Nickle

Physiological Role
A second microbial function of Ni may be important to ruminants
Ni may have a biological role that interacts with vitamin B-12
Ni may play a role in lipid metabolism
Metabolism and Homeostatic Control
Nickel Requirements
Sources of Ni
Deficiency Signs
Toxicity

I.  Physiological Role

1. Ni meets criteria for essentiality
2. Nonspecific activator of enzymes
3. Ni can replace the natural metals in numerous enzymes in vitro
4. Ni containing enzymes have been identified in plants and microorganisms but no enzyme in animals has been shown to be activated specifically by Ni
5. Ni may be specific for ruminal bacterial urease
6. Spears et al (1977) reported bacterial urease activity was much lower in lambs fed only 60 ppm rather than 5 ppm Ni
7. Urease appears to be a Ni metalloenzyme
8. Largest responses to Ni supplementation in ruminants occur when diets high in concentrate but low in protein are fed
9. When dietary N is low, Ni may function to enhance recycling of N to the rumen by increasing ruminal urease activity
10. Ureolytic bacteria adhere to the rumen epithelium surface and produce urease which may facilitate transfer of ureaN from the blood across the rumen wall

II.  A second microbial function of Ni may be important to ruminants

1. Ni is a component of factor F430 which is present in methanogenic bacteria.  At least one species of methanogenic bacteria requires Ni for growth
2. Addition of Ni to in vitro cultures stimulates methanogenesis

III.  Ni may have a biological role that interacts with vitamin B-12

(J. Trace Elem. Exp. Med. 2:21, 1989) and folic acid (Biol. Trace Elem. Res. 52:23, 1996)

IV.  Ni may play a role in lipid metabolism

1. Regulation of lipid content in tissues
2. Synthesis of phospholipids (J. Nutr. 126:2466, 1996)

V.  Metabolism and Homeostatic Control

1. The major excretory route for oral Ni is the feces
   1. Absorption of dietary Ni is in the range of 1-10%
   2. Fecal excretion increases with increasing intake
2. Urine is the primary excretory route for intravenously administered Ni
3. Tissue concentrations of Ni are maintained at fairly constant levels until homeostatic controls are exceeded (> 250 ppm Ni in calf diets)

VI.  Nickel Requirements

1. Most nonruminant animals have a Ni requirement of < 200 ug/kg of diet
2. Ruminants may have higher Ni requirements than other animal species that have been studied
   1. Ni deficiency has been observed with diets containing 100 ppb
   2. Ni requirement of young ruminants is approximately 1 ppm

VII.  Sources of Ni

1. Ni is ubiquitous and selection of low Ni feeds is difficult
2. Ni in plants is influenced by a number of factors
   1. Legumes are generally higher than grasses
   2. Ni decreases with advancing maturity
   3. Concentration and availability in the soil

VIII.  Deficiency Signs

(Nelson suggests earlier reported signs listed below may have been misinterpreted manifestations of pharmacologic actions of Ni)

1. Chick
   1. Pigmentation changes and dermatitis in shank skin
   2. Leg abnormalities
      1. Reduced length: width ratio of tibia
      2. Slight thickening of long bones
      3. Selling of hock joint
2. Swine
   1. Decreased growth rate
   2. Delayed estrus
   3. Increased neonatal mortality
   4. Scaly, entrusted skin similar to parakeratosis
3. Ruminants
   1. Reduced ruminal urease activity
   2. Skin dermatitis
   3. Decreased growth rate
   4. Increased mortality

IX.  Toxicity

1. Contact with skin can cause dermatitis
2. Toxicity to domestic animals in relation to requirement is low
   1. 250 ppm caused slight growth depression in calves but had no adverse effects on milk production, milk composition, or health of cows
   2. 700 ppm caused growth depression in chicks
3. Toxicity threshold may be < 600 ug/day in sensitive human subjects (J Nutr. 126:2452S, 1996)
   1. Conventional diets usually provide, 150 UG/DAY
   2. Diets high in chocolate, nuts, dried beans and peas, and grains could provide 900 ug/day

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