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)

Acetaminophen (APAP) overdose is often fatal, leading to fulminant hepatic and renal tubular necrosis in humans and animals. We studied the effect of a nutrient mixture (NM) containing, among other nutrients, lysine, proline, ascorbic acid, N-acetyl cysteine, and green tea extract, which has previously been demonstrated to exhibit a broad spectrum of therapeutic properties on APAP-induced hepatic and renal damage in ICR (Imprinting Control Region) mice. Seven-week-old male ICR mice were divided into four groups (A-D) of five animals each. Groups A and C mice were fed a regular diet for 2 weeks, while groups B and D mice were supplemented with 0.5% NM (w/w) during that period. Groups A and B received saline i.p., while groups C and D received APAP (600 mg/kg) i.p. All animals were killed 24 h after APAP administration, serum was collected to assess the liver and kidney functions, and the livers and kidneys were excised for histology. Mean serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, BUN (Blood Urea Nitrogen), creatinine, and BUN/creatinine ratios were comparable in groups A and B, increased markedly in group C and significantly lower in group D compared with group C. APAP caused significant centrilobular necrosis and glomerular damage in unsupplemented animals, while NM prevented these alterations. The results indicate that NM has potential to protect against APAP-induced liver and kidney damage.
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PMID:A nutrient mixture prevents acetaminophen hepatic and renal toxicity in ICR mice. 1865 Feb 54

A bienzyme electrochemical probe has been assembled and used to monitor the inhibition of the enzyme protein phosphatase-2A (PP2A) by okadaic acid (OA), taking advantage of the particular characteristics of a biochemical pathway in which PP2A is involved. This enzyme has significant activity toward glycogen phosphorylase a (PHOS a), which in turn catalyzes the conversion of glycogen to glucose-1-phosphate (G-1-P). In addition, PP2A is strongly inhibited by OA and its derivatives. Due to this combination of properties, PP2A was employed to develop an assay system involving a preliminary phase of off-line enzymatic incubations (OA/PP2A, PP2A/PHOS a, PHOS a/glycogen+phosphate). This off-line step was followed by the electrochemical detection of H2O2, which is the final product of two sequential enzymatic reactions: G-1-P with alkaline phosphatase (AP) producing glucose, then glucose with glucose oxidase (GOD) producing hydrogen peroxide. These two enzymes were coimmobilized on a nylon net membrane that was placed over an H2O2 platinum probe inserted into a flow injection analysis (FIA) system. During a first phase of the study, all analytical parameters were optimized. During a subsequent phase, the inhibition of PP2A enzyme by OA was evaluated. The calibration of the system shows a working range for detection of OA between 30 and 250 pg ml(-1). The total analysis time is the sum of 50 min for the off-line enzymatic incubations and 4 min for the biosensor response.
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PMID:A bienzyme electrochemical probe for flow injection analysis of okadaic acid based on protein phosphatase-2A inhibition: an optimization study. 1901 24

Ethanol extract of Clausena dentata (Willd.) M. Roem (Rutaceae) was evaluated for hepatoprotective activity in rats. The plant extract (250 mg/kg, p.o.) showed a remarkable hepatoprotective activity against acetaminophen-induced hepatotoxicity as judged from the serum markers for liver damage. Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP) and decrease in total protein. Treatment of rats with ethanol extract (250 mg/kg) significantly (P<0.001) altered serum marker enzymes levels to near normal against acetaminophen treated rats. The activity of the extract was comparable to the standard drug, silymarin (50 mg/kg, p.o.). Histopathological changes of liver sample were compared with respective control. Results indicate that Clausena dentata possesses hepatoprotective effect on acetaminophen-induced hepatotoxicity in rats.
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PMID:Effect of Clausena dentata (Willd.) M. Roem. against paracetamol induced hepatotoxicity in rats. 1916 28

The hepatoprotective potential DTS (1.5 g/kg bw, Denshici-to-Chiusei, Kyotsu Jigyo, Tokyo, Japan) was evaluated against either toxic (1.5 g/kg bw) and sub-toxic (150 mg/kg bw) dosage of paracetamol-induced liver injury in Sprague-Dawley rat. Paracetamol intoxication caused a reduction of serum total protein and increase levels of serum alkaline phosphatase (ALP), aspartate aminotranferase (AST) and serum alanine aminotranferase (ALT) at higher extent in the toxic group. This phenomenon was paralleled by an impaired liver redox status (reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) and increased MDA in both paracetamol-administered groups. Moreover, a marked reduction of ATPase and thiols together with DNA fragmentation occurred in liver tissue. Animals pretreated with DTS showed a marked mitigation of the severity of liver enzyme and of the impaired redox status of the liver. Moreover, DTS partly prevented the DNA fragmentation and the decline of liver tissue ATPase and protein thiol assay as compared with both groups treated with paracetamol alone. Although more detailed studies are awaited to ascertain the detailed mode of action of DTS, it wouls seem to be related to the prevention of formation of the reactive oxygen groups thereby preventing the damage on the hepatocytes and possibly modulating the genes responsible for synthesis of liver antioxidant enzymes thus providing marked DNA protection.<br />
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PMID:Protective effect of a phytocompound on oxidative stress and DNA fragmentation against paracetamol-induced liver damage. 1922 34

