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)

We established a versatile method for the measurement of indocyanine green maximal removal rate (ICG Rmax) to detect hepatic functional mass in conscious rats using a repeated blood sampling procedure. On investigation of the optimal technical conditions, the appropriate intravenous administered doses of ICG were 2.5, 5, 10 or 20 mg/kg, and the best blood collection times for calculating plasma half-life at these doses were immediately before, and 4, 7 and 10 min after ICG injection. The interval among the respective ICG injections was more than 4 hr. In hepatectomized rats, the ICG Rmax value was reduced to about 50% and 20% of sham-operated rats in mean 2/3 and 4/5 liver resections, respectively, suggesting that it would almost extrapolate to hepatic surviving reserves under these experimental conditions. In rats treated subcutaneously with carbon tetrachloride (CCl4, 0.1 and 0.25 ml/kg) thrice weekly during a 17-week period (120 days), a decrease in ICG Rmax value did not correlate with increases in serum alanine transaminase (ALT), alkaline phosphatase (ALP) and total bilirubin values throughout the experimental periods. However, the reduced ICG Rmax well correlated with decreases in serum albumin and cholinesterase (CHE) values from day 50. Histological examinations in the liver revealed that nodules of hepatocytes were separated by thick fibrous bands, defining the typical aspect of cirrhosis on day 30 to 90. These results suggest that the measurement of ICG Rmax is a valuable tool for the estimation of hepatic functional integrity in rats.
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PMID:Application of maximal removal rate of indocyanine green to the determination of hepatic functional mass in conscious rats. 919 53

Syh-Mo-Yin (SMY), Guizhi-Fuling-Wan (GFW), Shieh-Qing-Wan (SQW) and Syh-Nih-San (SNS) are prescriptions of Traditional Chinese Medicine (TCM) for liver disease. The effects of these four prescriptions against experimental liver injury induced by alpha-Naphthylisothiocyanate (ANIT) and carbon tetrachloride (CCl4) were studied. Rats treated with ANIT (100 mg/kg) exhibited elevations of serum total bilirubin (TBI), alkaline phosphatase (ALP), glutamate-oxalatetransaminase (sGOT) and glutamate-pyruvate-transminase (sGPT) as well as cholestasis and parenchymanecrosis. In rats receiving SMY, SQW and SNS treatment after ANIT challenged, the biochemical and morphological parameters of liver injury were significantly reduce. Elevated lipid peroxidation (LPO) level in liver tissue, associated with an increase in serum GOT and GPT level, was observed in CCl4-treated rats. Treatment with these four prescriptions on CCl4-induced liver injury rats showed a remarkable hepatoprotective effect. A significant decrease in peroxidative level suggested that these prescriptions have anti free radical properties.
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PMID:Ameliorative effect of traditional Chinese medicine prescriptions on alpha-naphthylisothiocyanate and carbon-tetrachloride induced toxicity in rats. 928 66

Present work was undertaken to ascertain the hepatoprotective effect of Swertia chirata in albino rats. Intraperitoneal injection of CCl4 (1 ml/kg body wt on every 72 hr. for 16 days) significantly increased serum aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), and alkaline phosphatase (ALP) activities and bilirubin level in rat, but liver glycogen and serum cholesterol levels were decreased. Histologically it produced hepatocytic necrosis especially in the centrilobular region. Simultaneous treatments with S. Chirata (in different doses, viz, 20, 50 and 100 mg/kg body wt daily) and CCl4 (similar dose to that mentioned earlier) caused improvement at both biochemical and histopathological parameters compared to that of CCl4 treatment alone but it was most effective when S. chirata was administered in a moderate dose (50 mg/kg body wt).
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PMID:Hepatoprotective effect of Swertia chirata on rat. 931 40

