Bone mobilization

According to USNRC Regulatory Guide 8.22, the acceptable methods for the quantification of uranium in urine must have a detection limit of 5 pg/mL and a precision of 30% (Kressin 1984). A urinary concentration >100 pg/L is indicative of recent absorption, while a concentration of <40 pg/L may be due either to slow uptake from the site of absorption or to bone mobilization (Butterworth 1955). Variations in background levels of uranium from drinking water in different locations may also result in higher or lower urinary concentrations of uranium. 

Bone contains a small amount of zinc, Studies have shown that feeding growing rats a zinc-free diet results in low levels of bone zinc. Normal bone contains 0,4 mg zinc per gram of bone salts (bone ash), whereas deficient bone contains one-quarter of that lev el Swenerton and Hurley, 1963). The zinc that is present in bone cannot be readily tapped as a reservoir during a dietary deficiency in the mineral. Only under one condition can this zinc be used when bone mobilization is stimulated (i.e, by feeding a low-catcium diet) as shown in a clever experiment by Hurley and Tao (1972). Zinc deficiency during pregnancy produced birth... 

Estrogen inhibits the bone-mobilizing effect of parathyroid hormone (PTH) by a direct effect on the osteoblasts (Chapter 37). 

Assay for intestinal calcium transport and in vivo bone mobilization... 

The activities of la,25(OH)2D4 on a calcium transport and bone mobilization in vitamin D deficient SD rats were less than (about 1/2) those of la,25(OH)2D3. This is well understood by stronger affinity of la,25(OH)2D4 for DBP than that of la,25(OH)2D3 because of the decreased availability for target cells (decreased uptakes into the cells)[43,44], The hypercalcemic activities of 24-epi-la,25(OH)2D2 and la,25(OH)2D7 were negligible as compared with that of la,25(OH)2D3. Their effects on intestinal calcium transport was significantly smaller than that of la,25(OH)2D3 and it is required 10 fold more of these compounds to produce a similar activity to la,25(OH)2D3 [35]. 

Estrogens inhibit the actions of parathyroid hormone, resulting in decreased bone mobilization. 

Another well-known function of l,25-(OH>2D2 is the mobilization of calcium from bone so as to maintain normal plasM calcium concentration.This l,25-(0H)2D2-mediated process, however, cannot occur unless parathyroid hormone is present, " and it is probable that parathyroid hormone is responsible for bone mobilization, but reouires for its action certain l,25-(OH)2D2 induced cellular events." "... 

Vitamins A, D, and E are required by mminants and, therefore, their supplementation is sometimes necessary. Vitamin A [68-26-8] is important in maintaining proper vision, maintenance and growth of squamous epitheHal ceUs, and bone growth (23). Vitamin D [1406-16-2] is most important for maintaining proper calcium absorption from the small intestine. It also aids in mobilizing calcium from bones and in optimizing absorption of phosphoms from the small intestine (23). Supplementation of vitamins A and D at their minimum daily requirement is recommended because feedstuffs are highly variable in their content of these vitamins. 

Dihydroxyvitamin (283) is the endogenous ligand for the vitamin receptor (VDR). It modulates genomic function in a tissue and developmentaHy specific manner and affects ceU proliferation, differentiation, and mineral homeostasis (74). Vitamin mobilizes calcium from the bone to maintain plasma Ca " levels. Vitamin and VDR are present in the CNS where they may play a role in regulating Ca " homeostasis. Vitamin D has potent immunomodulatory activity in vivo. 

Hydroxy vitamin D pools ia the blood and is transported on DBF to the kidney, where further hydroxylation takes place at C-1 or C-24 ia response to calcium levels. l-Hydroxylation occurs primarily ia the kidney mitochondria and is cataly2ed by a mixed-function monooxygenase with a specific cytochrome P-450 (52,179,180). 1 a- and 24-Hydroxylation of 25-hydroxycholecalciferol has also been shown to take place ia the placenta of pregnant mammals and ia bone cells, as well as ia the epidermis. Low phosphate levels also stimulate 1,25-dihydtoxycholecalciferol production, which ia turn stimulates intestinal calcium as well as phosphoms absorption. It also mobilizes these minerals from bone and decreases their kidney excretion. Together with PTH, calcitriol also stimulates renal reabsorption of the calcium and phosphoms by the proximal tubules (51,141,181—183). 

