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:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cathepsin D, acid phosphatase, beta-galactosidase, N-acetyl hexosaminidase, leucine aminopeptidase (LAP), lactate dehydrogenase, glucose-6-phosphate dehydrogenase (g-6-PDH), and peroxidase activities were measured in the buccal mucosa of rats kept for 60 days on high-sucrose (68% of sucrose) caries-inducing diet. The findings evidence that this diet observed for 30 days results in a significant elevation of beta-galactosidase and LAP activities and in reduction of peroxidase level. After 60-day diet the examined parameters virtually did not differ from the reference characteristics (a control group kept on 68% starch diet), except elevated g-6-PDH and lowered peroxidase activities. Enzymic activity changes are adaptive and evidence changes in the metabolic processes in the buccal mucosa, that may eventuate in the development of periodontal diseases.
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PMID:[The effect of a high-saccharose diet on the enzymatic activity of the oral mucosa in rats]. 192 95

Within the uterine glands, the following enzymes were demonstrated by histochemical methods after 30, 58, 80, 100, and 110 d of pregnancy, respectively: beta-N-acetyl-hexosaminidase, beta-galactosidase, beta-glucuronidase, alpha-mannosidase, acid phosphatase, alkaline phosphatase, esterases, cytochrome oxidase, 5-nucleotidase, leucine aminopeptidase, adenosine triphosphatase, diaphorases (NADH, NADPH), glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, succinate dehydrogenase, isocitrate dehydrogenase (NAD, NADP), beta-hydroxybutyrate dehydrogenase, glycero-3-phosphate dehydrogenase, NAD-glycero-3-phosphate dehydrogenase, glutamate dehydrogenase (NAD, NADP), lactate dehydrogenase. The results show that the activities of G-6-PDH, 6-PGDH, and cytochrome oxidase increase within secreting cells during the 2nd half of pregnancy. The activities of the other enzymes remained almost unchanged during the period of investigation. The description of our results distinguishes between gland neck, middle, and distal part of the secretory unit, respectively. In general, the enzyme activities are similar within the middle and distal gland segments, but lower in the epithelia of the neck region. The activity of dehydrogenases was medium to intensive within the middle and distal gland segments, but only low to medium within the neck portion. Of the hydrolases, the acid phosphatase, ATPase, leucine aminopeptidase, and beta-galactosidase demonstrated an intensive activity within activity secreting cells. The enzyme activities of the gland epithelia are compared with these of the uterine surface epithelia and the histochemical results are discussed in context with their significance in histiotrophic nutrition.
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PMID:[Enzyme histochemistry of the pig placenta. III. Histotopics of enzymes in the uterine epithelium]. 309 49

We suggest that polymyalgia rheumatica with giant cell arteritis (PR-GCA) is an arachidonic acid metabolites mediated disease which can be diagnosed more accurately and monitored more precisely for therapeutic benefits by the serial determinations of the major urinary prostaglandin F, serum urinary lysozymes, serum acid phosphatase, and serum angiotensin converting enzyme rather than by the erythrocyte sedimentation rate, and, when necessary by temporal artery biopsy. The pathogenetic role proposed for prostaglandins (PG) and, even more precisely perhaps, the leukotrienes in this disease is consistent with the several published clinical observations that non-steroidal anti-inflammatory drug treatment produces in some cases a therapeutic paradox of symptomatic relief with concurrent, if clinically silent, progression of the arteritis, even to blindness. Furthermore, the impressive response of PR-GCA to low maintenance dose steroid therapy, a clinical conundrum for decades, is rationally explained on the basis of depressed or obstructed PG metabolism early on in the metabolic cascade. These views warrant clinical evaluation, confirmation or correction in whole or in part, and may increase our understanding of PR-GCA.
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PMID:Polymyalgia rheumatica and giant cell arteritis--rational diagnosis and treatment predicated and disordered prostaglandin metabolism. 627 May 20

