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)

D-Galactosamine (800 mg/kg, intraperitoneally) caused significant decrease in the activities of 5'-nucleotidase, glucose-6-phosphatase and cytochrome P450 and increase in activities of gamma-glutamyl transpeptidase, succinate dehydrogenase, acid phosphatase and acid ribonuclease in liver after 24 hr. The levels of RNA, protein and glycogen decreased while total lipids, phospholipids, cholesterol and lipid peroxides increased. It also increased the serum levels of transaminases, alkaline phosphatase and bilirubin while protein concentration decreased significantly. Oral administration of Picroliv (12 mg/kg/day for 7 days), a standardised iridoid glycoside fraction of Picrorhiza kurroa, significantly prevented the biochemical changes in liver and serum of galactosamine-toxicated rats. Kutkoside (12 mg/kg/day for 7 days) also protected against changes in most of the hepatic and serum constituents studied. Another iridoid glycoside from Picroliv, Picroside I, at the same dose level could only prevent toxicant-induced changes in acid phosphatase, phospholipids and lipid peroxides in liver and alkaline phosphatase in serum. Mixture of Picroside I and Kutkoside in the ratio of 1:1.5 at 12 mg/kg dose elicited lesser response than Picroliv.
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PMID:Picroliv and its components kutkoside and picroside I protect liver against galactosamine-induced damage in rats. 133 78

The present study examined the preventive effects of green tea extract on D-galactosamine (GalN)-induced hepatic injury in rats, an animal model of viral hepatitis. A single i.p.-injection of GalN (700 mg/kg) to male Wistar rats caused fulminant hepatitis by 48 hr as assessed by marked increases in the serum aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and alkaline phosphatase (ALP) activities; decreases in the serum protein and cholesterol levels and the amount of liver microsome P-450; and marked changes in organ weights. The lecithin: cholesterol acyltransferase (LCAT) activity markedly increased at 8 hr and markedly decreased at 24 hr after the GalN injection. In the experiment, animals were orally administered green tea extract at doses of 50, 100 or 200 mg/kg five times each before and after the GalN injection. Treatment with green tea extract significantly prevented the increases in the GOT, GPT and ALP activities in a dose-related manner. It also significantly prevented the decreases in serum albumin and total cholesterol, although not in a dose-related manner. A tendency to prevent the increase in LCAT activity and the decrease in liver microsome P-450 was also noted. Little effect was found on the other abnormal changes in the serum lipids and proteins and the organ weights. These results suggest that green tea may have an ameliorating effect on hepatic dysfunction.
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PMID:[Effects of green tea extract on galactosamine-induced hepatic injury in rats]. 146 98

N-(2-Hydroxypropyl)methacrylamide (HPMA) copolymers containing doxorubicin (DOX) and galactosamine can be targeted to the hepatocyte galactose receptor for organ-specific chemotherapy of primary and metastatic liver cancer. Here we report the dose-dependent pharmacokinetics of this macromolecular conjugate. Following intravenous administration to mice most efficient liver targeting was seen at low dose (0.05 mg DOX kg-1), with receptor saturation observed using higher bolus doses. Repeated low dose bolus injections did not cause down-regulation of the galactose receptor and targeted drug delivery rates of greater than or equal to 2 micrograms DOX g-1 liver h-1 were achieved. DOX is released from such conjugates intracellularly via action of lysosomal proteinases. It was shown that isolated rat liver lysosomal enzymes (Tritosomes) can release unmodified DOX from the peptidyl side chain Gly-Phe-Leu-Gly at a rate greater than or equal to 3 micrograms DOX g-1 liver h-1 i.e. the hydrolytic capacity is greater than the observed rate of drug delivery to the liver lysosomes in vivo. Although most conjugate would be captured by normal hepatocytes following intravenous administration, it was shown that the human hepatoma cell line HepG2 retains the galactose receptor, accumulating and processing the conjugate efficiently. Potential dose limiting toxicities of such drug conjugates could include cardio- or hepatotoxicity. Administration of conjugate reduced the 15 min heart level of DOX approximately 100-fold compared with that observed for an equivalent dose of free drug. Preliminary experiments showed that plasma levels of alkaline phosphatase, alanine transaminase and asparate transaminase did not change following administration of HPMA copolymer-daunorubicin (DNR) (10 mg DNR kg-1) indicating no significant heptatoxicity.
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PMID:N-(2-hydroxypropyl)methacrylamide copolymers targeted to the hepatocyte galactose-receptor: pharmacokinetics in DBA2 mice. 164 46

