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)

The gamma-glutamyltransferase isoenzymes in the sera of patients with extrahepatic biliary obstruction have been studied, using electrophoretic, gel filtration, and ultracentrifugation techniques, and compared with those present in normal sera. Five isoenzymes were shown to exist in patients' sera, three of which were not demonstrated in normal sera. The observations are discussed in relation to the influence of biliary regurgitation and the possible solubilisation of membrane-bound enzymes. The results are compared with those of previous studies on alkaline phosphatase.
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PMID:Serum gamma-glutamyltransferase isoenzymes in extrahepatic biliary obstruction. 4 51

Earlier studies have identified two main isoenzymes of alkaline phosphatase in the sera of patients with obstructive liver disease. This paper reports on a study of these isoenzymes in specific types of liver disease where the pathology in relation to bile duct obstruction is known. The results have been used to support the theory that in biliary obstruction the increase in serum alkaline phosphatase is in part due to regurgitation of the biliary isoenzymes.
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PMID:An interpretation of the serum alkaline phosphatase isoenzyme patterns in patients with obstructive liver disease. 100 41

Various tissues were extracted with either normal saline or heat inactivated serum (HIS) and the heat stability and electrophoretic migration of the alkaline phosphatase enzymes (AP) of the extracts were compared to the heat stability and electrophoretic properties of serum AP. The electrophoretic pattern of HIS extracts of liver and bone differed from that of saline extracts but the pattern was unaffected if HIS was added to the saline extracts. The heat stabilities of the tissue AP also differed depending on whether they were extracted with saline or HIS. However, serum AP heat stability can help differentiate between liver and bone disease. It is concluded that the comparison of serum and tissue AP heat stabilities or the comparison of serum and tissue AP electrophoretic patterns as criteria for identification of the tissue source of the serum enzyme may be misleading since both these parameters vary, depending on the medium used for extracting the tissue and the extract(s) may contain a mixture of enzymes different from that in serum. It is further concluded from the electrophoretic studies on tissue AP that the increased serum AP in patients with hepatobiliary disease was unlikely to be due to regurgitation of bile but due to increased synthesis and release of alpha 1 and alpha 2 AP isoenzymes from liver, bile ducts or gall bladder. In patients with bone disease the increased serum AP is derived from bone. The source of the serum AP of "normal" subjects may be either liver or vascular tissue or both.
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PMID:Observations on the heat stability and electrophoretic pattern of alkaline phosphatases extracted from various tissues. 112 1

1. Administration of alpha-naphthylisothiocyanate (ANIT) to rats produced dose-dependent increases in plasma bile acid and bilirubin concentrations. Similar increases in plasma bile acid and bilirubin concentrations were evident in bile duct ligated rats, indicating that the severity of cholestasis is almost identical in both models. 2. Plasma alkaline phosphodiesterase I was increased by only 50-80% while alkaline phosphatase was increased more than threefold after ANIT administration. This is in contrast to an earlier study [S. R. Simpson, K. Rahman & D. Billington (1984) Clinical Science 67, 647-652] where, after bile duct ligation, serum alkaline phosphodiesterase I was elevated sixfold before any increase in alkaline phosphatase activity became apparent. Thus, plasma alkaline phosphodiesterase I does not offer as sensitive a marker of intrahepatic cholestasis (induced by ANIT) as it does of extrahepatic cholestasis (induced by bile duct ligation). 3. Hepatic alkaline phosphodiesterase I was unaffected by ANIT pretreatment while hepatic alkaline phosphatase was increased up to seven times. It is suggested that raised plasma alkaline phosphodiesterase I is due to regurgitation of the biliary enzyme rather than overspill of the enzyme from liver into blood. 4. Gel filtration showed that 24 h and 96 h after ANIT administration, rat serum contained a high molecular weight form of alkaline phosphodiesterase I, suggesting a different isoenzyme profile.
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PMID:Plasma alkaline phosphodiesterase I in intrahepatic cholestasis induced by alpha-naphthylisothiocyanate in rats. 284 2