Monocytes purified with cell scatter monitored counterflow centrifugation were cultured in plastic (adherent) and in teflon culture bags (suspension). Sequential changes were monitored during 15 days by measuring intracellular activity of three enzymes of intermediary metabolism: glucose-6-phosphate dehydrogenase (G-6-PDH), phosphohexose isomerase (PHI) and isocitrate dehydrogenase (ICDH), and the two acid hydrolases: acid phosphatase (ACP) and N-acetyl-beta-glucosaminidase (NAG). In teflon grown macrophages a significantly lower G-6-PDH activity was seen after 15 days in comparison to plastic adherent macrophages (P less than 0.0002). For the other enzymes similar values for both culture modalities were found. The significantly, cycloheximide insensitive, higher values for G-6-PDH, PHI and ICDH in 2 h plastic adherent monocytes in comparison with plastic non-adherent monocytes, suggest a relationship between adherent capacity and the level of intermediary metabolism. The overall yield of plastic adherent macrophages after 15 days was 35% in contrast with 89% for the in suspension cultured macrophages. This corroborates the existence of adherent and non-adherent monocytes, both capable of differentiation in vitro. In 14 patients with advanced Hodgkin's disease (HD) and 14 normal controls, monocyte differentiation was studied applying both culture modalities. The enzyme levels, reflecting growth and intermediary metabolism, were similar for both groups. The adherent capacity and yield, both in teflon and in plastic, after 15 days was comparable for both groups. It was concluded that in vitro monocyte differentiation in the presence of autologous serum was qualitatively and quantitatively normal in advanced HD; this is in favour of an intrinsically normal function of monocytes in HD.
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PMID:Characterization of monocyte maturation in adherent and suspension cultures and its application to study monocyte differentiation in Hodgkin's disease. 636 Apr 44

In porcine interareolar placental epithelia, the following enzymes were demonstrated by histochemical methods after 30, 58, 80, 100, and 110 d of pregnancy, respectively: beta-N-acetylhexosaminidase, beta-galactosidase, beta-glucuronidase, alpha-mannosidase, acid phosphatase, alkaline phosphatase, nonspecific esterases, cytochrome oxidase, 5-nucleotidase, leucine aminopeptidase, adenosine triphosphatase, diaphorases (NADH, NADPH), glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, succinate dehydrogenase, isocitrate dehydrogenase (NAD, NADP), beta-hydroxybutyrate dehydrogenase, glycero-3-phosphate dehydrogenase, NAD-glycero-3-phosphate dehydrogenase, glutamate dehydrogenase (NAD, NADP), lactate dehydrogenase. The results show that most of the enzyme activities remained almost unchanged during the period of investigation. Only G-6-PDH and 6-PGDH activities increased within the uterine epithelium and nonspecific esterase activity within uterine as well as chorionic epithelia during the 2nd half of pregnancy. Within chorionic and uterine epithelia, hydrolases but not dehydrogenases demonstrated a higher activity at the bases of chorionic villi as compared to the apices and flanks of the latter. The action and influence of the demonstrated enzymes on metabolism, energy transfer, secretory, and resorptive activities of chorionic and uterine epithelia are discussed.
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PMID:[Enzyme histochemical studies of the swine placenta. Histoptics of enzymes in interareolar placental epithelia]. 643 35

The gastric mucosa of marmosets is devoid of UDPG-GT; phosphorylases; G-6-PA; F-1,6-PA; alanyl aminopeptidase and leucine aminopeptidase. Only the acid phosphatase was seen with a stronger reactivity in the chief cells. The other enzymes (LDH; G-6-PDH; 6-PGDH; NADPH2-TR; cis-aconitase; ICDH; SDH; MDH; cytochrome oxidase; NADH2-TR; a-GPDH; b-OHBDH and nonspecific esterase) showed a stronger reactivity in the parietal cells.
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PMID:[Histoenzymologic data on the epithelial cells of the gastric mucosa of marmosets (Callithrix jacchus & Callithrix penicillata)]. 677 86

