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At least 199 records · Page 11Linked to original sources

PubMed1992

Effect of dietary calcium on tibial dyschondroplasia. Interaction with light, cholecalciferol, 1,25-dihydroxycholecalciferol, protein, and synthetic zeolite.

A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 micrograms/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.

Aluminum Silicates↗

PubMed1995

Comparison of dietary 25-hydroxycholecalciferol and cholecalciferol in broiler chickens.

We conducted a series of 10 feeding trials involving over 36,000 broilers. The effects of various dietary levels of cholecalciferol (vitamin D3) or 25-hydroxycholecalciferol (25-OH-D3) were compared using a "basal" dosage level of 69 micrograms/kg feed, as well as levels ranging from .5 to 1.5 times the basal level. For all 10 studies, average body weight increased by an average of .042 +/- .03 kg (P < .001) and adjusted feed efficiency decreased (improved) by an average of .026 +/- .0046 kg/kg (P < .001) in birds fed 25-OH-D3 in comparison to those fed vitamin D3 at the basal level. Changes in mortality were not detected. Evaluation of different dietary levels of 25-OH-D3 revealed a significant dose-response relationship, with maximal effects on weight gain, feed efficiency, and breast meat yield being observed in the range of 50 to 70 micrograms/kg feed. Preliminary studies with different levels of vitamin D3 suggested no additional benefits on weight gain or feed efficiency with higher dietary levels of vitamin D3. Serum 25-OH-D3 concentrations increased more rapidly in birds fed 25-OH-D3 than in birds fed vitamin D3. There were significant correlations with body weight, feed conversion, and serum 25-OH-D3 concentrations, with no correlations observed between serum 1,25-(OH)2D3 concentrations and these variables.

Analysis of Variance↗

PubMed1995

Safety of 25-hydroxycholecalciferol as a source of cholecalciferol in poultry rations.

We conducted two safety studies of 25-hydroxycholecalciferol [25(OH)D3] in poultry broilers at levels ranging from 1 to 200 times those commonly used for cholecalciferol (vitamin D3) supplementation in the industry. In the first experiment, 1-d-old male and female broiler chickens were fed commercial diets containing either vitamin D3 or 25(OH)D3 at concentrations of 69, 207, and 690 micrograms of 25(OH)D3/kg of feed. The second experiment compared effects of 25(OH)D3 and vitamin D3 on performance and survival of broilers at levels ranging from 1 to 200 times the basal level of 69 micrograms/kg feed. When 25(OH)D3 was fed in equal amounts (wt/wt) to vitamin D3, there was an increase in body weight and a decrease (improvement) in adjusted feed efficiency in both experiments, but the changes were significant only in the first experiment. In the first experiment, serum 25(OH)D3 concentrations increased from 13.3 +/- 4.3 to 42.5 +/- 18 ng/mL in birds fed vitamin D3 or 25(OH)D3, respectively, and rose to 246 +/- 38 ng/mL in birds fed the highest level of 25(OH)D3. Tissue 25(OH)D3 concentrations were much lower than serum concentrations and were highly correlated to the latter, regardless of dietary treatment. In Experiment 2, there was some evidence of renal calcification in birds fed 25(OH)D3 at 10 times the basal level, whereas dietary levels of vitamin D3 of 50 times the basal level were required to show some evidence of renal calcification. On the basis of both renal calcification and body weight, the present studies would suggest that 25(OH)D3 is 5 to 10 times more toxic than vitamin D3.

Animals↗

PubMed1996

The effect of different levels of vitamin C and cholecalciferol with adequate or marginal levels of dietary calcium on performance and eggshell quality of laying hens.

