The effect of pregnancy on the content of silicon, aluminum and titanium in the liver and in the blood flowing from the liver of angiostomized dogs.
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The urinary excretion of silicon in the rat was found to be enhanced beyond normal levels by the administration of various chemical forms of silicon. The excretion was enhanced to a much greater degree by the administration of ethyl silicate than by magnesium trisilicate, sodium metasilicate, or water glass. The tolerance level of rats to sustained daily doses of ethyl silicate fed via stomach tube was approximately 15 to 30 mg. of silicon per rat per day. Urinary silicon excretion was found to be a straight line function of the concentration of ethyl silicate administered, via stomach tube, with approximately 18 per cent of the administered silicon appearing in the urine at all levels tested. Using sustained dietary additions of ethyl silicate as a means of enhancing urine silicon levels, artificial siliceous urinary calculi were consistently produced on zinc pellets implanted in the bladders of rats.
1. Cells of the fresh water diatom Navicula pelliculosa may be grown in a mineral medium containing a low concentration of silicon. When transferred to a fresh silicate solution and incubated under non-growing conditions such deficient cells rapidly take up silicon from the medium. 2. The utilization of silicon is an aerobic process. 3. When deficient cells are washed with distilled water or saline, their ability to utilize silicon is impaired whereas respiration is unaffected. 4. The ability of washed cells to take up silicon can be partially restored with sulfate or ascorbic acid, and is completely restored by Na(2)S, Na(2)S(2)O(3), glutathione, l-cysteine, dl-methionine, or ascorbic acid plus sulfate. 5. The sulfhydryl reagent, CdCl(2), inhibits silicon utilization of unwashed cells at concentrations which do not affect respiration. This inhibition similarly is reversed by glutathione or cysteine. 6. However, sodium iodoacetate or sodium arsenite inhibits respiration and silicon utilization at the same concentrations. 7. The silicon taken up by deficient cells is deposited at the cell surface as a thickening of the existing silica frustules. 8. Sulfhydryl groups in the cell membrane may be involved in silicon uptake by diatoms.
1. Evidence is presented that silicon uptake in the diatom Navicula pelliculosa is linked with aerobic respiration. 2. Cyanide, fluoride, iodoacetate, arsenite, azide, and fluoroacetate, at concentrations inhibitory to respiration, were also inhibitory to silicon uptake. 3. 2,4-Dinitrophenol (1 to 2 x 10(-5)M) stimulated respiration by 100 per cent, but almost completely inhibited silicon uptake. 4. The respiratory quotient of non-Si-deficient cells decreased from 0.93 to 0.75 after 4 days of starvation in darkness. Glucose (1 per cent) raised the respiratory quotient of such starved cells to 1.05. 5. Silicate (20 mg. Si/liter) stimulated respiration of unstarved Si-deficient cells by about 40 per cent. The effect of silicate on the respiration of Si-deficient cells which had been starved in darkness for 4 days was less marked. 6. The respiratory quotient of Si-deficient cells decreased from 0.8-0.9 to 0.3 after 4 days of starvation in darkness. The addition of silicate to starved cells raised the quotient to 0.5. This represented a 25 per cent stimulation of oxygen uptake concomitant with a 90 per cent stimulation of carbon dioxide evolution. 7. Glucose (1 per cent) caused an increase of respiratory quotient in starved cells from 0.3 to 0.7-0.8. The addition of silicate had no effect on the R.Q. during the oxidation of exogenous glucose. 8. Substrates (glucose, fructose, galactose, lactate, succinate, citrate, glycerol), which caused a stimulation of respiration in starved cells, also stimulated silicon uptake by those cells. However, the stimulation of silicon uptake (50 to 100 per cent) was not proportional to the respiratory stimulation by these substrates (30 to 300 per cent).
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