Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Calotes versicolor, thyroidectomy did not alter the blood glucose level, lactate dehydrogenase (LDH liver and heart), acid phosphatase (Ac.Pase liver and kidney), and alkaline phosphatase (Alk.Pase liver and kidney) activities; significantly decreased the activities of glucose-6-phosphatase (G-6-Pase liver and kidney), glutamic oxaloacetic transaminase (GOT liver and heart), glutamic pyruvic transaminase (GPT liver), and urea concentration (liver and kidney); and increased liver cholesterol when compared to sham-operated controls. Administration of L-thyroxine (L-T4) or triiodo-L-thyronine (L-T3) to thyroidectomized lizards significantly stimulated the activities of G-6-Pase, Ac.Pase, GOT and GPT, concentration of glucose and urea, and decreased the cholesterol level. While the activities of all the enzymes studied and cholesterol level remain unchanged, glucose and urea levels decreased and increased, respectively, in thyroidectomized animals treated with actinomycin D. Chloramphenicol treatment did not affect any of the parameters studied. Simultaneous injections of actinomycin D or chloramphenicol with L-T4 prevented the hormone-stimulated activities of Ac.Pase, GOT, and GPT while the activities of LDH, G-6-Pase, Alk.Pase, glucose, urea, and cholesterol levels remain unchanged.
Gen Comp Endocrinol 1990 Feb
PMID:Intermediary metabolism in a lizard, Calotes versicolor: role of thyroid hormones. 215 52

A continued accumulation of vitellogenin was observed in the serum through 28 days after administration of spaced large doses of estradiol. The level of estradiol in the serum reached a maximum on Day 4, followed by a continued decrease until a basal concentration was reached at Day 15. The estradiol treatment increased the in vitro hepatic protein synthesis activity, measured as polyphenylalanine synthesis per unit cytoplasmic RNA, within 2-4 days reaching a maximum after 7 days. The effect was transitory and reduced to less than 50% within 15 days. After restimulation a second rise in protein synthesis activity was observed. The cellular content of bulk RNA i the liver showed a slow but steady accumulation through the 28 days. The specific activity of glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase in the liver decreased 35 and 20% relative to control, respectively, within 7 days after the first stimulation and again 14 days after restimulation. The concentration of serum protein showed a steady increase throughout the experimental period. The concentration of serum ninhydrine positive substances was lowered to 50% relative to the controls within the first 7 days after start of treatment with hormone.
Gen Comp Endocrinol 1983 Apr
PMID:Estradiol-induced hepatic protein synthesis and transaminase activity in the male flounder, Platichthys flesus (L.). 618 62

Factors influencing the replication of varicella-zoster virus (VZV) in guinea-pig embryo cells were evaluated using both diploid cells (GPEC) and a chemically transformed cell line (GPT). Wild-type and vaccine strains of VZV were successfully isolated and serially propagated in GPEC prepared from early gestation whole embryos (less than 2 cm in length). Low passage GPEC (less than or equal to 5 subcultivations) were more susceptible to VZV infection than high passage GPEC (greater than 5 subcultivations), and guinea-pig cells were consistently less permissive than human diploid cells. Cell-free virus was produced from VZV-infected GPEC cultures by sonication and peak yields of 10(3) p.f.u./ml were obtained. In addition, we report the isolation and propagation of VZV, as well as production of cell-free virus, in GPT. Both GPEC and GPT cells were less susceptible to VZV infection than human cells. However, viral replication was enhanced by incubation of VZV-infected GPT cultures at 32 degree C rather than 36 degree C.
J Gen Virol 1981 Jun
PMID:Varicella-zoster virus infection of diploid and chemically transformed guinea-pig embryo cells: factors influencing virus replication. 627 Feb 57