Three experiments were conducted to determine whether shell quality, bone mineralization, and other production traits could be improved by adding vitamin C (ascorbic acid) to laying hen diets. The period of each experiment was 12 wk. Experiment 1 consisted of a 2 x 2 x 3 factorial design with two levels of Ca (2.8 and 3.8%), two levels of cholecalciferol (vitamin D3; 2,200 and 4,400 IU/kg diet), and three levels of vitamin C (0, 125, and 250 ppm). Experiment 2 consisted of a 2 x 3 x 2 factorial design with two levels of Ca (2.8 and 3.8%), three levels of vitamin D3 (250, 500, and 2,000 IU/kg diet), and two levels of vitamin C (0 and 250 ppm). Experiment 3 consisted of a 2 x 4 factorial design with two sources of vitamin D3 (12.5 micrograms vitamin D3/kg diet or 12.5 micrograms 25-OH-D3/kg diet) and four levels of vitamin C (0, 250, 500, and 1,000 ppm). Calcium level was kept constant at 3.5% for all the diets in Experiment 3. Production performance was not influenced by dietary treatments in Experiment 1. In Experiment 2, feed conversion was improved (P < 0.05) due to increasing the dietary Ca, and egg weight and egg size were increased (P < 0.05) due to adding 250 ppm vitamin C to the diet. In experiment 3, albumen quality was increased by the addition of 1,000 ppm vitamin C to the diet. Egg specific gravity was increased in Experiments 1 and 2 only, due to increasing the Ca level (P < 0.05). In Experiment 2, increasing the Ca level and increasing the vitamin D3 level from 250 to 2,000 ppm reduced (P < 0.05) the number of cracked eggs, but incidence of cracked eggs was increased with the addition of 250 ppm vitamin C to the diet. In Experiment 1, plasma level of 1,25(OH)2D3 was greater (P < 0.05) for hens fed 2.8 than 3.8% Ca, but blood acidbase balance was not influenced by dietary regimens. Bone ash was not influenced by dietary treatments in any of the experiments. The data indicated that a supplemental level of vitamin C had no beneficial effects on shell quality and bone mineralization under the conditions of the current experiments.

Aging↗

PubMed1992

Effect of pamidronate in a rat hypercalcemia model induced by cholecalciferol.

Pamidronate (disodium 3-amino-1-hydroxypropylidene-1,1-bisphosphonate pentahydrate, CGP 23339A, CAS 57248-88-1) has been show to provide a potent antihypercalcemic effect through the inhibition of calcium release from the bone. The time course study on the antihypercalcemic effect of pamidronate was performed using a rat hypercalcemia model induced by orally administered cholecalciferol. The onset of the antihypercalcemic effect was observed within 48 h after a single i.v. injection of pamidronate at 1 mg/kg and this effect was sustained for 19 days. The time course of the antihypercalcemic effect of pamidronate in combination with calcitonin was also examined in the same model. The onset of the antihypercalcemic effect was observed within 4 h after combination therapy with a single i.v. injection of pamidronate at 1 mg/kg and successive i.m. injections of calcitonin at 3.2 IU/kg and the effect was of sufficient duration. These results suggest that pamidronate has a pronounced effect in controlling hypercalcemia and provides a long-lasting effect by a single i.v. administration. Moreover, the use of pamidronate in combination with calcitonin may be useful when a quicker onset of action is required clinically.

Animals↗

PubMed1992

[The effectiveness of cholecalciferol and flumethasone for the prevention of hypocalcemic parturient paresis in dairy cows].

Investigations on the efficacy of high doses of cholecalciferol and flumethasone for prophylaxis of hypocalcemic milk fever were performed in dairy cows. Only one cow in the group of 25 treated animals diseased by milk fever, but 5 of 25 control animals showed signs of hypocalcemia. A placenta retention was observed in three treated animals and in four control animals. The results show that the additional application of flumethasone for birth induction after the injection of vitamin D3 was unchanged.

Animals↗

PubMed2004

Estimation of influence of high doses of cholecalciferol on thyroid parafollicular and respiratory tract neuroendocrine cells; preliminary investigations.

