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)

Thirty outpatients with active RA were treated with Sudoxicam, a nonsteroidal antirheumatic drug, for periods of 6-10 months. Gamma-GT, alkaline phosphatase and transaminase were estimated at 2 week intervals. During treatment, the frequently elevated values showed a significant tendency towards normality (time trend analysis). During a second drug trial with Piroxicam in 32 RA outpatients over a period of 18 months, the mean value of gamma-GT and alkaline phosphatase did not decrease significantly. With regards to liver function tests, there was no significant difference between 19 patients receiving and 13 patients not receiving simultaneous gold therapy. During gold treatment periods of 26 patients with a total dose of 3.8 g Fosfocrisolo (0.8 g Au) the mean value of gamma-GT decreased from 26 to IU/l. Cyclophosphamide treatment of 13 patients, with daily doses of 50-150 mg to a total dose auf 48 g, had no significant influence on gamma-GT and alkaline phosphatase. Our results indicate that the very frequent elevations of gamma-GT and of other liver data in RA are caused by the rheumatoid process itself and not induced by drugs.
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PMID:[Gamma-glutamyltranspeptidase in chronic polyarthritis. II. Influence of drugs]. 1 56

Cyclophosphamide administered intraperitoneally in 20 mg/kg doses at intervals of six days for six weeks caused focal morphological and histochemical lesions of low intensity in rat myocardium. From the third week of the experiment focal eosinophilia and fuchsinophilia of the cytoplasm of a part and later on, of the whole cytoplasm of myocardial fibres, contraction nodes, undulant shape of the fibres, rupture of intercalated discs, very rarely in the sixth week small focal infiltrations composed of mononuclear cells at the site of damaged and disintegrated myocardial fibres, small amount of glycogen, focal increase of acid phosphatase activity and low-grade loss of alkaline phosphatase and magnesium and calcium-dependent ATPases in the sixth week, and unchanged activity of succinic dehydrogenase. Simultaneous use of cyclophosphamide and low-magnesium diet increased the intensity of degenerative changes, which appeared from the second week on, and necrotic changes appearing from the third week on, with more pronounced disturbances in the activity of all studied enzymes, including succinic dehydrogenase, in the sixth week.
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PMID:Histological and histochemical examinations of the myocardium of rats kept on low-magnesium diet and treated with cyclophosphamide. 213 21

Cyclophosphamide must be metabolically activated to produce malformations in limbs developing in culture; 4-hydroperoxycyclophosphamide is an analog of the active metabolite of cyclophosphamide, 4-hydroxycyclophosphamide, that breaks down spontaneously in solution to form 4-hydroxycyclophosphamide. To study the mechanism by which metabolites of cyclophosphamide produce limb malformations in vitro we determined the effects of exposure of cultured limb buds to 4-hydroperoxycyclophosphamide. Fore- and hindlimbs were excised from ICR mice on day 12 of gestation and cultured in roller bottles for 6 days. Limbs were exposed to 4-hydroperoxycyclophosphamide for the first 20 hours of the culture period. Addition of 10 micrograms/ml of 4-hydroperoxycyclophosphamide to forelimb or to hindlimb buds in culture produced limb reduction malformations. A dramatic decrease in total limb bone area in fore- and hindlimbs was observed with 10 micrograms/ml of 4-hydroperoxycyclophosphamide. In forelimbs, the long bone area decreased and the paw area remained constant so that the relative contribution of the long bone area to total limb bone area was decreased. In hindlimbs treated with 10 micrograms/ml of 4-hydroperoxycyclophosphamide, no paw skeleton was observed. The DNA, RNA, and protein contents of the limbs were not affected by exposure to 1 microgram/ml of 4-hydroperoxycyclophosphamide, but were decreased by exposure to 10 micrograms/ml of this compound. Exposure to the higher concentration of 4-hydroperoxycyclophosphamide also decreased alkaline phosphatase activity, a marker for osteogenesis, in both fore- and hindlimbs; in contrast, neither concentration of 4-hydroperoxycyclophosphamide had an effect on creatine phosphokinase activity, a marker for myogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of 4-hydroperoxycyclophosphamide on limb development in vitro. 243 73

Spermatogenically active testes of rat challenged by 100 mg/kg body weight of p- Chlorophenylalanine for 45 days displayed marked and drastic changes in the seminiferous epithelium. Degenerative changes followed by immense necrosis of germ cells lead to complete breakdown of seminiferous tubules. Leydig cells, however, remained unaffected histologically in the treated animals. Among the accessory sex organs, epididymis alone showed a marked decrease in its weight. A biochemical study in the drug treated rats revealed a significant accumulation of glycogen in the testes accompanied by increase in the activities of enzymes like the succinic dehydrogenase, glucose-6-phosphatase, ATP-ase and acid phosphatases. However, a marked decrease was noticed in the activities of enzymes like alkaline phosphatase, phosphohexose isomerase and lactate dehydrogenase. No significant change was found in the protein, DNA and RNA concentrations in the drug treated testes. The histological and biochemical changes induced in the testes by p-CPA suggest the deleterious effect of the drug on the seminiferous tubules of the testes.
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PMID:Effect of para-chlorophenylalanine on male rats: histopathological and biochemical changes in the testes. 303 Sep 34

The BUN, serum creatinine, creatinine clearance and the urinary excretion of leucine aminopeptidase (LAP), alkaline phosphatase (ALP), beta 2-microglobulin (beta-m), and N-acetyl-beta-glucosaminidase (NAG), were measured in 21 gynecological cancer patients treated with CAPF (CPA + ADM + CDDP + 5-FU) to evaluate the sensitivity of these indices to renal tubular damage. After receiving CDDP almost all patients displayed an increase in excretion of beta-m but no urinary enzyme activities. However, NAG index (NAG activity/urinary creatinine) rose markedly in all patients. We concluded that NAG index is a valuable method in providing sensitive indices for detecting renal tubular damage caused by CDDP.
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PMID:[Comparison of methods for evaluating the nephrotoxicity of cisplatin]. 304 73

