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)

16 adult female rhesus monkeys received combined oral quingestanol acetate and ethinyl estradiol in a 10:1 ration, 4 received steroids in a 20:1 ration. After 6 cycles of 21 days on and 7 days off the uterine alkaline and acid phosphatases were analyzed histologically. Dose groups included: 4 monkeys given 4 mcg per kg ethinyl estradiol and 40 mg quingestanol acetate, 4 given 20 and 200, 8 given 10 and 100, 4 given 50 and 1000. Most monkeys were killed 8 days after the last dose. In the 6 controls glandular phosphatases were low in early follicular phase, highest in late follicular phase, and declining in the stratum functionale in luteal phase; also acid phosphatase appeared in the stromal cells with eccentric nuclei in luteal phase. 90% of the low and middle dose monkeys were in follicular phase and had normal menstrual cycles. Their alkaline phosphatase was greater in stratum functionale than in stratum basale, and the acid phsophatase resembled controls in follicular phase. Most monkeys given high doses were in luteal phase and their enzymes were correlated with cycle phase.
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PMID:Influence of an oral contraceptive progestin-estrogen combination on simian uterine phosphatases. 498 Aug 17

This study concerns the effect of graded doses of estrogen, alone or in combinations with progesterone, on the biochemical composition of the rat seminiferous tubules. Data on the accessory genital organs and pituitary gonadotrophic activity are added. Adult male albino rats received estradiol dipropionate (.1, 1 and 5 mcg/rat) injected intramuscularly, in .1 ml olive oil, daily for 30 days. Animals given the 5 mcg dose were given a 30 day rest period to determine reversibility of effects. In another group estrogen (5 mcg/rat) and progesterone (1 mg/rat) were given concurrently but at different sites for 30 days. Controls received vehicle only. Animals were sacrificed 24 hours after the last injection or rest period and genital organs and the pituitary were removed for study. A progessive reduction in testis weight with dosage was found after estrogen or the combination (p is less that .01). The low dose (.1mcg) had an inconsistent effect on spermatogenesis and endocrine function of the testis. Diameter of the tubules was reduced. Spermatogenesis was arrested in 25% of the tubules at the spermatid of secondary spermatocyte stage. Some normal spermatozoa were seen. Tunica propria was thickened. Some Leydig cells showed atrophy. Vascularity was increased. The median dose (1 mcg) caused spermatogenic arrest at the spermatid or secondary spermatocyte stage but the Sertoli cells were prominent. Only a few spermatozoa were seen. There was some desquamation of seminiferous epithilium. Tubular diameter was still further reduced and the tunica propria thickened. Leydig cells were atrophied. Few spermatozoa were found although 25-30% showed some spermatogenesis. The high dose (5 mcg) caused marked reduction in the diameter of the tubules. Spermatogenesis was arrested at the primary spermatocyte or spermatogonial stage. The tunica popria was much thickened. There was much desquamation and tubular lumeus were filled with debris. The Sertoli cells were hypertrophied. The Leydig cells were atrophied. The tunica albuginea was thickened. There were no spermatozoa. In the recovery group estrogen effects had disappeared, but the tubular diameter remained reduced. Tunica propria was normal. Spermatogenesis progressed to the spermatid stage and in 50% of the tubules many spermatozoa were present. The Leydig cells appeared normal. However spermatozoa were not found in the vas defereus. The histological appearance of the teatis in the estrogen and progesterone group was of the high dose estrogen type but with arrest of spermatogenesis at the spermatid, spermatocye or spermatogonial stage. The Sertoli cells remained hypertrophied. Leydig cells were atrophic. The large blood vessels were engorged. Weight of organs returned almost to normal. Estrogen .1 and 1 mcg had no effect on pituitary weight or gonadotrophin content. The high dose (5 mcg) alone or with progesterone caused a significant increase in pituitary weight (p is less than .0). Estrogen alone (5 mcg) caused a significant decline in pituitary gonadotrophin content (p is less than .0) but the combined therapy had no effect. None of the biochemical constituents of the seminiferous tubules showed any change after injection of .1 mcg of estrogen but 1 mcg dose caused an increase in protein nitrogen, alkaline phosphatase activity and total lipids. The high dose (5 mcg) provoked higher levels.
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PMID:Effect of estrogen on biochemical composition of the rat seminiferous tubules. 514 19