The aim of this study was to compare what changes are caused by high doses of cholecalciferol (100,000 UI vD3) and CaCl2 on thyroid parafollicular (C) cells and airways neuroendocrine (NE) cells in rat. Overdosage of vD3 and CaCl2 causes hypocalcaemia and strong hypercalcitoninemia in blood; C cells showed mainly signs of hypertrophy; simultaneously, the number of strong calcitoninpositive cells decreased significantly (statistically significant changes). Immunohistochemical reactions, detecting CGRP, somatostatin, synaptophysin and neuronspecific enolase did not fall under statistic analysis. Airways NE cells re-acted to hypercalcemia differently than C cells--they probably respond to different regulatory mechanisms.

Animals↗

PubMed1991

The influence of excipients and technological process on cholecalciferol stability and its liberation from tablets.

The influence of excipients, used in tablet technology, and technological processes on cholecalciferol (1) stability was investigated. It was observed that 1 degrades in the presence of some excipients. The stability of 1 may be increased by antioxidant addition. The best stabilizing effect was achieved by a alpha-tocopherol and ascorbic acid mixture. On the basis of the achieved results, tablets with 1 were prepared. Their physical and chemical properties, the content of 1, its stability and its pharmaceutical availability were determined.

Antioxidants↗

PubMed1975

Substrate specificity of lecithin:cholesterol acyltransferase. Esterification of desmosterol, b-sitosterol, and cholecalciferol in human plasma.

Desmosterol and beta-sitosterol were esterified when incubated with normal human plasma. The initial rate of demosterol esterification was 1.7 times faster, and that of beta-sitosterol 0.4 times slower, than the esterification rate of cholesterol. These ratios were found to be almost the same when plasma from different normal individuals was tested. Plasma from a patient with familial lecithin:cholesterol acyltransferase deficiency did not esterify any of the sterols. The esterification of desmosterol and beta-sitosterol was considerably slower in normal plasma in which in vitro cholesterol esterification previously had taken place. The different esterification rates could not be explained by a different affinity of the plasma lipoproteins for the sterols tested. Cholecalciferol added to normal plasma did not become esterified.

Acyltransferases↗

PubMed1990

Hypercalcemia secondary to cholecalciferol rodenticide toxicosis in two dogs.

Hypercalcemia secondary to cholecalciferol rodenticide toxicosis was identified in two dogs. The first dog died shortly after admission. The second dog responded to treatment with sodium chloride solution, prednisolone, furosemide, and calcitonin. Treatment was needed for a longer period than anticipated and the serum calcium concentration did not stabilize for approximately one month. Although not conclusively demonstrated, calcitonin was considered the cause of severe anorexia. This new class of rodenticides has great toxic potential for dogs, and it is recommended that serum calcium concentration be carefully monitored as treatment for hypercalcemia is gradually withdrawn.

Animals↗

PubMed1989

Acute intraperitoneal cholecalciferol (vitamin D3) toxicosis in mice: its nature and treatment with diverse substances.

To study the overt toxicosis of intraperitoneally (IP)-administered single doses of cholecalciferol (D3), groups of male CF-1 mice (N = 12) were given graded doses of D3 in corn oil and observed for 21 days. There was a 2- to 4-day onset of signs, including ocular squinting, reluctance to move, lethargy, weakness, anorexia, hunched posture, rough haircoat, and dehydration. This was followed by tremors, coma, and death (large doses) or gradual recovery. Deaths occurred 3 days (larger doses) to 21 days after D3 injection. The linear regression of mortality probits on log10 dose was Y = 7.332X-10.653. The median lethal dose (LD50) of D3 and 95% confidence limits were 135.4 mg/kg (112.2-157.4 mg/kg). To screen potential antidotes against acute D3 toxicosis, groups of mice (N = 12) were given subcutaneous (SC) injections of various substances beginning 2 days after IP injection of a large dose of D3 (300 mg/kg). Substances were given once or twice daily in constant volumes of saline solution (66.8 ml/kg) for 7 days. Two control groups were given D3 but no treatment. They both had 91.7% mortality; their mean (+/- SD) survival time (MST: censored to 21 days observation) was 6.8 +/- 4.7 days and 10.3 +/- 7.0 days. Mortality and MST were not affected significantly (P greater than 0.05) by once-daily injection of saline solution, saline containing dexamethasone (DEX), or saline containing the following substances with or without DEX: ascorbate; citrate; dimercaptosuccinic acid; oxytetracycline; ZnSO4; or MgCl2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

[Study of hard mineralized tissues effect of calcium-deficient diets with and without cholecalciferol supplementation on the incisor dentine of rats].

