Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0205700 (ash)
 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gallium nitrate is a clinically effective agent for the treatment of cancer related hypercalcemia. The mechanism of action of this agent was investigated following development of a quantitative in vivo bone resorption assay modified from the method of Glowacki. In a preliminary study, the time course of resorption of 50 mg subcutaneous implants of bone powder in growing rats was followed by chemical analysis of mineral (ash and Ca) contents, enzymatic and histochemical assay of tartrate resistant acid phosphatase (TRAP) activity, and image analysis of changes in particle size using von Kossa stained sections. Day 21 was chosen as a single time point for the comparison of the extent of resorption of gallium-containing and control bone particles. Resorption of bone particles containing 0.39 micrograms Ga/mg bone was significantly inhibited relative to control particles. Mineral content (6.7 vs. 3.6 mg), Ca content (1.72 vs. 1.37 mg), and the percentage of the field covered by bone particles (12 vs. 9%) were greater in the animals which received gallium-containing bone particles. Similarly, the number of osteoclast-like cells and the TRAP activity in the gallium-containing bone particle implants at 21 days were increased relative to controls. These data indicate that gallium incorporation into bone matrix confers resistance to resorption.
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PMID:Bone particles from gallium-treated rats are resistant to resorption in vivo. 202 8

We studied changes in bone mass induced by immobilization and the ability of salmon calcitonin to inhibit immobilization osteoporosis in rat. The bone mass of the immobilized hind leg of rat was compared with the contralateral non-treated leg. Neurectomy and cast immobilization reduced the bone mineral mass to an equal extent. However, the dose-response of calcitonin was different with these immobilization techniques. Calcitonin 15 IU kg-1 administered once daily reduced bone ash weight difference significantly after 2 weeks' neurectomy (P less than 0.001). This had no significant effect on the bone loss induced by cast immobilization, but the dose had to be delivered as two injections given every 12 h. Two weeks' immobilization decreased the incorporation of 45Ca into bones. Calcitonin could not prevent this. However, calcitonin tended to inhibit the overall incorporation of 45Ca into bones in immobilized rats but yet had no effect on 45Ca incorporation in non-immobilized rats. Immobilization decreased serum alkaline phosphatase activity in cast-immobilized animals. Neurectomy did not change serum alkaline phosphatase activity from a sham operation level. The tartrate-resistant acid phosphatase to total acid phosphatase ratio in the serum increased significantly in neurectomized rats and in cast-immobilized calcitonin-treated rats.
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PMID:Calcitonin treatment of immobilization osteoporosis in rats. 205 38

The alteration in bone metabolism with increasing age was investigated in the femoral diaphysis of male rats. Calcium content was highest in the bone from 3-week-old rats (491 +/- 13 mg/g bone ash), falling gradually with aged to 357 +/- 7 and 306 +/- 9 mg/g bone ash in 28- and 52-week-old rats, respectively. Bone zinc content increased until rats were 3 weeks of age, and thereafter remained constant. Deoxyribonucleic acid (DNA) content was highest in the bone from 1-week-old rats, and it decreased markedly with increasing age. Alkaline phosphatase and acid phosphatase activities increased up to 3 weeks, then subsequently declined with age. Thus, the retardation of bone metabolism was induced by ageing. When zinc sulfate (5.0, 10.0 and 20.0 mg Zn/kg body weight) was administered orally for 3 d to 28-week-old rats, alkaline phosphatase activity and calcium content in the femoral diaphysis was elevated markedly by all doses. The oral administration of vitamin D3 (2.0 and 20 micrograms/kg) for 3 d in 28-week-old rats did not produce an appreciable increase in bone alkaline phosphatase activity or calcium content, while 1,25-dihydroxyvitamin D3 (1.5 micrograms/kg) caused a significant increase in those biochemical indices. These results indicate that zinc and 1,25-dihydroxyvitamin D3 play a role as activators in bone metabolism of ageing rats.
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PMID:Alteration in bone metabolism with increasing age: effects of zinc and vitamin D3 in aged rats. 254 53

The effect of inhalation of coal fly ash for 6 hr daily for 15 days has been studied on the hematology, blood chemistry, and histopathology of lungs and liver of rats up to 4 months from the first day of exposure. Fly ash inhalation significantly reduced WBC, RBC, and hemoglobin contents at earlier periods after exposure but tended to return to normal values at later periods. Fly ash inhalation reduced lymphocytes and increased polymorphonuclears up to 60 days after exposure and after that the alterations were reversible. Blood glucose increased and blood urea and acid phosphatase decreased at early periods after inhalation, but at later periods returned to control group values. Fly ash inhalation profoundly affected the histological structure of lungs and liver at early periods after inhalation. Numerous fly ash-laden macrophages, thickening of alveolar septa, and alveolar dilatation were noted. In the liver, periportal necrosis was also observed. These changes, however, were reversible.
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PMID:Cytotoxicity of inhaled coal fly ash in rats. 358