Protective effect of emodin (1,3,8-trihydroxy-6-methyl anthraquinone), an active compound of Ventilago madraspatana Gaertn., was evaluated against acetaminophen-induced biochemical and histological alterations in rats. Acetaminophen (2g/kg, po) administration caused significant elevation in the release of serum transaminases, alkaline phosphatase, lactate dehydrogenase, serum bilirubin and serum protein with concomitant decrease in hemoglobin and blood sugar after 24h of its administration. Toxicant exposure intensified the lipid peroxidation and altered glutathione status, activities of adenosine triphosphatase, acid phosphatase, alkaline phosphatase as well as major cellular constituents i.e., protein, glycogen and total cholesterol in liver and kidney. Treatment of emodin (20, 30 and 40 mg/kg, po) significantly lessened the toxicity by protecting acetaminophen-induced alterations in various blood and tissue biochemical variables after 24h of its administration. Acetaminophen administration initiated histological damage in liver. Some degree of protection was seen after emodin therapy in a dose-dependent manner. Emodin at doses of 30 and 40 mg/kg effectively reversed toxic events induced by acetaminophen as same as silymarin (50mg/kg, po). Thus, the study concluded that emodin at a dose of 30 mg/kg (po) possesses optimum hepatoprotective ability against acetaminophen-induced toxicity.
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PMID:Dose-dependent hepatoprotective effect of emodin against acetaminophen-induced acute damage in rats. 1980 Jul 73

ABSTRACT The aim of this study was to evaluate the hepatoprotective role of a 43-kD protein (Hp-P) isolated from the leaves of Cajanus indicus L. against acetaminophen (APAP)-induced toxicity in mouse liver and in isolated hepatocytes. The hepatotoxicity of APAP and the hepatoprotective activity of Hp-P in vivo were determined by measuring the liver-specific serum marker enzymes alanine amino transferase (ALT) and alkaline phosphatase (ALP) in murine sera and observing the histological changes in the mice liver treated with the protein before and after (2 mg/kg body weight for 5 days) APAP (at a dose of 300 mg/kg body weight for 2 days) administration. The cell viability, LDH leakage, GSH level, and lipid peroxidation were measured in isolated hepatocytes to evaluate the cytotoxic effect of APAP and the protective role of Hp-P in vitro. Experimental results showed that APAP induced hepatotoxicity in vivo as revealed from the changes in serum-specific marker enzyme levels and histology of liver. It also induced cytotoxicity in hepatocytes as observed from the changes in cell viability and LDH leakage. Pretreatment with Hp-P prevented the APAP-induced elevation of ALT and ALP in murine sera. In addition, posttreatment with Hp-P significantly altered most of the changes induced by APAP. Although some natural recovery has been observed in toxin controls, the Hp-P-induced recovering process is more rapid than the natural ones. In histological studies, less centrilobular necrosis was found in the liver treated with Hp-P before and after APAP intoxication compared to the liver treated with APAP alone. Radical scavenging experiment showed that Hp-P scavenges DPPH radicals directly. Studies also showed that APAP-induced reduced cell viability and cellular LDH leakage could be prevented by the combinatorial effect of Hp-P. Besides, treatment of hepatocytes with Hp-P and APAP together maintained the normal GSH level. APAP-induced enhanced lipid peroxidation was also decreased when cells were treated with APAP and Hp-P together. Hp-P alone, on the other hand, did not induce any alterations of the studied parameters. Results of this study have been compared with a known antioxidant, alpha-tocopherol. Data from both the in vivo (before and after APAP administration) and in vitro studies suggest that Hp-P has potent hepato- and cytoprotective properties against APAP-induced toxicity.
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PMID:Attenuation of Acetaminophen-Induced Hepatotoxicity In Vivo and In Vitro by a 43-kD Protein Isolated from the Herb Cajanus indicus L. 2002 Sep 54

