Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two strains of broiler chickens selected for a high and a low incidence of tibial dyschondroplasia were fed a standard broiler starter ration with and without added chloride. Development of tibial dyschondroplasia was studied by radiography and serial necropsies. Lesions of tibial dyschondroplasia were mild in the low-incidence strain, regardless of ratio. The defect was more severe in the high-incidence strain and most severe in those birds fed the high-chloride ration. An abnormal thickening of the growth plate was apparent in the high-incidence strain as early as 2 weeks of age and became progressively more severe with age. No significant differences were noted in serum calcium, phosphorus, alkaline phosphatase, pCO2, or bone ash between strains of birds or between birds of the same strain fed different rations. Birds fed the high-chloride ration had a higher serum chloride and a lower serum bicarbonate and blood pH than birds on the standard ration.
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PMID:The development of tibial dyschondroplasia in broiler chickens. 116 13

Studies were conducted to determine the nutritional interrelationship between different fat sources, vitamin D3 (vit D) and excess dietary vitamin A (vit A) in the growing chick. Birds tolerated as much as 30 times the recommended level of vit A without compromising performance or skeletal development as measured by bone ash. The response to excess dietary vit A was not influenced by the type of dietary lipid (corn oil, tallow, or poultry oil). No nutritional interaction between vit A (1,500, 15,000, or 45,000 IU/kg) and vit D (100 or 1000 ICU/kg) was detected as measured by growth, bone ash, growth hormone, incidence of tibial dyschondroplasia (TD), or rickets. Serum alkaline phosphatase activity, however, was significantly affected by vit A, vit D, and age of the chicks. The higher vit D level significantly enhanced growth, bone ash, and reduced incidence of rickets, although it had no effect on incidence of TD.
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PMID:Excess dietary vitamin A in the growing chick: effect of fat source and vitamin D. 396 Aug 10

Large White male turkeys were fed rations containing 0, 12.5, 25, 50, 100, 200, 400, and 800 ppm added fluoride (F) from sodium fluoride in a corn-soybean assay diet containing tricalcium phosphate and 3 to 5 ppm F. The 800 ppm treatment was discontinued at 8 weeks because of low weight gains and a high incidence of leg disorders. Turkeys receiving defluorinated phosphate (32% calcium, 18% phosphorus) had significantly higher 4-week body weights than turkeys receiving tricalcium phosphate. Turkeys fed 0, 400, and 800 ppm F had significantly lower body weights at 8 weeks than turkeys fed 50 ppm F. A similar weight pattern was seen at 18 weeks, although the differences were not statistically significant. Based on growth response in this study, a requirement of 20 ppm F is proposed. Increasing levels of dietary F resulted in large increases in tibia F. Removal of high dietary F in certain groups at 8 weeks resulted in growth recovery and reduction in tibia F by 18 weeks. Elevated plasma alkaline phosphatase activity was observed with added dietary F of 400 and 800 ppm. At 4 weeks, tibiae from turkeys receiving high F had a trend (not statistically significant) toward lower percentage ash and a significantly lower breaking strength than controls. Compared to controls, tibiotarsi from turkeys on high F rations were significantly shorter, had thinner cortices, and had a narrower proliferative zone of proximal growth plates. A high incidence of tibial dyschondroplasia was observed, but it was not correlated with dietary treatment.
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PMID:Effect of dietary sodium fluoride on growth and bone development in growing turkeys. 663 81

The effect of thiram, a fungicide that increases the incidence of tibial dyschondroplasia (TD) in poultry, was studied in vitro using growth plate chondrocyte culture. Thiram caused a significant reduction in alkaline phosphatase, acid phosphatase, and lactate dehydrogenase (LDH) activities at concentrations of 5 microM and above. It was highly cytotoxic to chondrocytes at and above this concentration as determined by their ability to reduce 3(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (triazolyl blue, MTT), a marker of cellular viability. An increase in the leakage of LDH into culture media was evident at concentration as low as 1 microM. Very few differences were noticed in the electrophoretic migration profiles of cell-extract proteins at any treatment level relative to control. The cytotoxic effect of thiram is possibly due to its damaging effect on the cell membrane, which may be responsible for chondrocyte death.
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PMID:Effect of thiram on chick chondrocytes in culture. 789 97

