Two experiments were conducted using a completely randomized design to study the effects of high levels of silicon (Si) supplementation on bone development, structure, and strength in growing rats and turkeys. Rats were supplemented at two dietary Si levels: 0 and 500 ppm; and the turkeys were supplemented at four dietary Si levels: 0, 135, 270, and 540 ppm in semi-purified diets of dextrose-albumin for rats and dextrose-casein for turkeys. The experiments lasted 8 and 4 weeks for the rats and turkeys, respectively. Physical, mechanical, and chemical parameters of bones were measured. All the physical and mechanical measures of bone size and strength were not different (P > 0.05) between treatments in rats and turkeys except the moment of inertia, which was lower (P < 0.01) in rats on the 500 ppm Si level of supplementation. There were small but consistent reductions in structural and strength parameters with Si supplementation which were not wholly due to differences in bodyweights of the rats and turkeys. Although bone mineral composition was not affected (P > 0.05) by Si supplementation, plasma magnesium (P = 0.08) in rats and plasma calcium (P < 0.05) in turkeys were reduced by high levels of Si supplementation. The antagonistic relations of high Si levels with calcium and magnesium were deemed to be the mechanisms through which high Si imposes its deleterious effects on bone size and strength.
Flow-cytometric procedures were used to determine effects of dietary Zn and Si variations on rat testicular cell development, including integrity of caudal epididymal sperm chromatin structure defined as the susceptibility of DNA to denaturation in situ. Concentrations of 4 (deficient), 12 (adequate), and 500 (excessive) mg of Zn/kg of diet were used with Si concentrations of 0 (low), 540 (medium), and 2,700 (high) mg/kg of diet in a 3 x 3 factorial arrangement. Three-week-old Sprague-Dawley male rats were fed the experimental diets for 8 wk. Rats fed the Zn-deficient/Si-low diet demonstrated significant deviations in the ratio of testicular cell types present, including a reduction of S phase and total haploid cells. Furthermore, approximately 50% of epididymal sperm had a significant decrease in resistance to DNA denaturation in situ. In the Zn-deficient/Si-medium treatment, the effects of Si on animal and testicular growth, distribution of testicular cell types, and sperm chromatin structure integrity were quite similar to the effects of the Zn-adequate diets. A toxic effect of Zn on sperm chromatin structure integrity observed in the Zn-excess/Si-medium treatment seemed to be counteracted by Si in the Zn-excess/Si-high treatment. Silicon at medium and high levels seems to affect Zn metabolism through potentiation and antagonistic reactions, respectively. Zinc deficiency likely disrupts the normal sperm chromatin quaternary structure in which Zn plays a role by providing stability and resistance to DNA denaturation in situ.
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