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)

Although it is generally believed that hepatic alkaline phosphatase is localized to liver plasma membranes, 63% is present in the cytosol fraction after ultracentrifugation of rat liver homogenates. Divalent cation requirements, heat inactivation, pH optima, Km and chemical inhibition characteristics of partially purified alkaline phosphatase enzymes prepared from membrane and cytosol fractions suggested different structural forms. Furthermore, bile duct obstruction and ethinyl estradiol administration preferentially increased membrane-bound alkaline phosphatase activity, while cytosol activity was unaltered. In contrast, phenobarbital treatment decreased membrane-bound alkaline phosphatase and increased cytosol activity. These studies support the presence of two forms of hepatic alkaline phosphatase in rat liver which are regulated by different control mechanisms.
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PMID:Hepatic alkaline phosphatase isoenzymes: isolation, characterization and differential alteration. 1 30

Sequential therapy to regulate menstruation was administered to 30 women to determine if liver functions are disturbed by contraceptive use. 15 women aged 16-22, used a sequential preparation consisting of ethinyl estradiol and norethisterone acetate. These patients showed significant decreases in aminotransferase GPT and alkaline phosphatase in the last (gestagen) stage of treatment, and slight increases in alpha-amylase and beta-globulin throughout the therapy. In the 15 women aged 17-34 who used ethinyl estradiol and chlormadinone acetate, the ZST showed a significant increase during the therapy. No significant changes in the liver function could be shown by these tests. These preparations are recommended for treatment of disturbances of menstrual cycles; tests of liver functions during treatment are unnecessary. The length of the estrogen and estrogen-gestagen phases of the treatment should be equal to prevent hormonal imbalance.
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PMID:[Liver function tests under the influence of sequential treatment using ethinyl estradiol-norethisterone acetate and ethinyl estradiol-chlormadinone acetate]. 6 69

During the first cycle of treatment the influence of four forms of sequence therapy with mestranol and ethinyl estradiol as estrogen and the two gestagens chlormadinone acetate and norethisteron acetate in women at fertile age was examined for the aminotransferases (GOT and GPT), the activity of alkaline phosphatase and alpha-amylase, for the cholesterol, total bilirubin and total protein content of the serum and for the half-life period of indocyanine green. Under the application of mestranol/chlormadinon acetate an estrogen-induced increase of the activity of the alanine aminotransferase (GPT) from 6.38 units/l to 12.14 units/l may be established, after addition of the gestagen chlormadinon acetate a decrease to 5.34 units/l was to be established. Under the sequence therapy with mestranol/norethisteron acetate only an increase of the alpha1-globulin proportion was to be ascertained. All the other changes of the tested parameters including the half-life period of indocyanine green were not essential.
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PMID:[Liver function studies under the effect of 4 sequential hormonal contraceptives]. 8 73

Cells of sarcoma 180 and of Ehrlich's carcinoma were maintained by serial transplantation in male and female Swiss mice. Either estrogen, progesterone, or testosterone were injected im at doses of 1 mg/mouse. Ascitic fluid was aspirated at intervals of 1, 3, 6, 24, and 48 hours following hormone injections. Enzyme activities were analyzed by subjective grading according to the intensity of staining reaction. Estrogen produced enhancement of alkaline phosphatase activity in both types of cells in both sexes of mice. Progesterone produced increased alkaline phosphatase activity in both types of cells from female hosts but an inhibitory effect in male hosts' cells. Testosterone produced no change in enzyme activity in tumor cells of female hosts but in male hosts it inhibited enzyme activity of sarcoma 180 cells and activated activity in carcinoma cells. The effect of all 3 hormones on acid phosphatase activity was activation. With adenosine triphosphatase, estrogen stimulated the activity in both types of tumor in both sexes. Progesterone stimulated cells from male hosts with little or no effect on cells from female hosts. This enzyme was resistant to testosterone. Succinate dehydrogenase activity under similar conditions was different. Estrogen reduced this activity and progesterone produced some inhibition of activity. Testosterone inhibited the sarcoma cells but had no effect on carcinoma cells of either sex. Others have shown that sex hormones affect the enzyme activities beyond the target tissues, particularly in the liver, kidney, and pancreas. Different responses of the enzymes seemed to depend on the endogenous hormonal status of the mice.
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PMID:Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone. 13 8