Although it is being found that vitamin D metaboUtes play a role ia many different biological functions, metaboHsm primarily occurs to maintain the calcium homeostasis of the body. When calcium semm levels fall below the normal range, 1 a,25-dihydroxy-vitainin is made when calcium levels are at or above this level, 24,25-dihydroxycholecalciferol is made, and 1 a-hydroxylase activity is discontiaued. The calcium homeostasis mechanism iavolves a hypocalcemic stimulus, which iaduces the secretion of parathyroid hormone. This causes phosphate diuresis ia the kidney, which stimulates the 1 a-hydroxylase activity and causes the hydroxylation of 25-hydroxy-vitamin D to 1 a,25-dihydroxycholecalciferol. Parathyroid hormone and 1,25-dihydroxycholecalciferol act at the bone site cooperatively to stimulate calcium mobilization from the bone (see Hormones). Calcium blood levels are also iafluenced by the effects of the metaboUte on intestinal absorption and renal resorption. 

The absorption, distribution, and accumulation of lead in the human body may be represented by a three-part model (6). The first part consists of red blood cells, which move the lead to the other two parts, soft tissue and bone. The blood cells and soft tissue, represented by the liver and kidney, constitute the mobile part of the lead body burden, which can fluctuate depending on the length of exposure to the pollutant. Lead accumulation over a long period of time occurs in the bones, which store up to 95% of the total body burden. However, the lead in soft tissue represents a potentially greater toxicological hazard and is the more important component of the lead body burden. Lead measured in the urine has been found to be a good index of the amount of mobile lead in the body. The majority of lead is eliminated from the body in the urine and feces, with smaller amounts removed by sweat, hair, and nails. 

The most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. 

Hip replacement surgery is now routinely used to relieve pain and restore mobility in patients suffering from osteoarthritis. In this condition the surfaces of bone in contact with each other within the joint become worn and the layer of lubricating cartilage disappears. This makes movement of the joint both difficult and painful. By replacing the hip with an artificial joint patients stop experiencing pain and are once again able to move freely. 

D Calciferol Maintenance of calcium balance enhances intestinal absorption of Ca and mobilizes bone mineral Rickets = poor mineralization of bone osteomalacia = bone demineralization... 

Stimulating activation of vitamin D by 1-a-hydroxylase to cal-citriol (1,25-dihydroxyvitmin D3) to promote calcium absorption in the GI tract and increased calcium mobilization from bone... 

All of these actions are directed at increasing serum calcium levels and decreasing serum phosphorus levels, although the activity of calcitriol also increases phosphorus absorption in the GI tract and mobilization from the bone, which can worsen hyperphosphatemia. Calcitriol also decreases PTH levels through a negative feedback loop. These measures are sufficient to correct serum calcium levels in the earlier stages of CKD. 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

The prevalence of obesity in older adults is increasing therefore, it should not be surprising that more cardiovascular risk factors are present in this group of individuals. Additionally, obesity is a major predictor of functional limitation and mobility problems in older persons. Age alone should not prejudice the clinician from treating geriatric patients, whereas the benefits of cardiovascular health and functionality should be considered. Treatments should be initiated that minimize adverse effects on bone health and nutritional status and should include dietary and activity modifications.6... 

Studies of other bone-seeking radionuclides provide further support for increased vulnerability during periods of rapid bone growth such as adolescence (Carnes et al. 1997 Lloyd et al. 1999). On the other hand, americium uptake into maternal bone of lactating rats was similar to that of nonlactating rats, while concurrent calcium uptake into bone was lower in lactating rats (Hollins and Durakovic 1972). Thus, active mobilization of bone mineral, per se, may not always promote release of americium from bone (see Section 3.4.2.1). 

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