To elucidate the mechanism of action of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP, formerly APD) on bone metabolism, we have studied the influence of low doses of AHPrBP on bone resorption and formation in the mouse. Thirty-five-day-old mice were given daily injections of 0.16, 1.6, or 16 mumol/kg BW per day of AHPrBP for 10 days. At sacrifice biochemical parameters were measured in serum and bone ash, and histomorphometric parameters of bone formation and resorption were determined on undecalcified sections of caudal vertebrae after double 3H-proline and double tetracycline labelings. Serum calcium and 1,25-dihydroxyvitamin D levels remained normal at all dosage levels. Compared to controls, AHPrBP at doses of 1.6 and 16 mumol/kg per day increased the number of osteoclasts and the number of nuclei per osteoclast but markedly decreased the number of acid phosphatase-stained osteoclasts. Thus, AHPrBP appears to inhibit osteoclastic activity in vivo in part through reduction of acid phosphatase activity. At doses of 1.6 and 16 mumol/kg per day AHPrBP reduced serum alkaline phosphatase and the osteoblastic surface and decreased the endosteal osteoid surface and thickness. Both the matrix apposition rate and the mineral apposition rate were progressively reduced at the endosteal level, although they were not significantly changed at the periosteal level. Greater inhibition of bone resorption than bone formation resulted in increased endosteal bone density and bone mineral content. AHPrBP at a dose of 0.16 mumol/kg per day did not alter either the osteoclastic bone resorption or the mineral and matrix apposition rates.
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PMID:Inhibition of bone matrix apposition by (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (AHPrBP) in the mouse. 402 97

Lactating female rats were fed diets containing 1.0, 0.1, or 0.04% Ca for 21 days. Fat-free dry weight, ash weight, calcium and phosphorus content of the humerus, plasma calcium levels, and bone acid and alkaline phosphatase activities were compared to those of nonlactating rats fed the same diets. Bone, plasma, and urinary cAMP levels were also studied. Dietary calcium deficiency and/or lactation caused significant loss of bone mass from experimental animals. Urinary cAMP levels reflecting increased parathyroid activity were elevated by the stresses of lactation and calcium deficiency over those of control animals. Plasma and bone levels of cAMP were not different. Bone alkaline and acid phosphatase activities were affected only by the most extreme stress. The results demonstrated that the calcium-deficient lactating rat is an excellent model for bone resorption studies.
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PMID:Metabolic aspects of bone resorption in calcium-deficient lactating rats. 625 31

The effects of dietary phosphorus and sulphaguanidine levels, and sex differences on: (a) phytate digestibility, (b) calcium and P utilization, (c) the activities of alkaline phosphatase (EC 3.1.3.1), alkaline phytase (EC 3.1.3.8) and acid phosphatase (EC 3.1.3.2) in the intestinal mucosa of male and female rats were investigated. There was a linear increase in femur ash, Ca and P contents and the maximum force withstood by the fresh femurs as dietary P level was increased from 1.5 to 3.0 to 4.5 g/kg diet. The apparent digestibilities of Ca, P and phytate-P decreased as the level of P in the diet increased. Rats given the diets with 1.5 or 3.0 g P/kg were hypercalciuric and hypophosphaturic compared with rats receiving 4.5 g P/kg diet. The level of Ca retained was similar for all treatments. The level of P retained increased as the dietary P level increased. This suggests that P deprivation was a result of inadequate amounts of P retained and not due to the absorption of inositol phosphates formed during the enzymic hydrolysis of phytate. The addition of sulphaguanidine increased phytate digestibility without changing the activities of acid and alkaline phosphatase or alkaline phytase of the intestinal mucosa. This suggests that these enzymes did not play a role in the increase in phytate digestibility. However, dietary sulphaguanidine enhanced phytate digestibility, suggesting that alterations in the diet which modify either the composition or metabolism of the gastrointestinal microflora may be beneficial in enhancing the in vivo hydrolysis of phytate. Differences between males and females are reported and discussed.
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PMID:Influence of dietary phosphorus and sulphaguanidine levels on P utilization in rats. 632 99

