function, particularly biological half-life, receptor-ligand interactions, and estrogen-inducible gene expression as related to bone mineral density.
Studies of the possible role of boron in human neurophysiological and cognitive function that include delineation of a biochemical or other physiological basis for this function, in young as well as older populations.
There have been no studies to determine the nutritional importance of nickel in humans, nor has a biochemical function been clearly demonstrated for nickel in higher animals or humans (Uthus and Seaborn, 1996). Nickel may serve as a cofactor or structural component of specific metalloenzymes of various functions, including hydrolysis and redox reactions and gene expression (Andrews et al., 1988; Kim et al., 1991; Lancaster, 1988; Przybyla et al., 1992). Nickel may also serve as a cofactor facilitating ferric iron absorption or metabolism (Nielsen, 1985). Nickel is an essential trace element in animals, as demonstrated by deficiency signs reported in several species. Rats deprived of nickel exhibit retarded growth, low hemoglobin concentrations (Schnegg and Kirchgessner, 1975), and impaired glucose metabolism (Nielsen, 1996). Nickel may interact with the vitamin B12- and folic-acid dependent pathway of methionine synthesis from homocysteine (Uthus and Poellot, 1996).
The absorption of nickel is affected by the presence of certain foods and substances including milk, coffee, tea, orange juice, and ascorbic acid. Plasma 62Ni was shown to peak between 1.5 and 2.5 hours after the ingestion of the stable isotope by four fasted, healthy men and women (Patriarca et al., 1997). The investigators reported no evidence that absorbed nickel was excreted via the gut. The percentage of nickel absorbed ranged from 29 to 40 percent. Urinary excretion of the 62Ni dose ranged from 51 to 82 percent of the absorbed dose. Solomons and coworkers (1982) investigated absorption of nickel ingested with food and found that the presence of