Three experiments were carried out to investigate the effects of supplemental dietary 1,25-dihydroxycholecalciferol (1,25(OH)2cholecalciferol) and a low dietary Ca:P ratio on the occurrence of tibial dyschondroplasia (TD) in 3-week-old broilers. Histopathology was used to diagnose TD. In the first experiment, feeding a diet containing 7.5 g Ca and 7.6 g P/kg gave a higher incidence of TD than a control diet containing normal amounts of Ca and P (12 and 6 g/kg respectively). Increasing the dietary supplement of cholecalciferol in the imbalanced diet prevented rickets but did not decrease the incidence of TD. In the second experiment, supplementing the imbalanced diet with 10 micrograms 1,25(OH)2cholecalciferol/kg prevented TD completely but also gave a slight growth depression. In the third experiment the imbalanced diet was supplemented with 0, 2.5, 5 or 10 micrograms 1,25(OH)2 cholecalciferol/kg. The supplement of 2.5 micrograms/kg depressed and the higher supplements prevented the occurrence of TD, this time without a growth depression. Feeding the 10 micrograms/kg supplement for the first week only did not prevent TD. Plasma total Ca, inorganic P and alkaline phosphatase (EC 3.1.3.1) were unaffected by diet but 1,25(OH)2cholecalciferol was higher on the imbalanced than on the control diet. Supplementation of the imbalanced diet with 1,25(OH)2cholecalciferol did not increase plasma levels. It is concluded that 1,25(OH)2cholecalciferol is exerting a powerful biological effect in this model of TD, but the mechanism is unclear.
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PMID:The effect of dietary 1,25-dihydroxycholecalciferol in preventing tibial dyschondroplasia in broilers fed on diets imbalanced in calcium and phosphorus. 832 55

Tibial dyschondroplasia (TD) is a disorder of endochondral bone growth and results in the retention of a mass of unmineralized, avascular cartilage extending into the metaphysis. We have studied various parameters of chondrocyte differentiation, both in isolated chick chondrocytes and growth plate sections, in an attempt to determine whether the inhibition in chondrocyte differentiation seen in TD is a consequence of an inherent incapability of chondrocytes to differentiate terminally and mineralize. Results from in vitro experiments indicated that both normal and lesion chondrocytes synthesized a matrix that stained with antibodies to types II and X collagen and displayed foci of mineralization. Alkaline phosphatase activity in lesion chondrocytes was significantly increased in comparison to that in normal hypertrophic chondrocytes. In addition, normal and lesion chondrocytes in culture synthesized transforming growth factor-beta and 24,25(OH)2D3 but not 1,25(OH)2D3. There was no significant difference in the production rate of these growth regulators between normal and lesion chondrocytes. In contrast, in growth plate sections, alkaline phosphatase activity was markedly reduced in the lesion chondrocytes and sites of mineralization were not evident. Type II collagen was located throughout the growth plate and lesion, but type X collagen was not present within the lesion except at sites of vascularization. These results indicate that, in culture, lesion chondrocytes have the ability to differentiate terminally and mineralize, and suggest that the primary abnormality in TD is related to a developmental fault which is only operative in vivo. This may include a defect in cartilage vascularization and/or impairment of chondrocyte differentiation by mechanisms that have not yet been elucidated but may involve the abnormal production of regulatory factors.
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PMID:Regulators of chondrocyte differentiation in tibial dyschondroplasia: an in vivo and in vitro study. 854 Nov 42

In order to assess alterations in the collagen network during endochondral ossification the pyridinium cross-links of collagen were quantified in sequential transverse sections through the chick growth plate. This was accomplished using both morphological (alkaline phosphatase (ALP) histochemistry and collagen type X immunostaining) and analytical (HPLC) analyses. In articular cartilage, pyridinoline concentrations were maximal in the deep mature zones. In contrast, the proliferating chondrocyte zone of the growth plate had approximately a 10-fold greater pyridinoline cross-link concentration than the mature hypertrophic zone. Deoxypyridinoline was first found in the prehypertrophic zone of the growth plate cartilage that reacted positively for ALP activity but before collagen type X was detected. However, deoxypyridinoline concentrations were highest in the most differentiated regions of the growth plate where it was the principal pyridinium cross-link. In tibial dyschondroplasia, where chondrocyte differentiation is arrested in the prehypertrophic zone, higher concentrations of both cross-links were found with increasing distance down the lesion. We conclude that the decrease in pyridinoline cross-link concentration down the growth plate may be an essential adaptation (via increased collagenase activity and collagen turnover) of the matrix for vascular invasion and osteoclastic resorption to occur.
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PMID:Distribution and quantification of pyridinium cross-links of collagen within the different maturational zones of the chick growth plate. 876 27