In a search for additional antigens associated with virus-induced human liver disease a radioimmunoassay (RIA) was developed using IgG from sera of a multiply transfused person. Polystyrene beads coated with IgG F(ab)'2 fragments, dinitrophenylated F(ab)'2 fragments and 125I-labelled anti-2,4-dinitrophenyl antibodies (Neurath & Strick, 1979) were used in the RIA. An apparently new antigen or the corresponding antibodies were detected in 155 serum specimens from 35/37 (94%)individuals who developed non-A, non-B hepatitis. The antigen was also present in hepatitis B surface antigen-negative sera of blood donors with normal (13.2%) and elevated levels of alanine aminotransferase (34%). The antigen has an approximate mol. wt. of 45,000, a buoyant density of 1.23 g/ml and an isoelectric point of 7.
J Gen Virol 1980 Jun
PMID:An antigen detected frequently in human sera with elevated levels of alanine aminotransferase: a potential marker for non-A, non-B hepatitis. 677 39

1. Effect of aqueous-methanolic extract of Artemisia absinthium (Compositae) was investigated against acetaminophen- and CCl4-induced hepatic damage. 2. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 20%. 3. Pretreatment of rats with plant extract (500 mg/kg, orally twice daily for two days) prevented (P < 0.01) the acetaminophen (640 mg/kg) as well as CCl4 (1.5 ml/kg)-induced rise in serum transaminases (GOT and GPT). 4. Post-treatment with three successive doses of extract (500 mg/kg, 6 hr) restricted the hepatic damage induced by acetaminophen (P < 0.01) but CCl4-induced hepatotoxicity was not altered (P > 0.05). 5. Plant extract (500 mg/kg) caused significant prolongation (P < 0.05) in pentobarbital (75 mg/kg)-induced sleep as well as increased strychnine-induced lethality in mice suggestive of inhibitory effect on microsomal drug metabolizing enzymes (MDME). 6. These results indicate that the crude extract of Artemisia absinthium exhibits hepatoprotective action partly through MDME inhibitory action and validates the traditional use of plant in hepatic damage.
Gen Pharmacol 1995 Mar
PMID:Preventive and curative effects of Artemisia absinthium on acetaminophen and CCl4-induced hepatotoxicity. 759 79

1. The effects of racemic thalidomide (D[+]/L[-] alpha-phthalimido-glutarimide) on acetaminophen (AAP)-induced hepatitis were tested in male NMRI mice (n = 133) and quantified as serum activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT). 2. A 2.1-fold increase of GOT and a 1.9-fold increase of GPT activities (P < 0.001) were observed in mice treated perorally with 500 mg/kg of AAP plus 150 mg/kg of thalidomide (Thal). In the absence of AAP, Thal did not display any detectable hepatotoxic effects. 3. The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P < 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation. 4. We see the main application of nicotinic acid amide as for the combinational use in pharmaceutical preparations of AAP in order to avoid hepatic damage in patients treated with AAP and Thal.
Gen Pharmacol 1995 Oct
PMID:Exacerbation of acetaminophen hepatotoxicity by thalidomide and protection by nicotinic acid amide. 759 Jan 13

The response of adenylate cyclase to GTP and to dopamine (DA) was investigated in striatal membranes from desipramine (DMI)-treated rats (10 mg/kg, b.i.d., for 5 days). GPT exerted the same biphasic effect on basal and DA-stimulated enzyme activity in membranes from DMI-treated rats as on saline-treated rats. Rats were injected intraventricularly once with islet activating protein (IAP), pertussis toxin, and given extended treatment with DMI in order to study the effects on the inhibitory GTP-binding protein (Gi). Gi loses its function as a signal transducer on being ADP-ribosylated selectively by the IAP. D2 inhibition of adenylate cyclase by DA was attenuated by the IAP treatment in both DMI-and saline-treated rats; peak levels of DA plus GTP stimulation shifted from 1 microM to 100 microM GTP. D1 stimulation of adenylate cyclase by DA was also attenuated by the IAP in the DMI-treated rats. Since long-term treatment with DMI (15 mg/kg, once a day, for 3 weeks) resulted in suppression of D1 stimulation similar to that seen in the present findings, uncoupling between D2 receptors and Gi due to IAP treatment might accelerate DMI-induced adaptive changes of dual control of adenylate cyclase system by DA.
J Neural Transm Gen Sect 1994
PMID:Acceleration of desipramine-induced changes on the dopamine receptor-coupled adenylate cyclase system by pertussis toxin. 773 10

