Infants selenium levels

Selenium levels vary in infant formulas, depending mainly on the Se content of their cow s milk source. In any case, Se concentrations in formulas are usually... 

Studies with infants have clearly shown that plasma Se levels respond to dietary Se levels. A very rough correlation may be made from the available data. A 2.5-fold increase in selenate intake provoked a 66% rise in plasma selenium levels (T5o ala et al, 1996). 

No studies have demonstrated that selenium or its compounds are teratogenic in humans. Robertson (1970) reported on the outcome of pregnancies in a laboratory in which workers handled sodium selenite. Of the five pregnancies, four ended in spontaneous abortion and one resulted in an infant with bilateral clubfoot. The urinary selenium levels in all subjects were similar to those in other individuals living in the same area. The limited number of cases, possible exposure to other toxic agents, and other confounding factors leave the relationship between sodium selenite and developmental effects inconclusive. 

Selenium presence in the human food chain is mainly affected by its levels in agricultural soils. Hence, its daily uptake varies depending heavily on the geographical area. 50-200p.g/day were proposed as normal uptake selenium levels, with the exception of infants and children under 6 years of age where it is suggested as 10-40 g/day and 20-120 J,g/day, respectively. 

Selenium status may be a concern for premature infants, since this population may have lower levels of plasma Sc and of GSH peroxidase. Full-term infants have 0.6-1. pM Se, while premature infants have been found to have 0.3-0.5 pM Se, though levels as high as 1.1-1.6 pM have also been found (Tyrala et uL, 1996). 

Wilson DC, Tubman R, Bell N, et al. 1991. Plasma manganese, selenium and glutathione peroxidase levels in the mother and newborn infant. Early Hum Dev 26 223-226. 

The lack of suitable chelating agents for some analytes of interest is the main limitation of GC/MS. However, Reamer and Veillon (1981b) have developed a suitable chelate and method for the determination of selenium in biological materials. This method has been further adapted to a double-isotope method for studies of selenium metabolism (Reamer and Veillon, 1983 Swanson et al., 1983a, 1983b Moser-Veillon et al., 1992). Under routine conditions this method has proven to be well suited to determine total selenium in foods, diets, human breast milk, infant formulae, plasma and serum, red blood cells, feces and urine. The method has the accuracy expected for a definitive method, the precision is about 2% at the 100/absolute detection limit is about 50 pg. 

In animals, selenium deficiency is known to induce growth retardation in second-generation selenium-deficient rats (Ewan, 1976 Thompson et ai, 1995), but the mechanism involved remains unclear. Observations suggest that in humans, bone tissue is also affected by selenium deficiency. In healthy infants, a significant correlation has been observed between urinary levels of selenium and pyridin-ium cross-links of collagen, a marker of bone metabolism (Tsukahara et ai, 1996). This suggests a link between bone turnover and selenium status. The osteopenia observed in some phenylketonuric children may be related to their low selenium intake, but selenium-supplementation studies have not been performed so far to test this hypothesis. 

Hemolytic anemia of newborn infants—Newborn infants are more prone than other people to have abnormally shortlived red blood cells because blood levels of vitamin E— which together with selenium protects the membranes of red cells from premature disintegration are often subnormal at birth. Hence, it is suspected that selenium deficiency might tend to aggravate this condition, since the selenium enzyme glutathione peroxidase protects against this disorder. It is noteworthy, therefore, that cow s milk contains only half as much selenium as human milk, and that both types of milk are relatively poor sources of the mineral. 

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