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

The antiinflammatory, antioxidant activity of taurine and niacin against cyclophosphamide-induced early lung injury in rats was investigated. A single intraperitoneal injection of cyclophosphamide markedly altered the levels of several biomarkers in bronchoalveolar lavage fluid: total protein, albumin, angiotensin converting enzyme, lactate dehydrogenase, lactate, N-acetyl-beta-D-glucosaminidase, alkaline phosphatase, acid phosphatase and lipid peroxidation product were significantly elevated. In contrast, decreased levels of total reduced glutathione (GSH) and ascorbic acid were observed. Cyclophosphamide significantly increased malondialdehyde levels in serum and lung. Significant increases in lung content of lipid hydroperoxides were seen that paralleled the decreased levels of total reduced glutathione and total sulfhydryl groups. Pretreatment of rats with daily intraperitoneal injection of taurine plus niacin 7 days prior to and 2 days after cyclophosphamide insult significantly inhibited the development of lung injury, prevented the alterations in lavage fluid biomarkers associated with inflammatory reactions, with less lipid peroxidation and restoration of antioxidants. In conclusion, our results suggest that taurine and niacin in combination is efficient in blunting cyclophosphamide-induced pulmonary damage.
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PMID:In vivo administration of taurine and niacin modulate cyclophosphamide-induced lung injury. 786 92

In the course of a long-term L-DOPA administration (14 days) and 2 weeks after its cessation the activities of some protein enzymes (aminopeptidase, acid phosphatase), neuromediator (MAO, ACE) and oxidative (glutamate dehydrogenase, glucose-6-phosphate dehydrogenase) metabolism were studied by quantitative cytochemical methods in brain motor structures (sensorimotor cortex, caudate nucleus) and in structures not directly related to motor functions (hippocampus) of rats with high and low motor activity. After L-DOPA (madapar) cessation significant changes were revealed in the formation of motor system of the brain, primarily in the group of rats with low motor activity. It is suggested that a decrease in MAO activity after madapar cessation may be responsible for dyskinesia arising after cessation of L-DOPA preparations treatment.
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PMID:[Pathochemical changes in the motor structures of the brain under the influence of the administration of L-DOPA preparations and their withdrawal (experimental research)]. 790 Apr 46

The present investigation evaluated the changes in bronchoalveolar lavage fluid (BALF) biochemical constituents and indices of bronchoalveolar lavage cell functions to detect early lung injury in rats following intraperitoneal administration of cyclophosphamide (CP). Rats were exposed to a single intraperitoneal injection of CP (200 or 300 mg/kg body weight). Experimental and control rats were sacrificed at various time intervals (2, 3, 5, 7, 11, 21, and 42 days after cessation of exposure), and lung lavage was performed to examine several markers of lung injury. Biochemical analyses revealed dose-related increases in BALF angiotensin converting enzyme activity, total protein, lactate, lactate dehydrogenase, and N-acetyl-beta-D-glucosaminidase (NAG) levels on days 2, 3, 5, 7, and dose-related increases in albumin, alkaline phosphatase, acid phosphatase, and lipid peroxidation on days 2, 3, 5, 7, and 11 after CP treatment. In contrast, reduced levels of ascorbic acid and glutathione (GSH) content were observed in lung lavage fluid. We also examined bronchoalveolar lavage cells for acid hydrolases (acid phosphatase, beta-glucuronidase, NAG) and GSH content. Activity of acid hydrolases was slightly elevated on day 2 and peaked on days 3, 5, and 7. However, lavage cell GSH content was decreased. Thus, measurements of pulmonary changes by analyzing lavage fluid and lavage cell functions seems to be a useful marker for assessing the early onset and development of CP-induced lung injury.
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PMID:Cyclophosphamide induced early biochemical changes in lung lavage fluid and alterations in lavage cell function. 820 29


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