The efficacy of a new estrogen-progestin contraceptive agent Ovidon was evaluated in 65 women. The women were taking the contraceptive for 47 cycles (each Ovidon pill contained 0.25 mg of D-norgestrel and 0.05 mg of ethinyl estradiol). Prior to the Ovidon treatment, 15 women did not use any contraceptive agents or devices, 5 used hormonal contraceptives, 2 used IUDs, 4 used mechanical devices, 20 practiced coitus interraptus, and 9 used a biological method. Ovidon administration provided a 100% contraceptive effect. Side effects of Ovidon included fatigue (15 women), headache (4), irritability (3), fullness of the breast (27), hemorrhage (12), vaginal discharge (6), and changes in libido (22). Ovidon administration did not induce amenorrhea. A 1-3 kg weight gain was observed in 5 women. Laboratory studies showed no changes in hemoglobin levels, leukocyte count, cholesterol, and alkaline phosphatase levels. These findings indicated the safety and contraceptive efficacy of Ovidon.
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PMID:[Clinical trial of the combined contraceptive preparation, Ovidon]. 39 Oct 67

Ethinyl estradiol treatment to female rats resulted in increased levels of serum alkaline phosphatase, but was not associated with any other manifestation of toxicity such as increased serum transaminases or toxic lesions. Elevated serum alkaline phosphatase seen in rats treated with chloroform was associated with frank hepatotoxicity. Induction of hepatic drug metabolising enzymes in rats by phenobarbitone treatment did not result in raised serum alkaline phosphatase levels. Estradiol benzoate treatment to rats also did not increase serum alkaline phosphatase levels. Ethinyl estradiol also resulted in increased alkaline phosphatase content in the liver, intestine and bone. The raised intestinal alkaline phosphatase content of rats treated with phenobarbitone or estradiol benzoate was not associated with an increase in the serum levels. There was histochemical evidence of induction of canalicular alkaline phosphatase in the liver in Ethinyl Estradiol treatment. The study of the electrophoretic separation of serum alkaline phosphatase of ethinyl estradiol treated rats revealed the presence of a new fast moving fraction, similar to those seen in bile duct ligated rats. It is concluded that the serum alkaline phosphatase increase during ethinyl estradiol treatment at least in part is from the liver, due to new synthesis.
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PMID:Serum alkaline phosphatase elevation in female rats treated with ethinyl estradiol. 67 18

A 15-year old Black teenager came to a clinic at the University of Alabama's School of Medicine in Tuscaloosa requesting oral contraceptives (OCs). The physical examination indicated that she was in good health and the physician prescribed an OC (1 mg norethindrone and .035 mg ethinyl estradiol). 21 months later she returned complaining of yellow eyes for 3 weeks. The oral mucosa was also jaundiced. She had considerably high levels of bilirubin and alkaline phosphatase. She had no hepatitis virus antibodies. 5 months later she returned for the physical examination required to renew the OC prescription. She did not have jaundice at this time. 10 months later she complained of malaise and muscular pain. Her alkaline phosphatase level was high, but her bilirubin level was normal. She had mild hepatosplenomegaly without focal defects. After reviewing her medical records, the physician diagnosed intrahepatic cholestasis and discontinued her OC prescription. Liver function tests were normal within 3 months. 14 months later, she returned complaining of malaise and reported taking OCs obtained at another clinic 3 months earlier. The physician advised her about the complications of OCs and about other contraceptive methods. The same physician also examined a 32-year-old Black woman who had intermittent epigastric and right-upper quadrant abdominal pain for 2 weeks. Eating worsened the pain, which lasted for up to 15 minutes. She had used an OC for 12 years. Ultrasound revealed a 4.2 cm hypoechoic mass in the left upper lobe of the liver. The physician discontinued the OCs. The tumor regressed over 12 months. Active liver disease is a contraindication to OC use. Women who had cholestatic jaundice while pregnant or have first degree relatives with cholestatic jaundice of pregnancy should not use OCs. Physicians may introduce OCs to closely monitored women with a history of liver disease whose liver function tests are normal. Women with a family history of biliary excretion defects should not use OCs.
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PMID:Hepatobiliary complications of oral contraceptives. 133 97