It has been known that both tooth and bone have an apatite structure similar to that of mineral hydroxyapatite. The apatite crystal in living tissues of tooth and bone generally is constructed from submicrocrystals and has many impurities. It seems that chemical and physical aspects of resistance of hard tissues depend on the diet. Consequently, the matrix of organic, free radicals in X-ray irradiated hard tissues were studied by means of electron spin resonance (ESR). The effects of calcium-deficient diets with and without cholecalciferol supplementation on the incisor dentine of rats were examined by the rate of decay of organic, free fadicals in X-ray irradiated incisor dentine of rats. The crystal size of incisor dentine became smaller in case of calcium contained diet.

Animals↗

PubMed1987

Phospholipid and fatty acid changes produced by cholecalciferol on intestinal mitochondrial membranes.

Cholecalciferol administration to vitamin D-deficient chicks produces, 24 h after treatment, a specific increase of the phosphatidylcholine content in the intestinal mitochondrial inner membrane plus matrix fraction without changes in its proportion in the outer membrane. The ratio of unsaturated/saturated fatty acids in the outer membrane phosphatidylcholine was increased by that treatment. The inner membrane plus matrix presents a decrease of 16:1 in phosphatidylethanolamine and 18:0 in the phosphatidylcholine fraction. Cardiolipin shows the largest change in the ratio of unsaturated/saturated fatty acids predominantly by an increase in the linoleic acid. The present data suggest that phosphatidylcholine and fatty acids modifications in both mitochondrial subfractions caused by vitamin D3 might have some role in the intestinal mitochondrial Ca transport.

Animals↗

PubMed1985

Cholecalciferol metabolites in polycythemic newborns.

Metabolites of cholecalciferol were measured in the sera of healthy and polycythemic newborns at 15.5 and 10.5 h of age (median), respectively. The serum concentrations of 1,25-dihydroxyvitamin D and 24,25-dihydroxyvitamin D were lower in the polycythemic group (P less than 0.003 and P less than 0.001, respectively). As the kidney is the main site of conversion of 25-hydroxyvitamin D to its dihydroxylated metabolites, it is possible that hyperviscosity and subsequent decrease in renal blood flow interfere with the efficiency of the process.

24,25-Dihydroxyvitamin D 3↗

PubMed1986

Cholecalciferol and placental calcium transport.

Transplacental movement of calcium from mother to fetus is essential for normal fetal development. In most species, fetal plasma calcium levels are higher than maternal levels at term. The role of cholecalciferol metabolites, with specific emphasis on 1,25-dihydroxycholecalciferol (1,25(OH)2D), in placental calcium transport and maintenance of the fetomaternal gradient has been extensively investigated. In rats, there is not an absolute demand for 1,25(OH)2D for maintenance of fetal calcium homeostasis in utero, even though it is essential for maintenance of maternal plasma calcium levels. However, in sheep, the absence of 1,25(OH)2D results in disruption of both maternal and fetal calcium homeostasis. It is known that rat and human placentas contain specific cytosolic binding proteins for 1,25(OH)2D that are similar to the well-characterized intestinal receptor. Two calcium-binding proteins (CaBP) have been detected in rat and human placentas: a protein immunologically identical to the vitamin D-dependent CaBP and a calcium-dependent ATPase. The levels of CaBP in rat placenta have been shown to increase in response to exogenously administered 1,25(OH)2D but cannot be obliterated with maternal vitamin D deficiency. No relationship has been shown between 1,25(OH)2D and placental Ca-ATPase in any species. Thus, the mechanism of action of 1,25(OH)2D in maintenance of the transplacental calcium gradient in sheep is unknown. In the pregnant rat (and perhaps human), 1,25(OH)2D is a critical factor in the maintenance of sufficient maternal calcium for transport to the fetus and may play a role in normal skeletal development of the neonate.

