Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pretreatment of rats with colchicine (10 micrograms/day) for 7 days protected against CCl4-induced acute liver damage. CCl4 intoxication was demonstrated histologically and by increased serum activities of glutamic-pyruvic transaminase, alkaline phosphatase and gamma-glutamyl transpeptidase. Furthermore, an increase in liver lipid peroxidation and a decrease in plasma membrane gamma-glutamyl transpeptidase activity were found. Colchicine increased the LD50 of CCl4 2.5-fold and prevented the release of intracellular enzymes, as well as the decrease in gamma-glutamyl transpeptidase activity in the plasma membrane. It also completely prevented the lipid peroxidation produced by CCl4 and limited the extent of the histological changes. Our results suggest that the protective effect of colchicine may be mediated through its action on an early toxic event, because treatment of the animals with colchicine produced a significant decrease in CCl4-induced lipid peroxidation.
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PMID:Protective effect of colchicine on acute liver damage induced by carbon tetrachloride. 339 83

Male Baladi rabbits were acutely and sub-chronically intoxicated with cyanofenphos and profenophos. The levels of cholesterol, triglycerides, B-lipoproteins and total proteins were determined in the serum, brain, spinal cord and sciatic nerve of rabbits. Moreover, the activities of alkaline phosphatase, acid phosphatase and glutamic-pyruvic transaminase were determined in the liver of the animals. The whole studies revealed that the biochemical constituents were highly affected by the tested insecticides. Also, the liver function suffered from adverse effects of the tested insecticides.
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PMID:Effects of two organophosphorus insecticides on some biochemical constituents in the nervous system and liver of rabbits. 358 39

The in vivo-in vitro DNA repair and DNA replication assay in mouse hepatocytes has promise as a short-term test for detecting potential mouse liver carcinogens. In addition, this assay may provide information on the mode of action of known hepatic carcinogens. The induction of DNA repair is clearly a response to hepatic DNA damage. However, it is unclear whether induction of replicative DNA synthesis (S phase) represents regenerative hyperplasia in response to hepatotoxicity or is a result of direct mitogenic stimulation of the hepatocytes by the test compound. The objective of the present study was to examine the relationship between hepatotoxicity, which was assessed by measuring serum concentrations of glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), alkaline phosphatase (AP), and gammaglutamyl transferase (GGT), and induction of S phase following either single or multiple doses of the model mouse hepatocarcinogen carbon tetrachloride (CCl4). Under the experimental conditions in this study, CCl4 elevated SGPT and SGOT but did not affect serum concentrations of AP or GGT. CCl4 did not induce DNA repair. An increase in the percentage of hepatocytes in S phase followed the appearance of elevated SGOT and SGPT in all single-dose studies. The results from the multiple-dose studies showed a similar relationship except that with 20 mg/kg X d the concentrations of SGOT and SGPT decayed to control values after 14 d of dosing whereas the percentage of hepatocytes in S phase remained markedly elevated (greater than 10 X control). The daily dose of CCl4 that gave a no-observed-effect level for induction of S phase was lower with multiple administrations than it was following a single exposure. A single administration of CCl4 at 25 mg/kg did not increase S phase, SGOT, or SGPT, but if 20 mg/kg X d was given for 7 d the number of hepatocytes in S phase and the concentrations of SGOT and SGPT increased more than 10-fold. These data support the hypothesis that induction of replicative DNA synthesis in the mouse liver following CCl4 administration is related to hepatotoxicity. In single-dose studies elevation in S phase was always associated with elevation of SGOT and SGPT. However, in the multidose studies, SGOT and SGPT declined after 14 d of administering 20 mg/kg X d while S phase remained elevated.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relationship between hepatotoxicity and induction of replicative DNA synthesis following single or multiple doses of carbon tetrachloride. 361 36

Removal of the corpora allata from the emerging female adults of L. grandis caused a rapid and significant increase in the contents of total carbohydrate, glycogen, total lipids, cholesterol, total proteins and RNA in the fat body, and a significant drop in the contents of trehalose free fatty acids (FFA), phospholipids, free amino acids (FAA) and also in the activity of acid and alkaline phosphatase, glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and exterase in the fat body, in comparison with the sham-operated controls. Treatment with juvenile hormone analogue (JHa) of the allatectomized insects significantly reverses the effects produced by allatectomy (P less than or equal to 0.01). Similarly, removal of the brain produced similar responses in the fat-body but with some exceptions such as the decrease of total protein and RNA and increase significant of FAA as compared to the sham-operated controls. Simultaneous removal of corpora-allata and brain produces a rapid increase in the contents of total carbohydrate, glycogen, total lipid, cholesterol, FAA and the activity of acid phosphatase in comparison with all other treatments performed in this study, while the contents of trehalose, phospholipid, FFA, total protein, RNA and the activity of GOT, GPT, general esterase and alkaline phosphatase in the fat-body decreased compared to all other treatments. The results obtained are discussed in relation to the neuro-endocrine control of metabolism in insects.
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PMID:Role of corpora-allata and brain of adult female Lohita grandis gray. 370 75

When rats were exposed to 50 ppm NO2 gas for 36 h, remarkable changes in some biochemical levels compared with those of control rats were observed. Namely, levels of total cholesterol, ester cholesterol, total lipids, triglycerides, nitrogen of urea, uric acid, glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and cytochrome P-450 of the exposed rats were decidedly different from those of the control rats. Thus, it was suggested that functions of liver are acutely injured upon exposure to 50 ppm NO2 gas, although extensive pulmonary injury resulting from such an exposure may also be responsible for some of the abnormal serum values.
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PMID:Effects of 50 ppm NO2 gas exposure on physiological functions of rats. 373 29

