Silicon as a trace nutrient.

Silicon performs an important role in connective tissue, especially in bone and cartilage. Silicon's primary effect in bone and cartilage appears to be on formation of the organic matrix. Bone and cartilage abnormalities are associated with a reduction in matrix components, resulting in the establishment of a requirement for silicon in collagen and glycosaminoglycan formation. Additional support for silicon's metabolic role in connective tissue is provided by the finding that silicon is a major ion of osteogenic cells, especially high in the metabolically active state of the cell. Further studies also indicate that silicon participates in the biochemistry of subcellular enzyme-containing structures. Silicon also forms important relationships with other elements. Although it is clear from the body of recent work that silicon performs a specific metabolic function, a structural role has been proposed for silicon in connective tissue. A relationship established between silicon and aging probably relates to glycosaminoglycan changes.

Effect of dietary silicon and aluminum on silicon and aluminum levels in rat brain.

This preliminary study was undertaken to investigate the effect of dietary silicon and aluminum on levels of these elements in brain. Two ages of rats, 22 day and 10 month, were assigned to 1 of 4 diets: 1) low silicon; 2) low silicon plus aluminum; 3) silicon supplemented; and 4) silicon supplemented plus aluminum. Rats were 23 and 28 months old upon termination of the experiment. Twelve brain regions were analyzed for silicon and aluminum. Regional variations in silicon, which were independent of dietary silicon supplementation, suggest that silicon may be an essential element in brain. Aluminum supplementation decreased the silicon content in selected brain regions, including those thought to be involved in Alzheimer disease. A relationship has been established between silicon, aluminum and age. In 23-month rats, aluminum supplementation did not increase brain aluminum content. By contrast, in 28-month rats, aluminum supplementation of the low silicon diet increased brain aluminum content in most regions. No increase occurred in silicon supplemented groups of the same age. Dietary silicon supplementation thus appeared to be protective against aluminum accumulation in aging brain.

Silicon as an essential trace element in animal nutrition.

Within the last decade silicon has been recognized as participating in the normal metabolism of higher animals and as being an essential trace element. Silicon is found to perform an important role in connective tissue, especially in bone and cartilage. Bone and cartilage abnormalities are associated with a reduction in matrix components, resulting in the establishment of a requirement for silicon in collagen and glycosaminoglycan formation. Silicon's primary effect in bone and cartilage is on the matrix, with formation of the organic matrix appearing to be more severely affected by silicon deficiency than the mineralization process. Additional support for silicon's metabolic role in connective tissue is provided by the finding that silicon is a major ion of osteogenic cells and is present in especially high concentrations in the metabolically active state of the cell; furthermore, silicon reaches relatively high levels in the mitochondria of these cells. Further studies also indicate that silicon participates in the biochemistry of the subcellular enzyme-containing structures. Silicon also forms important interrelationships with other elements. Although it is clear from the body of recent work that silicon performs a specific metabolic function, a structural role has also been proposed for it in connective tissue. A relationship established between silicon and ageing probably relates to glycosaminoglycan changes.

Biochemical and morphological changes associated with long bone abnormalities in silicon deficiency.

The purpose of this paper was to investigate long bone changes in silicon deficiency more extensively and under a new set of conditions. Long bone abnormalities have been produced in silicon-deficient chicks fed a casein-based rather than amino acid-based diet and under an entirely new set of conditions. As demonstrated previously feeding amino acid diets, the long bones of cockerels fed a silicon-supplemented basal diet and sacrificed at 4 weeks had a significantly greater amount of articular cartilage and water content as compared with the silicon-deficient group. Biochemical analyses of tibia for bone mineral, non-collagenous protein, hexosamine and collagen demonstrated that tibia from supplemented chicks had a significantly greater percentage and total amount of hexosamine and greater percentage of collagen than deficient chicks, the difference being greater for hexosamines than collagen. Tibia from silicon-deficient chicks also showed marked lesions, profound changes being demonstrated in epiphyseal cartilage, especially striking in the proliferative zone. The disturbed epiphyseal cartilage sequences resulted in defective endochondral bone growth indicating that silicon is involved in the metabolic chain of events required for the normal growth of bone.

A silicon requirement for normal skull formation in chicks.

Studies were undertaken to investigate the effect of feeding a silicon (Si) -deficient diet containing a natural protein in place of the crystalline amino acid-based diets used in earlier studies. Feeding this Si-deficient basal diet with or without supplemental Si to day-old cockerels under trace element-controlled conditions resulted in the production of skull abnormalities in the deficient chicks under conditions of near optimal growth. On macropathological examination, gross changes were found in the architecture of the skulls of the deficient chicks; the frontal area was narrower and the dorsal median line at the frontal parietal junction was depressed with a narrowing both posterior and laterally, forming a stunted parietal, occipital and temporal bone area. X-ray and histological examination of this area showed less trabeculae and calcification. Biochemical analyses of the skull frontal bones for bone mineral, non-collagenous protein, hexosamine and collagen demonstrated that the frontal bones from the Si-deficient chicks had a significantly reduced collagen content. In this study, the major effect of Si appears to be on the collagen content of the connective tissue matrix, a deficiency resulting in abnormal skull matrix formation. Support is given to the earlier postulate that Si is involved in an early stage of bone formation.

In vivo requirement for silicon in articular cartilage and connective tissue formation in the chick.

Studies were undertaken to determine further effects of silicon deficiency in the chick. The diet and experimental conditions were the same as those used in previous studies to demonstrate the essentiality of silicon for growth and development. Skeletal and other abnormalities involving glycosaminoglycans in formation of articular cartilage and comb connective tissue were found to be associated with silicon deficiency. The bones of 1 day-old deutectomized cockerels fed a silicon supplemented diet and killed at 4 weeks of age had significantly greater amounts of articular cartilage and water as compared with the silicon deficient group and also a greater proportion of hexosamine in the cartilage. The greater water content in bones of the silicon supplemented chicks coincided with a larger content of glycosaminoglycans in the articular cartilage. A similar relationship was obtained in cockerel comb. In addition to larger amounts of connective tissue and of total hexosamine in combs of the supplemented group, a higher percentage of hexosamine and a higher silicon content was found. These findings provide the first evidence for a requirement for silicon in articular cartilage and connective tissue formation and that the site of action of silicon is in the glycosaminoglycan-protein complexes of the ground substance.

Silicon: an essential element for the chick.

Silicon is required for normal growth and development in the chick when a low silicon diet is fed in a trace element controlled environment. Day-old deutectomized cockerels fed a purified amino acid diet showed significantly retarded growth and development within 2 to 3 weeks. Chicks fed the same diet plus a silicon supplement showed 50 percent higher growth and normal development. Silicon meets the criteria for an essential trace element.

Silicon: a possible factor in bone calcification.

Silicon, a relatively unknown trace element in nutritional research, has been uniquely localized in active calcification sites in young bone. Silicon increases directly with calcium at relatively low calcium concentrations and falls below the detection limit at compositions approaching hydroxyapatite. It is suggested that silicon is associated with calcium in an early stage of calcification.