Besides rickets and osteomalacia, the X-linked hypophosphatemic male mouse (Hyp/Y) presents with low serum calcium (Ca) and increased urinary hydroxyproline (OH-Pro) excretion, suggesting a parathyroid hormone (PTH)-stimulated bone resorption despite reduced magnesium (Mg) bone content. In this study, we have investigated by histochemical methods the state of bone resorption in 50-day-old untreated Hyp/Y mice and the effects of 4 wk of Mg therapy or dietary lactose supplementation on bone formation and resorption. Mineral and skeletal changes were evaluated on serum, urinary and bone ash concentrations of Ca, phosphorus (P) and Mg, and by histomorphometric analysis of tetracycline double labeled undeclalcified caudal vertebrae. The number of acid phosphatase stained chondroclasts and osteoclasts was lower than normal in untreated Hyp/Y and was restored after Mg therapy while the osteoclastic surface was increased above normal. Accordingly, serum P and urinary Ca, P, Mg, cAMP and OH-Pro were increased while TmP/GFR was unchanged. On the other hand, dietary lactose corrected serum Ca which probably suppressed PTH secretion since the renal P conservation was improved and the osteoclast number and the osteoclastic surface were decreased. Both treatments reduced the growthplate and osteoid seam thickness and increased the bone calcification rate. The results indicate that the low skeletal Mg present in Hyp/Y partially impairs bone responsiveness to PTH since Mg therapy restored the osteoclastic bone resorption which secondarily provided new minerals for bone mineralization. The greater than normal bone resorption found in Mg treated-Hyp/Y and the decreased bone resorption observed in lactose treated animals indicate that the chronic hypocalcemia induces secondary hyperparathyroidism in Hyp/Y mice.
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PMID:Effects of magnesium and lactose supplementation on bone metabolism in the X-linked hypophosphatemic mouse. 682 87

An in vitro method was developed to predict inorganic P release from maize-soyabean poultry feeds containing supplemental phytase (EC 3.1.3.8), and to quantify the effect of acid phosphatase (EC 3.1.3.2), fungal protease (EC 3.4.23.6) and Aspergillus niger cellulase (EC 3.2.1.4) on phytate dephosphorylation. Pepsin (EC 3.4.23.1) and pancreatin digestion periods were preceded by a 30 min pre-incubation at pH 5.25 to simulate digestion in the crop of poultry. Pancreatin digestion was carried out in dialysis tubing, with a ratio of about 1:25 (v/v) between the digesta and dialysing medium, to simulate gradient absorption from the duodenum. The feed:water ratio was kept within physiological limits and a constant proportion of feed weight to digestive enzymes was maintained. There was a linear response to increasing dosages of phytase up to 1000 phytase units (FTU)/kg feed, and to increasing phosphate concentration in feeds. In vivo validation was performed with growing turkeys (1-3 weeks) fed on diets containing 12 g Ca/kg and 0, 500 or 1000 FTU phytase/kg in a factorial arrangement with 0, 1, 2 or 3 g supplemental phosphate/kg (from KH2PO4). After a simple transformation (variable/in vitro P = f (in vitro P)), amounts of P hydrolysed from feed samples by in vitro digestions correlated with 3-week body-weight gain (R 0.986, P < 0.0001), toe ash (R 0.952, P < 0.0001), feed intake (R 0.994, P < 0.0001) and feed efficiency (R 0.992, P < 0.0001). The dephosphorylating ability of phytase in vitro was significantly enhanced (P < 0.05) by the addition of acid phosphatase. Fungal acid protease and Aspergillus niger cellulase also enhanced the dephosphorylation process in vitro.
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PMID:An in vitro procedure for studying enzymic dephosphorylation of phytate in maize-soyabean feeds for turkey poults. 754 27

To investigate the possible mechanisms of the accumulation of particle-laden alveolar macrophages (AMs) in alveoli, male golden hamsters were exposed to coal fly ash (FA) at the concentration of 0 or 2 mg/m3 for 6 months (20 hr/day, 7 days/week) in the first series of experiments, and at 0, 1, 2, or 20 mg/m3 of FA for 3 months in the subsequent experiments. Particle-laden AMs accumulated dose- and time-dependently in alveoli. In the lungs of 1 and 2 mg/m3-exposed groups. AMs first appeared in a cluster in alveoli at the alveolar-bronchiole junctions proximal to the lobar bronchus. Agglomerated AMs in these regions were generally larger in size and ingested more particles than those in the peripheral regions. These results indicate that the accumulation of AMs is closely related to the amount of particles deposited in alveoli and that ingested by AMs. Histochemical analysis revealed that AMs with small amount of particles showed the positive activity of acid phosphatase. On the other hand, heavily particle-laden AMs showed no such activity. Scanning electron microscopic observations revealed the time-related formation of small blebs and loss of surface features on the cell surface of AMs. These results suggest that the accumulation of particle-laden AMs might be caused by the decrease and/or loss of their activities, especially their mobility during migration toward terminal bronchioles from alveoli, due to the increase of ingested particles in parallel with the prolongation of exposure time.
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PMID:Accumulation of alveolar macrophages induced by inhalation exposure of coal fly ash in golden hamster lungs. 811 44


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