24,25-Dihydroxyvitamin D 3↗

PubMed1981

[Hereditary pseudovitamin-D-deficiency rickets with alopecia as a consequence of extreme resistance of target organs to 1.25-(OH)2-cholecalciferol. Therapeutic progress in another disorder of vitamin-D-metabolism (author's transl)].

We report about a pair of Turkish siblings suffering from alopecia and severe rickets. In the elder sister we could show the causal role of extreme resistance of target organs to 1.25-(OH)2-cholecalciferol. The birth of a brother who developed the same symptoms together with two other similar cases in siblings recently published by other authors, made it possible to recognize the disorder as a typical syndrome-like entity, based on a hereditary defect. By successful administration of excessive (and so-far not previously published) doses of Vitamin-D3 a way for therapeutic progress in this new type of vitamin-D-dependent rickets is shown.

Alopecia↗

PubMed1981

Serum calcium, phosphorus and magnesium responses to massive dosing of cholecalciferol (CC) and 25-OH-CC in young and aged ewes.

Twenty-four ewes were divided into two age groups (one-year-old and nine-year-old) and used to determine the influence of cholecalciferol (CC) and 25-OH-CC on serum concentrations of Ca, P, and Mg with time post-injection. The ewes were maintained in slatted-floor pens and fed 800 g per head daily of a diet which analyzed 0.38% calcium, 0.31% phosphorus, and 0.14% magnesium. This diet was fed throughout the 21-day trial. The ewes were injected on days 0 and 7 as follows: (control) 5 ml ethanol; (CC) 50 mg CC in 5 ml ethanol; and (25-OH-CC) 25 mg 25-OH-CC in ethanol. Blood samples were pre-injection (day 0) and on days 1, 2, 3, 5, 7, 9, 12, 17 and 21 of the trial. Serum Ca averaged 10.81, 11.06 and 11.25 mg/100 ml for the one-year-old ewes and 10.51, 11.06 and 11.54 mg/100 ml for the nine-year-olds across sampling times in groups A to C, respectively. Serum P across sampling times averaged 6.58, 7.80 and 9.51 mg/100 ml in one-year-old ewes and were different (P less than .05) from each other. Serum P averaged 7.06, 8.56 and 8.59 mg/100 ml for the nine-year-old ewes. Serum Mg values were 2.51, 2.32 and 2.19 mg/100 ml for the one-year-old and 2.38, 2.14 and 2.00 mg/100 ml for the nine-year-old ewes across all sampling times for control, CC and 25-OH-CC groups, respectively. Serum Mg in one-year-old ewes was lower (P less than .05) in both CC and 25-OH-CC injected ewes than controls, and was lowest (P less than .05) for 25-OH-CC when compared with the control in nine-year-old ewes. External symptoms of hypervitaminosis (reduced feed intake and leg abnormalities) were apparent after the second injection with 25-OH-CC, and were most pronounced in the aged ewes.

Aging↗

PubMedDate not supplied

[Cholecalciferol metabolism of pregnant rats with vitamin D poisoning].

Four and 24 hours after administering toxic doses of vitamin D3 the concentration of unchanged cholecalciferol in the blood plasma, liver, kidneys, osseous and muscle tissues in pregnant rats was lower than in the control animals. The content of 25-hydroxycholecalciferol in all test tissues of the pregnant rats was higher than in non-pregnant animals. Particularly great amounts of this metabolite are accumulated by the osseous tissue, kidneys and intestine, i.e. by vitamin D target tissues. During vitamin D poisoning the content of 25-hydroxycholecalciferol in embryos and placenta is fairly high, the content in the placenta being greater as compared to the test tissues of the pregnant rats.

Animals↗