This randomized double-blind study of the metabolic effects of two low-dose oral contraceptives was conducted in 58 randomly selected Singaporean women. Study subjects were divided into two treatment groups: 1) norethisterone 1 mg/ethinyl estradiol 35 mcg (NET/EE) or levonorgestrel 150 mcg/ethinyl estradiol 30 mcg (LNG/EE) were given to 35 women; 2) a control group of 23 women using IUDs. Blood samples were taken on admission and at 3 and 12 months after pills or insertion of IUDs. Findings demonstrate a significant decrease in mean fasting glucose and in 2-hour glucose loading, while triglycerides were increased throughout the treatment period in the NET/EE group. The LNG/EE group only showed significant suppression of the 2-hour glucose loading at 12 months and low-density lipoprotein/high-density lipoprotein (LDL/HDL) cholesterol was significantly reduced by 12 months. Both groups had no change in hemoglobin, hematocrit and total protein levels, but alkaline phosphatase, bilirubin and aspartate transaminase (SGOT) were decreased. Decreased albumin was observed in the NET/EE group, but not in the LNG/EE group. Changes in total HDL and LDL cholesterol and SGOT were not significantly different in the treatment group compared to the IUD group, except for the 2-hour glucose loading. There was no increase in the number of abnormal parameters after treatment. On the contrary, there was a reduction of abnormal values in most liver function parameters. Thus, except for glucose intolerance, the observed changes in metabolic parameters may not be of any clinical significance.
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PMID:Lipid and biochemical changes after low-dose oral contraception. 145 19

Mineral metabolism was studied in 99 premenopausal and 80 postmenopausal women both before and after 9-14 months of treatment with 50 micrograms/day transdermal estradiol. In estrogen-repleted subjects (premenopausal women and postmenopausal women on estrogen replacement therapy) total serum calcium was significantly lower (0.065 mmol/l; p less than 0.001) than in those who were estrogen-depleted (untreated postmenopausal women). This difference was smaller but still significant for calculated ultrafiltrable calcium (UFCa: 0.02-0.03 mmol/l; p less than 0.001). However, ionized calcium (both calculated and measured) was not different in the two groups of women. This finding explains why estrogen repletion does not induce changes in the serum level of intact parathyroid hormone (PTH), despite lower total or ultrafiltrable serum calcium. In a parallel study we have shown that intravenous administration of aminobutane bisphosphonate, a powerful inhibitor of bone resorption, produces similar decreases in serum calcium which were associated with significant increases in intact PTH. Estrogen-depleted women had, on the one hand, significantly higher serum levels of bicarbonate, anion gap, complexed calcium, pH, phosphate and alkaline phosphatase, and higher rates of tubular reabsorption of phosphate and urinary excretion of calcium and hydroxyproline. On the other hand they had lower serum chloride levels and lower rates of tubular reabsorption of calcium. Altogether these findings might indicate that estrogen deficiency decreases renal sensitivity to PTH. This is responsible for the higher serum phosphate and bicarbonate levels, the resulting mild metabolic alkalosis leading to higher serum levels of complexed ultrafiltrable calcium and higher rates of urinary excretion of calcium, but unchanged serum levels of ionized calcium and PTH.
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PMID:The effects of menopause and estrogen replacement therapy on the renal handling of calcium. 161 Dec 23

An oral administration of antifertility drug Lyndral (17 alpha-ethinyl estradiol) at doses 5 micrograms/rat/a week for 3 consecutive weeks altered the internal biochemical milieu of uterus, showing a cyclic variation in both acid and alkaline phosphatase of the uterine fluid with high levels being present at proestrus and estrus in control rats. In Lyndral treated rats acid phosphatase showed a tendency to increase in estrus and metestrus rats, whereas alkaline phosphatase increased significantly during proestrus and estrus stages of the cycle. All these altered phosphatase levels in uterine fluid, after Lyndral treatment, gives some insight into the hormonal sensitiveness of these enzymes.
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PMID:Cyclic variation in rats's uterine fluid phosphatase level after administration of lyndral (17 alpha-ethinyl estradiol). 166 77


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