Swiss albino rats were treated in groups with CCl4, and flyash to induce cellular toxicity in the lungs and trachea. Animal groups received treatment of Koflet (K) with CCl4 (7 days) and with flyash (30 days); their general health and biochemical parameters were studied and used as an indication of cellular injuries. A significant loss was observed in body weight and food consumption in animals given only CCl4 or flyash, while simultaneous treatment with K resulted in a non significant alteration from normal control groups. Enzyme (alkaline phosphatase, Ca2+ -Mg2+ -ATPase, glutamic-oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT)) activities were estimated in tissue homogenate preparation of lung, trachea and serum, which showed no significant change except for GPT activity as compared to control animals which received CCl4 or flyash with K. Similarly lung, trachea and serum contents of carbohydrate, protein, sialic acid, serum protein, serum cholesterol were estimated and it was found that alteration caused by CCl4, or flyash becomes almost non-significant compared to that of the control after the treatment of K, except for carbohydrate and serum cholesterol values. The animal group which was only treated with K did not show any significant alteration in their biochemical markers or injuries, except for cholesterol.
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PMID:In vivo protective role of Koflet (an ayurvedic preparation) against cellular toxicity caused by CCl4 and flyash. 940 99

The possible modulatory effect of browned yam flour, a local dietary staple in south western Nigeria, on the toxicity of 7,12-dimethylbenzanthracene (DMBA), 3-methylcholanthrene (3-MC), carbon tetrachloride (CCl4) and bromobenzene (BrB) in rats was investigated. Feeding rats with 25% browned yam flour 2 wk before treatment with 65 mg/kg DMBA (single dose) and 5 mg/kg 3-MC and continued for 3 wk significantly decreased the reduction in final body weight or weight gain and organ weights caused by the two compounds. Similarly, the diet decreased the reduction in body weight or weight gain and the increase in relative liver weight mediated by oral treatment with 0.5 ml CCl4/kg and 2.5 mmol BrB/kg body weight. Incorporation of 25% browned yam flour into rat diet significantly reduced the DMBA-mediated decrease in haemoglobin content, packed cell volume, red blood cell count and white blood cell count by 7, 5, 20 and 10%, respectively; while the diet reduced the 3-MC-mediated decrease in these parameters by 15, 28, 9 and 17%, respectively. The same diet elicited 23, 45, 13 and 33% decreases in CCl4 mediated reduction in these parameters and 23, 18, 16 and 29% in the case of BrB. Browned yam flour diet caused 10, 14 (P < 0.001) and 4% (P < 0.05) reductions in the DMBA-mediated increase in serum aspartate aminotransferase, alanine aminotransferase and serum alkaline phosphatase, respectively; and 32, 31 (P < 0.05) and 13% (P < 0.001) in the case of the 3-MC-mediated increase. Also, the diet reduced CCl4-mediated increase in the activities of these by 40, 34 and 31%, respectively and by 23, 30 and 29% following BrB treatment. These results suggest that browned yam flour diet could possibly be a modulator of chemically induced toxicity.
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PMID:Possible modulatory effect of browned yam flour diet on chemically-induced toxicity in the rat. 946 31

Esculetin, a phenolic compound found in Cichorium intybus and Bougainvllra spectabillis was investigated for its possible protective effect against paracetamol and CCl4-induced hepatic damage. Paracetamol produced 100% mortality at the dose of 1 g kg-1 in mice while pre-treatment of animals with esculetin (6 mg kg-1) reduced the death rate to 40%. Oral administration of paracetamol (640 mg kg-1) produced liver damage in rats as manifested by the rise in serum enzyme levels of alkaline phosphatase (ALP) and aminotransferases (AST and ALT). Pre-treatment of rats with esculetin (6 mg kg-1) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl4 (1.5 ml kg-1; orally) also raised serum ALP, AST and ALT levels. The same dose of esculetin (6 mg kg-1) was able to prevent the CCl4-induced rise in serum enzymes. Esculetin also prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity. These results indicate that esculetin possesses anti-hepatotoxic activity and the presence of this compound in Cichorium intybus and Bougainvllra spectabillis may explain the folkloric use of these plants in liver damage.
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PMID:Esculetin prevents liver damage induced by paracetamol and CCL4. 950 77