Lead markedly augments the lethality of endotoxin lipopolysaccharide (LPS) in rats. In this model of LPS toxicity, the liver is severely injured. Much of the tissue injury produced by LPS is thought to be mediated by the cytokine tumor necrosis factor (TNF). Tumor necrosis factor recently has been speculated to be a mediator of several models of liver injury such as that produced by galactosamine. To investigate the possible role of TNF in the lead-enhanced LPS toxicity model, we administered doses of lead acetate (15 mg/kg), LPS (100 micrograms/kg), or TNF (6.25 x 10(6) U/kg) that produced minimal changes in liver enzymes. However, when lead was administered simultaneously with either LPS or TNF, serum aspartate transaminase, alanine transaminase, alkaline phosphatase, glutamyl transpeptidase, and plasma triglyceride levels were markedly increased. Lead + LPS treatment increased both peak serum TNF concentrations and TNF "area under the curve" as compared with LPS alone. We conclude that lead not only enhances LPS lethality but also LPS liver injury. Furthermore, lead enhances TNF liver injury and increases LPS-stimulated serum TNF levels. These data suggest that the lead-enhanced LPS model offers a system for studying TNF-induced liver injury.
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PMID:Lead enhances lipopolysaccharide and tumor necrosis factor liver injury. 167 39

The changes in the activity and the localization of alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP) and alpha-fetoprotein (AFP) were examined during cell regeneration in the galactosamine-injured rat liver. D-galactosamine was injected i.p. into rats at a single dose level of 400 mg/kg. The biochemical activities of ALP and gamma-GTP in rat liver homogenate increased significantly in comparison with those in the control rats 3 days and 4 days after administration of D-galactosamine. In the histochemical analysis, 3 days, 4 days and 5 days after the administration of the amino sugar, a high level of activity of both ALP and gamma-GTP was seen along the cell borders between adjacent hepatocytes. AFP was detected by the enzyme-labeled antibody technique in the cytoplasm of a few small hepatocytes around Glisson's sheath and epithelial cells of small tubules within Glisson's sheath which show morphological features similar to bile duct 3 days, 4 days and 5 days after the administration of the amino sugar. AFP was detected in serum by the western blotting method 3 days and 4 days after the administration of D-galactosamine, whereas serum albumin decreased significantly in the same period. In this study, it was shown that ALP, gamma-GTP and AFP were proper markers to justify the degree of the differentiation of hepatocytes during the state of proliferation.
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PMID:Histochemical and immunohistochemical study on the expression of alkaline phosphatase, gamma-glutamyl transpeptidase and alpha-fetoprotein during the process of rat hepatocyte proliferation. 171 Jun 83

Hepatoprotective effect of andrographolide (the major active diterpenoid lactone of the plant Andrographis paniculata) was studied on acute hepatitis induced in rats by single dose of galactosamine (800 mg/kg, ip)/paracetamol (3g/kg, po). Hepatoprotective activity was monitored by estimating the serum transaminases (GOT and GPT), alkaline phosphatase and bilirubin in serum, hepatic triglycerides, and by histopathological changes in the livers of experimental rats. Pre-treatment and/or post-treatment of rats at different time intervals with different doses of andrographolide in the two experimental models of hepatotoxicity showed that treatment of rats with 400 mg/kg, ip or 800 mg/kg, po, 48, 24 and 2 h before galactosamine administration or with 200 mg/kg, ip, 1, 4 and 7 h after paracetamol challenge leads to complete normalisation of toxin-induced increase in the levels of all the five biochemical parameters, and significantly ameliorates toxin-induced histopathological changes in the livers of experimental rats. The results confirmed the in vivo hepatoprotective effect of andrographolide against galactosamine or paracetamol-induced hepatotoxicity in rats. Since the protective effect of andrographolide was observed in two types of intoxication, which are very different in their primary mechanism of inducing hepatotoxicity, it is suggested that protective mechanisms of andrographolide which are not specific to galactosamine or paracetamol toxicity may be responsible for the hepatoprotective activity of the compound.
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PMID:Hepatoprotective activity of andrographolide against galactosamine & paracetamol intoxication in rats. 222 75

The hepatoprotective effect of colchicine in a model of liver intoxication with galactosamine (GalN), 375 mg/kg, i.p., was studied in rats. At 0.5, 1, 3, 6, 18 and 24 h after GalN intoxication the following markers of liver damage were measured: serum activity of alanine aminotransferase, alkaline phosphatase, gamma-glutamyltranspeptidase, hepatic calcium and glycogen contents, liver lipoperoxidation, and liver plasma membrane activity of alkaline phosphatase, gamma-glutamyltranspeptidase and high-affinity Ca2+-ATPase. 24 h after GalN intoxication increases in serum levels of alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase were observed along with decreases in plasma membrane activities of alkaline phosphatase, gamma-glutamyltranspeptidase, and high-affinity Ca2+-ATPase. A sharp increase of lipoperoxidative processes measured as malondialdehyde production was also observed. Pretreatment of rats with colchicine 10 micrograms/rat/day p.o. for 7 days before GalN injection prevented partially the toxic effects of GalN. When a dose of 50 micrograms/rat/day for 7 days was given the drug prevented almost completely the damage induced by galactosamine, with the exception of glycogen and serum alkaline phosphatase that remained different from controls. Time-course experiments showed that malondialdehyde formation increased 30 min after intoxication while all other changes became apparent from 6 h after treatment, suggesting that lipoperoxidation may be a prerequisite for galactosamine-induced damage. The protection offered by colchicine was related to its capacity to inhibit lipoperoxidation. Histochemical findings paralleled the biochemical results. The possible role of lipoperoxidation in galactosamine-induced liver damage is discussed.
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PMID:Colchicine prevents D-galactosamine-induced hepatitis. 256 25

