Silicon Articles

© 2011

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

            (Carlisle 1980) Download

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.

Silicon as a trace nutrient

            (Carlisle 1988) Download

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.

Silicon and bone health

         (Jugdaohsingh 2007) Download

Low bone mass (osteoporosis) is a silent epidemic of the 21st century, which presently in the UK results in over 200,000 fractures annually at a cost of over one billion pounds. Figures are set to increase worldwide. Understanding the factors which affect bone metabolism is thus of primary importance in order to establish preventative measures or treatments for this condition. Nutrition is an important determinant of bone health, but the effects of the individual nutrients and minerals, other than calcium, is little understood. Accumulating evidence over the last 30 years strongly suggest that dietary silicon is beneficial to bone and connective tissue health and we recently reported strong positive associations between dietary Si intake and bone mineral density in US and UK cohorts. The exact biological role(s) of silicon in bone health is still not clear, although a number of possible mechanisms have been suggested, including the synthesis of collagen and/or its stabilization, and matrix mineralization. This review gives an overview of this naturally occurring dietary element, its metabolism and the evidence of its potential role in bone health.

Soluble silica and coral sand suppress high blood pressure and improve the related aortic gene expressions in spontaneously hypertensive rats

            (Maehira, Motomura et al. 2011) Download

Silicon is rich in the normal human aorta but decreases with age and the development of atherosclerosis. We hypothesized that soluble silica (Si) and coral sand (CS), as a natural Si-containing material, would suppress high blood pressure (BP) in spontaneously hypertensive rats (SHRs), and clarify the observed antihypertensive mechanism by cell cultures by quantifying messenger RNA expressions in the aorta. In SHR fed diets containing 1% Ca supplemented with CaCO(3) as the control (CT) and CS in a Ca-deficient diet and containing 50 mg/kg Si in the CT diet for 8 weeks, systolic BP was significantly (P < .05) lowered by 18 mm Hg for the Si group and 16 mm Hg for the CS group compared with the control CT group with 207 mm Hg. Magnesium (Mg) uptake by rat aortic smooth muscle cells significantly increased (177%, P < .005) in cells cultured with a physiologic Mg level plus Si compared with those with no Si addition. Furthermore, the increase of systolic BP by the CT diet was significantly suppressed by 17 mm Hg (P < .001) in SHR fed the diet containing Mg along with Si, but not by the Mg-deficient diet with or without Si. Soluble silica and CS treatments suppressed the aortic gene expressions of angiotensinogen and growth factors related to vascular remodeling, whereas, Si stimulated the expression of peroxisome proliferator-activated receptor-gamma, the activation of which has anti-inflammatory and antihypertensive effects on vascular cells. These findings suggest that Si reduces hypertension in SHR by stimulating the intracellular Mg uptake and related gene expression in the aorta.

Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review

            (Nielsen and Sandstead 1974) Download

Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation

            (Nielsen 1991) Download

Definition of specific biochemical functions in higher animals (including humans) for the ultratrace elements boron, silicon, vanadium, nickel, and arsenic still has not been achieved although all of these elements have been described as being essential nutrients. Recently, many new findings from studies using molecular biology techniques, sophisticated equipment, unusual organisms, and newly defined enzymes have revealed possible sites of essential action for these five elements. Based on these findings and the response of animals and/or humans to low intakes of these elements, the following speculations have been presented: 1) Boron has a role that affects cell membrane characteristics and transmembrane signaling. 2) Silicon is necessary for the association between cells and one or more macromolecules such as osteonectin, which affects cartilage composition and ultimately cartilage calcification. 3) Vanadium reacts with hydrogen peroxide to form a pervanadate that is required to catalyze the oxidation of halide ions and/or stimulate the phosphorylation of receptor proteins. 4) Nickel is needed for the CO2-fixation to propionyl-CoA to form D-methylmalonyl-CoA. 5) Arsenic has an important role in the conversion of methionine to its metabolites taurine, labile methyl, and the polyamines. If any of these speculations are found to be true, the element involved will be firmly established as having a nutritional requirement because the body obviously cannot synthesize it. Based on animal findings, the dietary requirement is likely to be small; that is, expressed in micrograms per day.

Silicon, fibre, and atherosclerosis

         (Schwarz 1977) Download

A logical argument can be made for the hypothesis that lack of silicon may be an important aetiological factor in atherosclerosis. As silicic acid or its derivatives, silicon is essential for growth. It is found mainly in connective tissue, where it functions as a cross-linking agent. Unusually high amounts of bound silicon are present in the arterial wall, especially in the intima. Various kinds of dietary fibre have been reported to be effective in preventing experimental models of atherosclerosis, reducing cholesterol and blood-lipid levels, and binding bile acids in vitro. Exceptionally large amounts of silicon (1000 to 25 000 p.p.m.) were found in fibre products of greatly varying origin and chemical composition which were active in these tests. Inactive materials, such as different types of purified cellulose, contained only negligible quantities of the element. It is concluded that silicate-silicon may be the active agent in dietary fibre which affects the development of atherosclerosis. Two out of three samples of bran also had relatively low levels, which could explain why bran does not lower serum-cholesterol. The fact that atherosclerosis has a low incidence in less developed countries may be related to the availability of dietary silicon. Two instances are presented where silicon is reduced by industrial treatment: white flour and refined soy products were much lower in silicon than--their respective crude natural products. The chemical nature of silicon in different types of fibre is not known. It could exist as orthosilic acid, polymeric silicic acid, colloidal silica (opal), dense silica concentrations, or in the form of organically bound derivatives of silicic acid (silanolates). Possible mechanisms of action are discussed.


References

Carlisle, E. M. (1980). "Biochemical and morphological changes associated with long bone abnormalities in silicon deficiency." J Nutr 110(5): 1046-56.

Carlisle, E. M. (1988). "Silicon as a trace nutrient." Sci Total Environ 73(1-2): 95-106.

Jugdaohsingh, R. (2007). "Silicon and bone health." J Nutr Health Aging 11(2): 99-110.

Maehira, F., K. Motomura, et al. (2011). "Soluble silica and coral sand suppress high blood pressure and improve the related aortic gene expressions in spontaneously hypertensive rats." Nutr Res 31(2): 147-56.

Nielsen, F. H. (1991). "Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation." FASEB J 5(12): 2661-7.

Nielsen, F. H. and H. H. Sandstead (1974). "Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review." Am J Clin Nutr 27(5): 515-20.

Schwarz, K. (1977). "Silicon, fibre, and atherosclerosis." Lancet 1(8009): 454-7.