1. Hepatoprotective activity of hydro-methanolic extract of Artemisia scoparia (Compositae) was investigated against acetaminophen-induced hepatic damage. 2. Acetaminophen at a dose of 1 g/kg produced 100% mortality in mice while pretreatment of animals with plant extract (150 mg/kg) reduced the death rate to 20%. 3. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of GOT and GPT to 1528 +/- 310 and 904 +/- 261 IU/l (n = 10) respectively, compared to respective control values of 80 +/- 11 and 38 +/- 09. 4. Pretreatment of rats with plant extract (150 mg/kg) lowered significantly the respective serum GOT and GPT levels to 85 +/- 11 and 23 +/- 06. 5. These results indicate that Artemisia scoparia contains hepatoprotective constituents and this study rationalizes the traditional use of this plant in hepatobiliary disorders.
Gen Pharmacol 1993 Nov
PMID:Protective effect of Artemisia scoparia extract against acetaminophen-induced hepatotoxicity. 811 19

Recently, we demonstrated the hepatoprotective effects of nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP; EC 2.4.2.30) on mice suffering from acetaminophen (AAP)-hepatitis, suggesting that the AAP-induced liver injury involves a step which depends on adenoribosylation. The present study investigates the effects of a diet free of precursors of NAD, the substrate on which PARP acts, in female NMRI mice with AAP hepatitis and evaluates the influence of simultaneous ethanol consumption in these animals. Liver injuries were quantified as serum activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT). While AAP caused a 117-fold elevation of serum transaminase activities in mice kept on a standard laboratory diet, which was significantly exacerbated by ethanol and inhibited by nicotinic acid amide (NAA), adverse effects were noted in animals fed a diet free of precursors of NAD. In these animals, only minor increases of serum transaminase activities were measured in the presence of AAP, and unlike the exacerbation caused by ethanol in mice on a standard diet, the liver damage was inhibited by 50% by ethanol. A further 64% reduction of hepatitis was observed, when NAA was given to ethanol/AAP-mice. Our results provide evidence that the AAP-induced hepatitis and its exacerbation by ethanol can either be reduced by end-product inhibition of PARP by NAA or by dietary depletion of the enzyme's substrate NAD. We see the main application of NAA as for the combinational use in pharmaceutical preparations of acetaminophen in order to avoid hepatic damage in patients treated with this widely used analgesic.
Gen Pharmacol 1996 Jan
PMID:Influence of diet free of NAD-precursors on acetaminophen hepatotoxicity in mice. 874 98

An array of therapeutically used analgetic and antirheumatic drugs causes severe liver damage. The present study investigates the hepatoprotective effects of inhibitors of NAD-dependent adenoribosylation reactions in analgesics-induced hepatic injury. Male NMRI mice were treated perorally with 500 mg/kg of acetaminophen, and the activities of both glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) were determined in serum. In addition, the activity of poly(ADP-ribose)polymerase (PARP) was quantified in liver cell nuclei. While the PARP-activity remained essentially unchanged, the acetaminophen-induced release of both GOT and GPT from injured liver cells could be inhibited by 90-99%, when mice were injected additionally with the selective PARP-inhibitors nicotinic acid amide, benzamide, caffeine, theophyline, and thymidine, respectively. We see the main application of inhibitors of adenoribosylation reactions as for the combinational use in pharmaceutical preparations of analgesics and antirheumatic drugs in order to avoid hepatic damage.
Gen Pharmacol 1996 Jan
PMID:The influence of antagonists of poly(ADP-ribose) metabolism on acetaminophen hepatotoxicity. 874 16


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