The activity of dipeptidyl aminopeptidase IV was studied in the sera of 378 hospitalized patients. The mean activity of dipeptidyl aminopeptidase IV was elevated significantly in patients with neoplasmata and hepatitis, but not in patients with liver cirrhosis. Significant correlations (p less than 0.001) existed with gamma-glutamyl transferase, glutamate dehydrogenase, alkaline phosphatase and leucine aminopeptidase. A significant correlation with lactate dehydrogenase existed only in patients with neoplasmata. Principal component analysis, performed with aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, leucine aminopeptidase, lactate dehydrogenase and dipeptidyl aminopeptidase IV, revealed correlations between the activities of aspartate aminotransferase and alanine aminotransferase, and between alkaline phosphatase and leucine aminopeptidase, but neither dipeptidyl aminopeptidase IV nor lactate dehydrogenase showed any correlation with either of these two groups. In lectin affinity chromatography with concanavalin A and wheat germ lectin sepharose, serum dipeptidyl aminopeptidase IV from liver cirrhosis patients showed the same binding pattern as that from healthy subjects. The activity and glycosylation of dipeptidyl aminopeptidase IV in serum and hepatic plasma membranes was investigated in rats, following the induction of hepatitis with galactosamine. In the serum, dipeptidyl aminopeptidase IV activity was elevated as early as 6 h after galactosamine injection, and the elevated activity persisted until the 7th day. At the same time dipeptidyl aminopeptidase IV activity was also elevated in the hepatic plasma membrane. Ninety eight percent of hepatic dipeptidyl aminopeptidase IV bound to concanavalin A as well as to wheat germ lectin and this value was unchanged during hepatitis. In the serum of control rats, 90% of dipeptidyl aminopeptidase IV bound to concanavalin A but only 39% to wheat germ lectin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dipeptidyl aminopeptidase IV in hospitalized patients and in galactosamine hepatitis of the rat: Activity and lectin affinity chromatography in serum and hepatic plasma membranes]. 257 17

This study was aimed to examine whether disulfiram (DS) may exacerbate the pre-existing liver damage induced by D-galactosamine (GalN) in rats. DS, 600 mg/kg, administered by gavage for 3 days caused an increase in asparagine aminotransferase (AspAT) and alkaline phosphatase (AP) and a decrease in cholinesterase (ChE) activity in the serum and decrease in AspAT and ChE activity in the liver. DS given to rats with GAlN-induced liver injury caused significant increase in alanine aminotransferase (A1AT) and bilirubin level in serum in comparison with rats with GalN-damaged liver but without DS treatment. In summary, DS exacerbates a damage of the liver of rats. This study supported the clinical observations showing enhanced liver damage in alcoholics treated with DS.
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PMID:Effect of disulfiram on function of the liver of rats with galactosamine-induced hepatitis. 309 1

Experimental liver injury was provoked in test rats with intraperitoneal injections of D-galactosamine. Traumatized rats received further intraperitoneal injections of Hepasor, a protoberberine alkaloid mixture from Enantia chlorantha (Annonaceae). Biochemical assays from blood plasma, serum alanine transferase, serum alkaline phosphatase, serum creatinine, serum hydroxyproline and serum calcium were done and liver and kidney samples for histological processing were taken. The biochemical results obtained indicate a marked influence by Hepasor on the serum alanine transferase activities and serum hydroxyproline values in female rats, but more accidental ones in male rats. A reduction in serum alkaline phosphatase activity and the serum creatinine values was also found, being also dependent on sex. The histological findings in the liver sections of female rats show that 1 week Hepasor therapy greatly furthers the healing process in a D-galactosamine-pretraumatized liver, eliminating megalocytosis, contraction of chromatines and other disorders in the cell architecture. The inhibitory effect of Hepasor on proceeded traumatization caused by D-galactosamine was nearly complete.
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PMID:Regeneration of D-galactosamine-traumatized rat liver with natural protoberberine alkaloids from Enantia chlorantha. 341 61


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