A model for hepatic arterial chemotherapy studies using large dogs and an implantable infusion pump has been developed. Using this technique near complete perfusion (greater than 90%) of the liver can be achieved in vivo as determined by hepatic arterial perfusion scintigraphy with technitium 99m macroaggregated albumin. The system is reliable and has been in use for a total of 1353 days (mean of 104 days, range 52-239) in 13 dogs. Pump implantation causes no apparent acute liver damage based on pre- and post-operative alkaline phosphatase and serum glutamic-pyruvic transaminase determinations and does not affect the general mobility or behavior of the animals. Careful placement of the catheter and attention to the physicochemical properties of the solutions loaded are factors contributing to the success of the model. The model permits comprehensive preclinical pharmacokinetic and toxicologic studies of new or preexistent chemotherapeutic agents in the same device that will be used for later administration in human subjects. By providing the means to examine and develop new treatment modalities, it enables the design of even more potent cytotoxic therapy directed into the tumor vascular bed.
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PMID:A dog model using an implanted system for protracted hepatic arterial chemotherapy. 377 8

A male born to first cousins presented at 12 months with hypocalcemic convulsions, rickets, epistaxis due to vitamin K deficiency, and extremely low serum levels of beta-carotene and vitamin A. Liver function was altered moderately (glutamic-oxaloacetic transaminase, 55 U/L; glutamic-pyruvic transaminase, 37 U/L; lactate dehydrogenase, 255 U/L; alkaline phosphatase, 437 U/L). To correct the deficiencies, 8,000 IU vitamin D/day, 10,000 IU vitamin A/day, and intramuscular administration of vitamin K1 were required. At 9 years, he presented signs of neuromuscular affection, and the serum vitamin E level (measured for the first time) was extremely low. Classic lipid malabsorption syndromes (abetalipoproteinemia, chronic cholestasis, mucoviscidosis, coeliac disease, Whipple's disease) were excluded by appropriate examinations. Composition of duodenal bile acids was characterized by undetectable levels of cholic acid metabolites, and only chenodeoxycholic acid metabolites were present. Serum total bile acid concentration was normal, with an atypical low cholic acid/chenodeoxycholic acid ratio and abnormal presence of 3 beta-OH-delta 5-cholenic acid and 6-OH-bile acids. Urinary bile acid composition was also characterized by elevated 6-OH-bile acids. Known enzymopathies of the bile acid synthetic pathway were excluded (cerebrotendinous xanthomatosis, cerebro-hepato-renal syndrome of Zellweger, coprostanic acidemia). Bile acid pool sizes were determined by using stable isotopes: cholic acid pool size [2.90 (N, 32 +/- 16) microM/kg] and chenodeoxycholic acid pool size [10.8 (N, 32.6 +/- 9.9) microM/kg] were extremely low; fractional turnover rates of both bile acids were in a normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malabsorption of liposoluble vitamins in a child with bile acid deficiency. 379 31

To explore a possible relationship between metabolism and lethality, the acute toxicity of naturally occurring perilla ketone (PK), 1-(3-furyl)-4-methyl-pentan-1-one, was examined in the uninduced mouse, hamster, rabbit, dog and pig. The LD50 (+/- SE), determined using intraperitoneal (ip) injection, for the mouse and hamster were low at 5.0 +/- .3 and 13.7 +/- .9 mg/kg, respectively. The rabbit died from an ip dosage of near 14 mg/kg and estimated ip LD50 dosages were quite high for the dog and pig, being 106 +/- 25 mg/kg and over 158 mg/kg, respectively. Dogs and the pig that died from ip injections of PK displayed varying degrees of midzonal and centrilobular liver damage and dogs also had elevated serum alkaline phosphatase and glutamic-pyruvic transaminase activities. In contrast, rodents and rabbits display only pulmonary toxicity from this agent. Cytochromes P-450 and b5 concentrations and NADPH-cytochrome c reductase activity were determined for the lung, liver and kidney of mice, hamsters, rabbits, dogs, swine, sheep and cattle. High correlation between lethality and enzyme concentration further supports the hypothesis that enzymatic bioactivation of PK is required for toxicity in all species.
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PMID:Species susceptibility to the pulmonary toxicity of 3-furyl isoamyl ketone (perilla ketone): in vivo support for involvement of the lung monooxygenase system. 397 46

The pesticide dichlorvos inhibits not only cholinesterase but also alkaline phosphatase, lactate dehydrogenase and glutamate dehydrogenase competitively. A mixed type inhibition of glutamic-oxaloacetic transaminase is in contrast to the increased activity of glutamic-pyruvic transaminase after dichlorvos application. The activity of leucine aminopeptidase is not affected by the substance. After administering rats an acutely toxic dose of dichlorvos (70 mg per kg b.w.) in vitro-inhibitions other than that of cholinesterase could not be found.
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PMID:Enzyme activities after in vitro and in vivo application of dichlorvos. 400 35

A retrospective study on 50 young and 35 aged patients with acute hepatitis B was performed. Clinical and laboratory parameters were evaluated. The most significant results obtained in the aged group when compared with the young were longer hospitalization, less elevated serum glutamic-pyruvic transaminase, serum bilirubin and alkaline phosphatase significantly higher, lower IgM and higher IgA levels. The results indicate that acute hepatitis B in elderly adults is characterized by a milder liver cell necrosis and a hypercholestatic pattern. The possible causes for these features are discussed.
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PMID:Different course of acute hepatitis B in elderly adults. 400 76


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