Nickel Deficiency Effects

Nickel is an essential micronutrient for maintaining health in certain species of plants and animals. Its deficiency effects from dietary deprivation have been induced experimentally in many species of birds and mammals. To prevent nickel deficiency in rats and chickens, diets should contain at least 50 pg Ni/kg ration, while cows and goats require more than 100 pg Ni/kg rations, perhaps reflecting the increased use by rumen bacteria. Nickel deficiency is not a public health concern for humans because daily oral intake is sufficient to prevent deficiency effects. 

In iron-deficient rats, nickel enhanced the absorption of iron (Nielsen 1980 Nielsen et al. 1980, 1984). This effect of nickel was only observed when ferric sulfate was given. No interaction was observed when iron was given as a 60% ferric/40% ferrous sulfate mixture. It has been proposed that nickel facilitates the passive diffusion of ferric ions by stabilizing the transport ligand (Nielsen 1980). 

No adverse effects nickel chloride, nickel subsulfide Diet To prevent deficiency Less than 0.1 mg/m ... 

Nickel is an essential micronutrient for maintaining health in certain species of plants and animals. Nickel deficiency effects from dietary deprivation of nickel has been induced experimentally in many species of birds... 

The alkylation of pyridine [110-86-1] takes place through nucleophiUc or homolytic substitution because the TT-electron-deficient pyridine nucleus does not allow electrophiUc substitution, eg, Friedel-Crafts alkylation. NucleophiUc substitution, which occurs with alkah or alkaline metal compounds, and free-radical processes are not attractive for commercial appHcations. Commercially, catalytic alkylation processes via homolytic substitution of pyridine rings are important. The catalysts effective for this reaction include boron phosphate, alumina, siHca—alurnina, and Raney nickel (122). 

Kirchgessner, M. and A. Schnegg. 1980. Biochemical and physiological effects of nickel deficiency. Pages 635-652 in J.O. Nriagu (ed.). Nickel in the Environment. John Wiley, NY. 

Stangl, G.I. and M. Kirchgessner. 1997. Effect of nickel deficiency on fatty acid composition of total lipids and individual phospholipids in brain and erythrocytes of rats. Nutr. Res. 17 137-147. 

Some experimental evidences are in agreement with this proposed mechanism. For example, coordinating solvents like diethyl ether show a deactivating effect certainly due to competition with a Lewis base (149). For the same reason, poor reactivity has been observed for the substrates carrying heteroatoms when an aluminum-based Lewis acid is used. Less efficient hydrovinylation of electron-deficient vinylarenes can be explained by their weaker coordination to the nickel hydride 144, hence metal hydride addition to form key intermediate 146. Isomerization of the final product can be catalyzed by metal hydride through sequential addition/elimination, affording the more stable compound. Finally, chelating phosphines inhibit the hydrovinylation reaction. 

Nickel has long been suspected to be an essential trace element for living organisms, but the identification of its functions in molecular terms is relatively recent. The first nickel protein to be identified was urease (urea ammonia hydrolase) (i). This was demonstrated 49 years after the original isolation and crystallization of the enzyme by Sumner (2). This enzyme is of widespread occurrence, and the specific requirement for nickel explains many of the effects of nickel deficiency in plants (3, 4). 

A recent review by Hausinger (29) deals with nickel utilization by microorganisms. In addition to known effects of nickel deficiencies, nickel and its compounds are known to have toxic and carcinogenic effects. The reader is referred to recent proceedings (30a, 30b). 

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