Cats most commonly receive toxic amounts of acetaminophen (APAP) because owners medicate them without consulting a veterinarian. The aim of this study was to compare the hepatoprotective action of silymarin and N-acetylcysteine (NAC) against APAP poisoning. Twenty healthy cats were randomly allotted to five equal groups. Animals in group A were given APAP (single dose 150 mg/kg, p.o.); groups B and C consisted of cats that received NAC (100 mg/kg, p.o.) or silymarin (30 mg/kg, p.o.) concurrent with APAP administration respectively; groups D and E were treated like groups B and C, respectively, but 4 h after APAP administration. The serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), methemoglobin, and total and direct bilirubin were measured before APAP administration and 4, 24, and 72 h later. A single oral administration of APAP significantly elevated serum concentrations of ALT, AST, ALP, LDH, methemoglobin, and total and direct bilirubin. In both the groups receiving APAP plus NAC or silymarin, levels of serum enzyme activities, methemoglobin, and total and direct bilirubin remained within the normal values. It was concluded that silymarin as well as NAC can protect liver tissue against oxidative stress in cats with an APAP intoxication.
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PMID:Evaluation of prophylactic and therapeutic effects of silymarin and N-acetylcysteine in acetaminophen-induced hepatotoxicity in cats. 2044 31

Acetaminophen, a pain-reliever, is one of the most widely used medications in the world. Acetaminophen with normal dosage is considered a nontoxic drug for therapeutic applications, but when taken at overdose levels it produces liver damage in human and various animal species. By a high energy mechanically activated method, we produced acetaminophen in a nanometer crystalline size (24 nm). Forty-eight hours after injection of crystalline particles with normal and reduced size of our drug, the effect of liver toxicity was compared by determination of liver transferase enzymes such as alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase (ALT). These enzymes were examined by routine colorimetric methods using commercial kits and pathologic investigations. Statistical analysis and pathological figures indicated that ALT delivery and toxicity in reduced size acetaminophen was significantly reduced when compared with normal size acetaminophen. Pathology figures exhibited reduced necrosis effects, especially the confluent necrosis, in the central part of the lobule in the reduced size acetaminophen samples when compared with the normal samples.
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PMID:The effect of acetaminophen nanoparticles on liver toxicity in a rat model. 2046 35

Extracts of Boerhaavia diffusa leaves were evaluated for antioxidant and hepatoprotective properties in the acetaminophen-induced liver damage model. Antioxidative evaluation of ethanolic extract gave total phenolic content, total flavonoid content, vitamin C content and vitamin E content and the levels of selenium and zinc as 6.6+/-0.2mg/g tannic acid equivalent, 0.092+/-0.003 mg/g quercetin equivalent, 0.21+/-0.03 mg/g, 0.054+/-0.002 mg/g, 0.52+/-0.05 ppm and 9.28+/-0.16 ppm, respectively. The DPPH scavenging capacity and the reductive potential were 78.32+/-2.41% and 0.65+/-0.02 mg/g ascorbic acid, respectively. Pretreatment with aqueous and ethanolic extracts decreased the activities of alkaline phosphatase, lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and the level of bilirubin in the serum that were elevated by acetaminophen. The two extracts also ameliorated the elevation in the activities of the enzymes in the liver. Acetaminophen intoxication led to reduction in serum and liver albumin levels which were not significantly increased by pretreatment with the extracts. The extracts also protected against acetaminophen induced lipid peroxidation. These results indicated that leaf extracts from B. diffusa possess hepatoprotective property against acetaminophen-induced liver damage which may be mediated through augmentation of antioxidant defenses.
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PMID:Antioxidant activity and hepatoprotective property of leaf extracts of Boerhaavia diffusa Linn against acetaminophen-induced liver damage in rats. 2055 84

Renal proximal tubule fragments (RPT) were prepared from young-adult, male F-344 rats by deferoxamine/collagenase perfusion and evaluated as a potential model for mechanistic studies and screening, using known nephrotoxins. Chloroform and S-(1,2- dichlorovinyl )- l - cysteine (DCVC) produced depressed O(2) consumption rates (basal and/or nystatin-stimulated) and lactate dehydrogenase (LDH) release during 8-hr incubations at 0.5 mg RPT protein/ml. Cytochrome P-450 inhibitors piperonyl butoxide and metyrapone were either without effect or potentiated chloroform-induced toxicity. DCVC was more cytotoxic to RPT than to rat hepatocytes. The cytotoxic potency for cephalothin relative to cefazolin decreased as RPT content in the medium was increased to 3.0 mg protein/ml, giving a rank order more in accord with results reported in vivo. Cephalosporins markedly depressed brush border alkaline phosphatase (ALP) activity, without affecting gamma-glutamyltranspeptidase activity; the effect on ALP was less sensitive to the RPT level. Acetaminophen (25 mm) and p-aminophenol (1.0 mm) induced LDH release without ALP depression and inhibited mitochondrial respiration. These results in general corresponded well with in vivo responses and indicate that this RPT system may be valuable for studies of chemical-induced nephrotoxicity.
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PMID:Studies of nephrotoxic agents in an improved renal proximal tubule system. 2070 4


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