Cyclophosphamide (Cy) treatment (150 mg/kg) of Sprague-Dawley rats 48 hr before immunization with a T-dependent antigen, ovalbumin (OVA), resulted in striking bone marrow, blood and tissue eosinophilia, maximal at 14 days and concurrent with profound lymphopenia. This phenomenon has been tentatively attributed to selective elimination by Cy of T-suppressor cells. In this study, T-cell subsets, B cells and monocytes/macrophages were enumerated following alkaline phosphatase-anti-alkaline phosphatase (APAAP) staining of mononuclear cells isolated from lymphoid tissues of rats exhibiting eosinophilia. In lymph nodes, a significant increase in the A3/25+:OX-8+ ratio compared with normal was maintained from Day 7 to Day 14; in the spleen, however, this effect was no longer apparent by Day 14, due to the emergence of a population of OX-8+, OX-19- large granular lymphocytes. A seven-fold rise in splenic B-cell numbers (OX-12+) between Day 7 and Day 14 coincided with the eosinophilia. These findings are consistent with the potentiated production of TH-cell derived soluble factors affecting eosinophil production and differentiation, including possibly a rat equivalent of eosinophil differentiation factor, which in the mouse has been reported to have B-cell growth factor activity linked with eosinophilia.
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PMID:Cyclophosphamide-induced eosinophilia in the rat: concomitant changes in T-cell subsets, B cells and large granular lymphocytes within lymphoid tissues. 349 68

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
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PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

Cyclophosphamide-induced changes in rodent odontogenesis were investigated by light and electron microscopy in four-day-old Sprague Dawley rats given one injection of 40 mg/kg of body weight of cyclophosphamide and killed at intervals of one hour, one day, one week and two weeks. Incisor and molar teeth were dissected from the animals, fixed in 2.0% glutaraldehyde in 0.1 M sodium cacodylate with 3.4% sucrose, and subsequently some were incubated for alkaline phosphatase reaction, and embedded in Spurr's medium for sectioning at light- and electron-microscopic levels. From three days a cell-sparse zone was created in the pulp in the growing end of the tooth and progressive cellular changes were observed which became more severe in the one-week and two-week specimens. Subodontoblast and adjacent pulpal cells were the most affected showing nuclear changes, damage to, or loss of, organelles, and inclusion bodies. Odontogenic epithelium was less affected and odontoblasts appeared to be unaffected by the drug. A new irregular matrix was laid down in the defect area and seemed to be the product of depolarized odontoblasts. This new matrix showed alkaline phosphatase activity, as did the cells embedded in it, and later it became mineralized. It is speculated that the polarity of odontoblasts might be maintained by an intact subodontoblastic layer; when this is lost the odontoblasts become depolarized and capable of secreting matrix from both ends.
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PMID:Cyclophosphamide-induced changes in rodent odontogenesis. A light- and electron-microscopic study. 666 56

Cyclophosphamide induced changes in the ovotestis of the snail Lymnaea acuminata, the vector of the giant liverflukes Fasciola hepatica and Fasciola gigantica were studied in order to explore potential of the drug as a chemosterilant for snails. The drug caused a dose dependent reduction in the levels of DNA, RNA and proteins and the activity of the enzyme alkaline phosphatase. It increased the activity of acid phosphatase and the levels of total free amino acids in the ovotestis. While the animals showed nearly total recovery in RNA and DNA levels 7 days after termination of drug treatment, changes produced in protein, amino acid levels and phosphatase activity did not show any recovery. It appears that cyclophosphamide, while affecting its primary targets i.e. DNA and RNA, irreversibly inhibits protein synthesis through other cellular enzymes as well.
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PMID:Cyclophosphamide as a potential chemosterilant for harmful snails. 733 77

Cyclophosphamide causes lung injury in rats through its ability to generate free radicals with subsequent endothelial and epithelial cell damage. In order to observe the protective effects of a potent anti-inflammatory antioxidant, curcumin (diferuloyl methane) on cyclophosphamide-induced early lung injury, healthy, pathogen free male Wistar rats were exposed to 20 mg/100 g body weight of cyclophosphamide, intraperitoneally as a single injection. Prior to cyclophosphamide intoxication oral administration of curcumin was performed daily for 7 days. At various time intervals (2, 3, 5 and 7 days post insult) serum and lung samples were analyzed for angiotensin converting enzyme, lipid peroxidation, reduced glutathione and ascorbic acid. Bronchoalveolar lavage fluid was analyzed for biochemical constituents. The lavage cells were examined for lipid peroxidation and glutathione content. Excised lungs were analyzed for antioxidant enzyme levels. Biochemical analyses revealed time course increases in lavage fluid total protein, albumin, angiotensin converting enzyme (ACE), lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase, alkaline phosphatase, acid phosphatase, lipid peroxide levels and decreased levels of glutathione (GSH) and ascorbic acid 2, 3, 5 and 7 days after cyclophosphamide intoxication. Increased levels of lipid peroxidation and decreased levels of glutathione and ascorbic acid were seen in serum, lung tissue and lavage cells of cyclophosphamide groups. Serum angiotensin converting enzyme activity increased which coincided with the decrease in lung tissue levels. Activities of antioxidant enzymes were reduced with time in the lungs of cyclophosphamide groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of cyclophosphamide-induced early lung injury by curcumin, an anti-inflammatory antioxidant. 775 45


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