58 postpartum patients between the ages of 20-35 were selected from a series of 208 oral contraceptive users for liver function studies. They had been treated with 1 of 3 anovulatory combined oral contraceptives for a period of 1 year. The preparations used were: 1) .05 mcg of ethinyl estradiol + 1 mcg of ethinyl-nortestosterone acetate (25 patients), 2) .075 mcg of ethinyl estradiol + 1 mcg of ethinyl-nortestosterone acetate (16 patients), and 3) .50 mcg of ethinyl estradiol + .50 mcg of norgestrel (17 patients). Studies were done trimestrally and included direct bilirubing, total bilirubin, turbidity of timol, SGOT, SGFT, alkaline phosphatase, and sulfobromophthalien retention. Menstruation was induced on the 28th day postpartum by administering 20 mcg of nortestosterone acetate and .04 mcg of ethinyl estradiol (Duogynon). The assigned contraceptives was taken on a normal basis thereafter. No changes in liver function that could be attributed to the pills were observed. Pathological modifications were, however, observed in the tests for turbidity (in 52.5%, 31.3%, and 25%, respectively), SGOY (0%, 0%, and 12.5%, respectively), and sulfobromophthalien retention (0%, 13.3%, and 11.76%); in some instances the changes persisted throughout the study. Alterations in turbidity, SGOT and SGFT that occurred in 1 patient with a history of hepatitis were an indication to the authors that hepatitis should be a contraindication for use of orals. Graphs of test results are included.
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PMID:[Liver function and iatrogenic anovulation]. 540 52

25 fertile women aged 25-36 with an average of 3 children were tested over 93 cycles to observe the effects of synthetic steroids on the neutrophil alkaline phosphatase. The women were using 3 different types of oral contraceptives: Anovlar, Lyndiol, and Enovid-E. 14 women using Anovlar were analyzed for 50 cycles and showed fluctuation in alkaline phosphatase activity with higher levels as compared to normal cycles before the use of Anovlar. 8 women receiving Lyndiol over 18 cycles indicated a low-rise, while 3 women on Enovid-E over 10 cycles showed a rise in alkaline phosphatase activity, but not as much as with the Anovlar. After a 5-cycle follow-up, 5 women who discontinued the pill showed a drop in alkaline scores. After pill discontinuation, there was a gradual return to the neutrophil alkaline phosphatase activity, but these levels did not indicate a correlation with the total leukocyte or absolute neutrophil count.
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PMID:Alkaline phosphatase activity of polymorphonulcear leukocytes in relation to oral contraceptives. 576 65

In vitro cultivated cells derived from normal human renal cortex were characterized morphologically and biochemically. Although the epithelial monolayer was composed of heterogeneous cells, it included cells with a surface structure similar to microvilli as well as some resembling the desmosome between neighboring cells. Enzymatic studies revealed a marked decrease in alkaline phosphatase activity, and the activity of gamma-glutamyl transpeptidase was also reduced to about one-fifth of that in the original tissue. The electrophoretic mobility of the enzyme was not identical with that of normal kidney or of the novel enzyme in renal neoplastic tissue. Lactate dehydrogenase activity was similar to that of normal kidney tissue but the isozyme pattern was completely inverted. These cells responded to the addition of 10 ng per ml of parathyroid hormone in culture medium and there was a 33 fold increase in intracellular cyclic adenosine monophosphate. Estrogen specific binding protein was not detectable in the monolayer cells. These results clearly indicated that the biologic transformation observed in the cultivated normal cells was not attributable to simple fetalism or dedifferentiation, but was a more complicated process.
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PMID:Morphologic and biochemical characteristics of human kidney cells in vitro. 611 28

Methyltestosterone (MT) or ethinyl estradiol (EE) was administered to adult rabbits for 20 weeks beginning with initial daily doses of 0.4 mg/kg MT and 0.015 mg/kg EE for three weeks, then these dosages were doubled at 3-week intervals to a maximum dosages 6.4 mg/kg and 0.24 mg/kg, respectively. Within 2 weeks, the serum gamma-glutamyltransferase activity of MT and EE treated rabbits was significantly greater than controls and increased progressively throughout the treatment period. Aspartate aminotransferase activity was also increased at 2 weeks and remained so for 17 weeks. Serum alkaline phosphatase was elevated at 2 weeks but thereafter was normal indicating that this enzyme is of no value in detecting steroid-induced hepatic dysfunction. Elevated serum bile acid concentration and prolonged BSP clearance indicated marked hepatic excretory dysfunction at higher dose levels. Histologic abnormalities were observed in the livers of both MT and EE treated rabbits. These lesions were more severe in the EE group in which there was marked bile duct proliferation, mononuclear cell infiltration of portal areas, and perilobular fibrosis. The studies indicate that the rabbit is susceptible to development of hepatic injury when receiving 17 alpha-alkyl substituted steroids and may be a useful animal model for investigations of the pathogenesis of steroid-induced cholestatic liver injury.
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PMID:Assessment of hepatic function in rabbits with steroid-induced cholestatic liver injury. 613 44