Gene expression and alkaline phosphatase (AP) activity, associated with chondrocyte differentiation, were evaluated in the epiphyses of normal and tibial dyschondroplasia (TD)-afflicted turkeys. In the normal turkey growth plate (GP), osteopontin (OPN) and type X collagen genes were expressed by the hypertrophic cells in both GP and secondary ossification center, parallel to manifestation of AP activity. Collagen type II gene expression was restricted to the nonhypertrophic chondrocytes at the upper part of the GP. OPN or collagen type X genes were not expressed within the TD lesion. However, these genes were expressed in areas proximal and distal to the lesion, suggesting that after reaching partial differentiation, chondrocytes within the developing TD lesion de-differentiate into cells that resemble chondrocytes in the prehypertrophic zone. This suggestion is supported by the observation that the cells in the lesion expressed the collagen type II gene. In some cases, the TD lesion was invaded by fibroblastlike cells that did not exhibit any AP activity or expressed the OPN gene. No lesions were observed in the secondary ossification centers.
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PMID:Gene expression during cartilage differentiation in turkey tibial dyschondroplasia, evaluated by in situ hybridization. 908 21

PTH/PTHrP receptor gene expression was evaluated in situ in avian epiphyseal growth plates taken from normal, rachitic and tibial dyschondroplasia (TD) afflicted chicks induced by thiram or by genetic selection. In the normal growth plates, PTH/PTHrP receptor gene expression was localized to the maturation zone as demonstrated by the expression of collagen type II (col II), osteopontin (OPN) genes and alkaline phosphatase activity (AP). In TD, either induced by thiram or by genetic selection, normal levels of PTH/PTHrP receptor gene expression were observed up to 21 days post-hatch. In rickets, on the other hand, no PTH/PTHrP receptor gene expression was observed in the growth plate from day 8 of a vitamin D-deficient diet. In cultured chondrocytes, PTH caused time-dependent down-regulation of its own receptor. These results suggest that alterations in the PTH/PTHrP receptor gene expression are associated with rickets but not with TD. The reduction in the PTH/PTHrP receptor gene expression in rickets may be due to the high plasma levels of PTH.
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PMID:Parathyroid receptor gene expression by epiphyseal growth plates in rickets and tibial dyschondroplasia. 1037 30

Four litters (41 pigs) of cross-bred pigs were studied from 6 to 26 weeks of age. Blood samples were collected at 6, 13, 21 and 26 weeks of age and analysed for contents of vitamin C, calcium (Ca), inorganic phosphorus (P) and alkaline phosphatase (ALP). The pigs were examined clinically for foreleg weakness at the ages of 21 and 26 weeks. At the age of 26 weeks the pigs were slaughtered and the right forelegs were examined macroscopically and selected samples were collected for radiological, histological and ultrastructural examination. The prevalence of foreleg lesions was high, with lesions of dyschondroplasia of the distal growth plate of the ulna in 30 pigs, synovitis of the elbow joint in 24 pigs and osteochondritis dissecans of the elbow joint in 25 pigs. At the ages of 21 and 26 weeks, five pigs had evidently crooked forelegs and 14 pigs (age 21 weeks) and 25 pigs (age 26 weeks) had mildly deformed forelegs. The serum levels of Ca, P and ALP were within normal values for growing-finishing pigs. The range of vitamin C concentrations in plasma showed a wide difference (7.1-49.8 mumol/l) but was not associated with deformed forelegs. The serum concentrations of Ca, P and ALP and the plasma concentration of vitamin C differed significantly (P = 0.05) between age groups and there was a significant (P = 0.001) positive correlation between the levels of vitamin C in plasma and the serum levels of ALP at 6 weeks of age. The aim of the present study was to determine if there was any association between the plasma levels of vitamin C and the extent of crooked or deviated forelegs in growing-finishing pigs. We could not find a vitamin C deficiency during the study and no association between low levels of vitamin C in plasma and the presence of deformed forelegs of these 40 pigs.
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PMID:Vitamin C plasma concentrations and leg weakness in the forelegs of growing pigs. 1137 90


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