to 90 days of age.
Ducklings fed 1.200 ppm nickel began to tremor and show signs of paresis after 14 days of
dosage and 71% of this group died within 60 days of age. Birds fed 1.200 ppm nickel
weighed significantly less at 28 days of age than birds fed the other diets. Liver and kidney
tissues from all ducklings that survived to 90 days of age contained less than 1.0 ppm nickel.
Numerous animal studies have revealed that nickel expresses embryotoxic and teratogenic
properties. The metal can be transferred from the mother to an infant in breast milk and can
cross the placenta. The circulation of the element through the foetus follows the direction:
maternal blood→ placenta → foetus → amniotic membranes → endometrium → maternal
venous blood. There are data that a direct embryo damaging effect of nickel crossing the
placenta (direct cytotoxic effect) is responsible for its embryotoxicity and teratogenicity21.
Parenteral administration of nickel to rabbits, chickens, and rats and oral administration of
nickel to rabbits induce hyperglycaemia and reduce the levels of prolactin releasing factor in
rats.
A number of experiments are conducted on the carcinogenicity of nickel compounds in
experimental animals. Generally, tumours are induced at the site of administration of the
nickel compound. Several nickel compounds induce injection-site sarcomas20. The exact
mechanisms of nickel-induced carcinogenesis are not known. The mechanisms are likely to
involve genetic and epigenetic routes. Ni genotoxicity may be aggravated through the
generation of DNA damaging reactive oxygen species (ROS) and the inhibition of DNA
repair. Broad spectrum of epigenetic effects of nickel includes alteration in gene expression
resulting from DNA hypermethylation and histone hypoacetylation, as well as activation or
silencing of certain genes and transcription factors, especially those involved in cellular
response to hypoxia6,
7&12
. The carcinogenic potency of nickel compounds depends on the
ability of nickel ions to enter target cells. Soluble nickel appears to increase respiratory cancer
risks at lower exposure than more water-insoluble nickel compound exposure. However, wellconducted inhalation studies in rats and mice, where exposure were solely to nickel sulphate
hexahydrate, failed to demonstrate a carcinogenic potential for this compound8. Similar
negative results were seen in animal studies through oral exposure and intramuscular injection
studies with soluble nickel compounds alone. It has been suggested on the basis of animal
experiments that soluble nickel compounds by themselves are not carcinogenic but that at
concentrations above those that result in chronic respiratory toxicity, they may enhance the
carcinogenicity of simultaneous inhalation exposure to carcinogens. However, some
experiments on human and mice showed the anti-tumour activity of some nickel complexes.
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Nickel, being one of the important metal pollutants is of considerable concern, because its
concentration is rapidly increasing in soils of different parts of the world and ultimately taken
up by plants. Thus, they can enter in the food chain and cause deleterious effects on animals.
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Conventional surface water treatment, comprising chemical coagulation, sedimentation, and
filtration, can achieve 35-80% removal of nickel. Better nickel removal occurs with waters
containing high concentrations of suspended solids; for waters low in solids, the addition of
powdered activated carbon can be used to enhance nickel removal. The optimum pH for
removal on activated carbon was reported to be pH 8. In the case of ground water, effective
removal of nickel can be achieved using chelating ion-exchange resins. Various adsorbents
could potentially be used to remove nickel from ground water. Response to nickel also was
suppressed in the presence of 1 g of ascorbic acid.
In case of nickel deficiency, using fertilizers to improve the nickel uptake of plants may be a
practical means of increasing animal productivity.
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Ni requirement for monogastric species may be between 50 and 200 ppb. It may be prudent to
formulate livestock diets to contain at least 0.2 mg nickel/kg. Nickel is an essential element
for the chick, rat, pig, sheep and goat. The requirement for Ni is low (50 to 60 ppb) in chicks
fed semi-purified diets. Most monogastric animals have a dietary nickel requirement of less
than 200 ng/g diet16. Signs of nickel deprivation have been described for six animal species
chick, cow, goat, minipig, rat, and sheep. For rats and chicks, the nickel requirement
apparently is about 50 µg/kg of diet or slightly less. For cows and goats this requirement may
be higher (>100 µg/kg of diet), possibly because some rumen bacteria use nickel as part of
their enzyme urease. The Ni requirement of ruminants may be less than 500 ppb, but since
normal feeding situation usually provide Ni in excess of this amount, a primary deficiency of
Ni is unlikely to be seen under practical conditions.
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The two most commonly used analytical methods for determination of nickel concentration in
water are atomic absorption spectrometry and inductively coupled plasma atomic emission
spectrometry. The limit of detection is approximately 20 µg/litre by flame atomic absorption
spectrometry, 15 µg/litre by inductively coupled plasma, 1 µg/litre by electrothermal atomic
absorption spectrometry, and 1 µg/litre by inductively coupled plasma optical emission
spectrometry. Alternatively, electrothermal atomic absorption spectrometry can be used. 2hydroxy-3-methoxy benzaldehyde thiosemicarbazone (HMBATSC) can also be used as a
spectrophotometric reagent for simultaneous determination of nickel.
,
The trace element like nickel may be added to the diets, although until today, there is no
conclusive evidence that this element is essential for any metabolic process. Studies have
shown that it may interact with other nutrients under various conditions to give beneficial
effects. At the same time, we have to take into account the toxic effects. Nickel may
accumulate and disrupt functions of vital organs thereby affecting health of animals. In this
context, the study of effects of trace minerals on animal health has become an upcoming
aspect of nutritional research.
8
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1. Ahmad, K., khan, Z.I., Ashraf, M., Valeem, E.E., Shah, Z.A. and Mcdowell, l.R.
(2009). Determination of forage concentrations of lead, nickel and chromium in
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3. Anke, M., Groppel, B., Kronemann, H., Grun, M. (1984). Nickel-an essential
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#
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$ 383:
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!
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compounds following 13-week inhalation exposure in the mouse. &
#
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%
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(
, 48: 47-52.
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administration of nickel: effects on behaviour and metallothionein levels.
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16. NieIsen, F.H. (1991). Nutritional requirement for boron, silicon, vanadium, nickel,
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mechanisms in rats.
(
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animals.
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zinc, manganese and copper in calves.
(
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' "
, 7: 377-398.
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)
$ 83: 3-12.
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#
$ 93: 141-154.
23. Yusuf, A.A., T.A. Arowola and O. Bamgesebese. (2003). Cadmium, copper and
nickel levels in vegetables from industrial and residential area of Lagos city, Nigeria.
&
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#
., 41: 375-378.