18 normal women, 20 with active schistosomiasis, and 25 with past histories of viral hepatitis were given a contraceptive pill containing 0.05 mg ethinyl estradiol and 0.5 mg levonorgestrel for 6 consecutive cycles. Serum bile acids were measured by enzyme immunoassay method before and after 3 and 6 months of use. Simultaneously, conventional liver function tests (serum bilirubin, transaminases, alkaline phosphatase, and albumin) were done. Serum bile acid concentration was not significantly changed by contraceptive use in any group. The concentration of cholylglycine (the main bile acid measured) did not correlate with the values of any of the other tests. Pretreatment values of serum cholylglycine were significantly lower in the past-hepatitis group. The difference was maintained during treatment.
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PMID:Effect of oral contraception on serum bile acid. 614 34

The short and longterm effects on the liver of oral contraceptives (OCs) containing the new progestational compound 13-ethyl-11-methylene-18,19-dinor-17alpha-pregn-4-en-20-yn-ol (desogestrel) and ethinyl estradiol (EE) were studied in multicenter efficacy trials. The following combinations (desogestrel/EE content/daily tablet in mcg) were investigated: 150/30, 125/50, 100/50, and 75/50 to be taken once daily for 21 days and normophasic preparation containing 7 tablets with 50 mcg EE and 15 tablets containing 125 mcg desogestrel and 50 mcg EE. Liver function parameters (SGOT, SGPT, alkaline phosphatase, and total bilirubin) were monitored in the serum of 1856 women for periods of up to 36 treatment cycles. The incidence of values (single and combined) above the upper normal limits before treatment was 3.3%. A combination of values above upper normal limits before treatment was observed in 31 women (1.6%). In practically all cases, values normalized during treatment; no deterioration was observed. During treatment, a combination of values above upper normal limits was seen in 30 women (with normal pretreatment values); these were distributed over the various preparations and unrelated to period of contraceptive treatment. Values normalized in the majority of women during treatment. This study shows that with OCs containing desogestrel and EE (30 or 50 mcg), liver function is not affected. (author's modified)
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PMID:Desogestrel, a new progestational compound, and the liver. 622 46

The effects of Triton WR-1339 and phenobarbital on ethinyl estradiol bile secretory failure were examined to determine the mechanism responsible for decreased bile salt excretion. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored bile salt independent bile flow and maximum taurocholate transport, whereas phenobarbital corrected bile flow only. Ethinyl estradiol decreased the activities of Na(+)-K(+)-ATPase, 5'-nucleotidase, while increasing the activities of Mg(++)-ATPase and alkaline phosphatase. In contrast to these heterogeneous changes in surface membrane enzyme activities, the number and affinity of [(14)C]cholic acid carriers were not altered. When administered in vivo or added directly to surface membrane fractions Triton WR-1339 restored the activities of Na(+)-K(+)-ATPase and Mg(++)-ATPase of rats treated with ethinyl estradiol through a process that did not require protein synthesis (unaffected by cycloheximide). Phenobarbital also restored the activity of Na(+)-K(+)-ATPase to control levels, but, unlike Triton WR-1339 it did not correct the defect responsible for reduced bile salt secretion. Ethinyl estradiol increased the concentration of cholesterol esters in surface membrane fractions. When administered to ethinyl estradiol-treated rats, Triton WR-1339 restored cholesterol ester concentrations to normal, whereas phenobarbital did not. These combined data suggest that decreased or altered bile salt carriers or reduced sodium driving forces resulting from impaired activity of Na(+)-K(+)-ATPase are not responsible for decreased bile salt excretion in ethinyl estradiol-treated rats. It is proposed that the diverse changes in surface membrane function, which are associated with ethinyl estradiol bile secretory failure, may be the result of a generalized alteration in membrane lipid structure.
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PMID:Reversal of ethinyl estradiol-induced bile secretory failure with Triton WR-1339. 624 35

Fourteen postmenopausal women with mild hyperparathyroidism were given conjugated estrogens. Serum calcium levels became normal and urinary calcium excretion was reduced for up to 2 years in ten patients taking an average dose of 1.25 mg of estrogen daily. Hypercalcemia returned quickly when therapy was interrupted. Estrogen did not systematically alter serum immunoreactive parathyroid hormone or calcitriol levels or urinary excretion of cyclic adenosine monophosphate. Significant reductions in urinary hydroxyproline and serum alkaline phosphatase activity during estrogen therapy indicate that the major effect of therapy was to decrease bone turnover. Iliac crest biopsy specimens taken before estrogen therapy showed normal trabecular bone volume and excessive osteoid seams. Follow-up biopsy specimens were taken from six patients after 1 year on therapy. Bone volume remained stable, but hyperosteoidosis had improved in only one patient. Without understanding the long-term impact of untreated mild hyperparathyroidism on bone, the benefits of estrogen therapy on bone remain uncertain. However, therapy with conjugated estrogens provides sustained control of serum and urine calcium in most women with hyperparathyroidism and is a reasonable alternative in patients who are not surgical candidates.
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PMID:Conjugated estrogens in the treatment of postmenopausal women with hyperparathyroidism. 632 24


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