Clinical and experimental studies on congenital dilatation of the bile duct (CDBD) were performed histologically as related to the regurgitation of pancreatic juice into the biliary tract. In all of the 40 patients, resected bile duct showed two characteristic findings such as grandular formation near the epithelial layfer with inflammatory cell infiltration and thickening of the wall occupied with increased collagen fibers. Twenty two of 26 patients (84.6%) who had abdominal pain showed both findings and 11 of 15 cases (73.3%) who had jaundice showed only thickening of the wall (p less than 0.01). Total bilirubin and alkaline phosphatase levels in serum were higher in latter patients and amylase level in bile was higher in the former (p less than 0.05). Grandular formation was shown in all of the 9 patients of which bile duct dilated cylindrically. A canine model in which total pancreatic juice passed via intact common bile duct was made in 10 mongrel dogs. Common bile duct showed cylindrical dilatation and grandular formation with inflammatory cell infiltration histologically. In conclusion, regurgitation of pancreatic juice into the bile duct was thought to take part in grandular formation with inflammatory cell infiltration shown in CDBD.
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PMID:[Histopathological studies on congenital dilatation of the bile duct--with special reference to the regurgitation of pancreatic juice into the bile duct]. 371

Evidence is presented in this paper which supports the hepatogenic theory for the mechanism by which the level of serum alkaline phosphatase is raised in liver disease and provides additional evidence that serum phosphatase is not excreted in the bile. By starch gel and paper electrophoresis the normal serum alkaline phosphatase isoenzyme is shown to be rarely present in hepatic bile. The action of neuraminidase demonstrates that beta-globulin isoenzymes of liver and bone are not identical. From these results a theory which clarifies the rationale of the elevation of alkaline phosphatase in bone and liver disease is postulated. The proposed mechanism may be summarized as follows. The normal serum level is the result of two factors, the rate of release of the enzyme from the tissues, principally liver and bone, and the rate of inactivation of the enzymes in the serum and body protein pool. In osteoblastic bone disease the elevated level is due to the rate of release of the enzyme exceeding the rate of inactivation. The raised level does not indicate an inability of the liver to excrete the enzyme via the biliary tract. In liver disease the increase in serum levels is a result of increased liberation of the enzyme from the sinusoidal surface of the liver cell and of regurgitation of the biliary isoenzyme back into the serum.
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PMID:An interpretation of the elevation of serum alkaline phosphatase in disease. 560 83

Alkaline phosphodiesterase I was present in rat liver at approx. 100-fold greater activity than alkaline phosphatase, and in rat bile at approx. 25-fold greater activity. Rat serum alkaline phosphodiesterase I was increased 6-fold whilst serum alkaline phosphatase was increased only 2-fold 96 h after bile duct ligation. In contrast to alkaline phosphatase, hepatic alkaline phosphodiesterase I was not affected by bile duct ligation, suggesting its raised serum activity was due to bile regurgitation rather than overspill of the enzyme from liver into blood. Gel filtration showed that 8 and 96 h after bile duct ligation the serum contained a high molecular weight form of alkaline phosphodiesterase I. It is suggested that alkaline phosphodiesterase I offers a potentially useful indicator of biliary obstruction in the rat.
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PMID:Serum alkaline phosphodiesterase I in experimental biliary obstruction in the rat. 609 81

Bile duct ligation in rats increased alkaline phosphatase activity in serum and liver. In the serum, the activity reached a peak 24 h after bile duct ligation, earlier than in the liver. This finding indicates that the elevation of serum alkaline phosphatase activity is not due to simple overspill of this enzyme from the liver into the circulation. An electrophoretic study, employing polyacrylamide gel with Triton X-100, and a gel filtration study disclosed that 24 h after bile duct ligation the serum contained a high molecular weight form of alkaline phosphatase in addition to the hepatic and intestinal isoenzymes. The high molecular weight form was also found in bile, indicating that regurgitation of bile contributed to the increase in alkaline phosphatase activity in the serum. The absence of the high molecular weight alkaline phosphatase in the sera of rats with intrahepatic cholestasis induced by alpha-naphthylisothiocyanate suggests that, in this type of cholestasis, regurgitation of bile alkaline phosphatase does not play an important role in the elevation of serum alkaline phosphatase activity. These findings indicate that the high molecular weight alkaline phosphatase in serum is a useful diagnostic marker of biliary obstruction.
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PMID:Mechanism of elevation of serum alkaline phosphatase activity in biliary obstruction: an experimental study. 742 80