The protective effect of tumeric extract (TE) in diet on CCl4-treated rats was studied. Rats were divided into 5 groups: (1) untreated, (2) CCl4 treated, (3) pre-TE for 2 weeks followed by CCl4, (4) TE + CCl4 given concurrently and (5) 5% TE as positive control. The serum levels of bilirubin, cholesterol, aspartate aminotransferase, (AST), alanine amino transferase (AST), (ALT) and alkaline phosphatase were estimated after 1, 2 and 3 months. CCl4 caused a maximum increase (2-3-fold in all the above parameters. As compared to CCl4 group, a short pre-treatment of TE showed reduction in cholesterol, bilirubin, AST, ALT and alkaline phosphatase activity whereas concurrent treatment of TE + CCl4 reduced to a greater extent the levels of all parameters except ALT. To conclude, concurrent treatment of TE gave significant protection against CCl4 though the values did not reach the normal levels.
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PMID:Protective effect of turmeric (Curcuma longa L.) extract on carbon tetrachloride-induced liver damage in rats. 973 71

The aim of this work was to determine if the inhibition or stimulation of NO synthesis modulates liver damage induced by the chronic administration of CCl4. CCl4 was administered three times a week for 8 weeks to male Wistar rats treated simultaneously with N omega-nitro-L-arginine methyl ester (L-NAME, 100 mg/kg, p.o., twice a day), aminoguanidine (AG, 4 g/L in the drinking water), or L-arginine (500 mg/kg, p.o., twice a day); appropriate controls were performed. Serum NO2- + NO3- increased in the groups treated with CCl4 and/or L-arginine, but the effect was prevented by either L-NAME or AG. In the liver, lipid peroxidation and collagen content increased, while glycogen content decreased in the CCl4-treated group (P < 0.05); L-NAME and AG accentuated these effects. Serum enzyme activities of alanine aminotransferase (ALT), alkaline phosphatase, and gamma-glutamyl transpeptidase (gamma-GTP) and bilirubin content increased about 2-, 3-, 2-, and 6-fold, respectively, after CCl4 intoxication (P < 0.05); L-NAME or AG cotreatment further increased the enzyme activities (P < 0.05). L-Arginine treatment protected the liver partially from the elevation of collagen, bilirubins, and alkaline phosphatase and from glycogen depletion induced by CCl4 intoxication (P < 0.05), but showed no significant effect on ALT, gamma-GTP, or lipid peroxidation. These results suggest that NO protects the liver against oxidative injury, because NO inhibition by L-NAME or AG increased lipid peroxidation and the other markers of liver injury studied herein.
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PMID:Nitric oxide protection of rat liver from lipid peroxidation, collagen accumulation, and liver damage induced by carbon tetrachloride. 975 Oct 83

Treatment with hepatotoxin namely carbon tetrachloride (CCl4) (0.1 ml/100 g of body weight; twice a week) induced acute hepatic necrosis in Swiss albino mice (male; body weight 30 g +/- 2), with significant alteration in the activities of glutamic oxaloacetic transaminase (GOT); glutamic pyruvic transaminase (GPT); alkaline phosphatase (AP) and serum bilirubin. Administration of a protein fraction isolated from the leaves of C. indicus counteracted the action of CCl4 on transaminase, phosphatase showing hepatoprotection. Daily treatment with a purified protein fraction 'X' from the above plant (0.5 mouse ml i.p; 50-60 micrograms/ml) for a period of 7, 14, 21 days respectively showed decreased activities of serum transaminases alkaline phosphatase and decreased levels of serum bilirubin. These findings were further confirmed by histopathological study of liver.
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PMID:Hepatoprotective effect of a protein isolated from Cajanus indicus (Spreng) on carbon tetrachloride induced hepatotoxicity in mice. 975 48

Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4 were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.
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PMID:Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats. 1007 38


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