To determine whether mitral valve or anular sclerosis or calcification (MC) is associated with reduced survival in patients with end-stage renal disease on continuous ambulatory peritoneal dialysis (CAPD), 53 CAPD patients were followed with echocardiography and Doppler echocardiography over 35 months. Both nonsurvivors and survivors with MC had higher systolic blood pressure before CAPD and calcium-phosphorus products during CAPD treatment than patients without MC (p < 0.05). Serum calcium and phosphorus concentrations, alkaline phosphatase and parathyroid hormone activities were higher in nonsurvivors and survivors with than without MC (p > 0.05). Left ventricular end-diastolic and end-systolic volumes were greater (p < 0.01), ejection fractions were smaller (p < 0.05) in nonsurvivors with than without MC, but not in survivors with versus without MC. Severe MC and grade III mitral valve regurgitation were more frequent in nonsurvivors than in survivors (p < 0.03). No valvular stenoses were found. It is concluded that the development of MC is favored by long-standing predialysis arterial hypertension and by high calcium-phosphorus products during CAPD. Nonsurvivors with MC are characterized by reduced systolic left ventricular function or severe valvular lesions. A close cardionephrologic cooperation is necessary to improve the survival of CAPD patients with these risk factors.
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PMID:Predictive value of mitral and aortic valve sclerosis for survival in end-stage renal disease on continuous ambulatory peritoneal dialysis. 850 38

A gene therapy strategy involving direct myocardial administration of an adenovirus (Ad) vector encoding the vascular endothelial growth factor 121 cDNA (Ad(GV)VEGF121.10) has been shown to be capable of "biological revascularization" of ischemic myocardium in an established porcine model [Mack, C.A. (1998). J. Thorac. Cardiovasc. Surg. 115, 168-177]. The present study evaluates the local and systemic safety of this therapy in this porcine ischemia model and in normal mice. Myocardial ischemia was induced in Yorkshire swine with an ameroid constrictor 21 days prior to vector administration. Ad(GV)VEGF121.10 (10(9) or 10(10) PFU), Ad5 wild type (10(9) PFU), AdNull (control vector with no transgene; 10(9) PFU), saline, or no injection (naive) was administered in 10 sites in the ischemic, circumflex distribution of the myocardium. Toxicity was assessed by survival, serial echocardiography, blood analyses, and myocardial and liver histology at 3 and 28 days after vector administration. All pigs survived to sacrifice, except for one animal in the Ad(GV)VEGF121.10 (10(10) PFU) group, which died as a result of oversedation. Echocardiograms of Ad(GV)VEGF121.10-treated pigs demonstrated no differences in pericardial effusion, mitral valve regurgitation, or regional wall motion compared with control pigs. Intramyocardial administration of Ad(GV)VEGF121.10 included only minimal myocardial inflammation and necrosis, and no hepatic inflammation or necrosis. Only a mild elevation of the white blood cell count was encountered on day 3, which was transient and self-limited in the Ad(GV)VEGF121.10 group as compared with the saline-treated animals. As a measure of inadvertent intravascular administration of vector, normal C57/BL6 mice received intravenous Ad(GV)VEGF121.10 (10(4), 10(6), 5 x 10(7), or 10(9) PFU), AdNull (5 x 10(7) or 10(9) PFU), or saline. Toxicity was assessed by survival, blood analyses, and organ histology at 3 and 7 days after vector administration. A separate group of C57/BL6 mice received intravenous AdmVEGF164 (Ad vector encoding the murine VEGF164 cDNA), Ad(GV)VEGF121.10, AdNull (10(8) PFU each group), or saline to assess duration of expression and safety of a homologous transgene. All mice survived to sacrifice except for 40% of the mice in the highest (10(9) PFU; a dose more than 10(3)-fold higher by body weight than the efficacious dose in pigs) Ad(GV)VEGF121.10 dose group, which died on days 5-6 after vector administration. The only differences seen in the blood analyses between treated and control mice were in the very high Ad(GV)VEGF121.10 dose group (10(9) PFU), which demonstrated an anemia as well as an increase in alkaline phosphatase when compared with all other treatment groups. Hepatic VEGF levels by ELISA in AdmVEGF164-treated mice did not persist beyond 14 days after vector administration, suggesting that persistent expression of a homologous VEGF gene transferred with an Ad vector is not a significant safety risk. Although this is not a chronic toxicity study, these data demonstrate the safety of direct myocardial administration of Ad(GV)VEGF121.10, and support the potential use of this strategy to treat human myocardial ischemia.
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PMID:Safety of direct myocardial administration of an adenovirus vector encoding vascular endothelial growth factor 121. 1036 64


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