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

---

Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pollution, industrial solvents, concentrations of metals and other environmental agents are widely related to biochemicals values which are used in disease diagnosis of environmental toxicity. A rat bioassay validated for the identification of toxic effects of eutrophication revealed increased serum activities of amylase, alanine transaminase (ALT) and alkaline phosphatase (ALP) in rats that received algae, filtered water and nickel or cadmium from drinking water. Serum Cu-Zn superoxide dismutase activity decreased from its basal level of 40.8 +/- 2.3 to 26.4 U/mg protein, at 7 days of algae and at 48 hr of nickel and cadmium water ingestion. The observation that lipoperoxide concentration was not altered in rats treated with filtered water, while amylase, ALT and ALP were increased in these rats and in those treated with nickel or cadmium, indicated that pancreatic, hepatic and osteogenic lesions by eutrophication were not related to superoxide radicals, and might be due to a novel toxic environmental agent found in filtered and non-filtered algae water.
...
PMID:Toxic effects of water eutrophication on pancreatic, hepatic and osteogenic tissues of rats. 753 73

1. Hepatotoxicity is the most common finding in patients with iron overload since the liver is the major recipient of iron excess, even though the kidney could be a target of iron toxicity. The effect of iron overload was studied in the early stages after iron-dextran injection in rats, as a model for secondary hemocromatosis. 2. Total hepatic and kidney iron content was markedly elevated over control values 20 h after the iron administration. Plasma GOT, GPT and LDH activities were not affected, suggesting that liver cell permeability was not affected by necrosis. 3. Spontaneous liver chemiluminescence was measured as an indicator of oxidative stress and lipid peroxidation. Light emission was increased four-fold 6 h after iron supplementation. 4. Increases in the generation of thiobarbituric acid reactive substances (TBARS in liver and kidney homogenates were detected after iron administration. 5. The activities of catalase, SOD and glutathione peroxidase were determined. Enzymatic activities declined in liver homogenates by 25, 36 and 32%, respectively, 20 h after iron injection. These activities were not affected in kidney as compared to control values, except for SOD activity that was decreased by 26%. 6. The content of alpha-tocopherol was decreased by 31% in whole kidney homogenates and by 40% in plasma. 7. Our data indicate that lipid peroxidation occurs after mild iron overload both in liver and kidney. Enzymatic antioxidants are consumed significantly in liver and alpha-tocopherol content decreases in kidney, suggesting an organ-specific antioxidant effect.
...
PMID:Effect of mild iron overload on liver and kidney lipid peroxidation. 764 Jun 23

Sixty gnotobiotic rats with 5 strains of bacteria in intestine were randomized to 4 groups: (1) Sham injury group (controls, n = 6). (2) Early fluid resuscitation (EFR) group (n = 24), receiving fluid resuscitation (Parkland formula) immediately after scald (40% TBSA, third degree). (3) Delayed fluid resuscitation (DFR) group (n = 24) receiving resuscitation 6 hours later after scald. (4) Treatment group (n = 12) receiving DFR and the therapy of VitC and VitE. At 8, 24, 48 and 72 hours after injury, the animals (n = 6, at each point) were sacrificed and the content of oxygen free radicals (OFR), SOD,GSHPx and MDA in the heart, liver, kidney and lung were determined. Morphological Changes of organs, PaO2, PaCO2 and the content of serum CPK, LDH, GPT, GOT, BUN and Cr were also examined. Both EFR and DFR groups demonstrated elevated content of OFR and MDA and reduced content of SOD and GSHPx in their organs. Morphological and serological changes were also observed. All these changes were more obvious in DFR group than in EFR group. After the treatment of VitC and VitE, the changes were ameliorated. Our results suggested that DFR induced the production of OFR, resulting in lipid peroxidation and that OFR injury might be one of the main factors in the pathogenesis of multiple organ injury after DFR.
...
PMID:[Multiple organ injury after delayed fluid resuscitation in severely scalded rats: role of oxygen free radicals]. 764 95

The effects of strenuous physical exercise on the serial changes in the haematological, biochemical and hormonal markers were investigated. A group of 14 soldiers, aged 24-36 years, took part in a military training course for about 13 weeks. After severe exercise stress, an increase (90%) in the number of peripheral blood leucocytes was observed. The degree of leucocytosis showed a close correlation with the values of some serum parameters, such as concentrations of aspartate aminotransferase (AST; r = 0.747), lactate dehydrogenase (LD; r = 0.748), blood urea nitrogen (r = 0.756), creatine kinase (CK; r = 0.637), manganese-superoxide dismutase (Mn-SOD; r = 0.508), alanine aminotransferase (ALT; r = 0.542) and uric acid (r = 0.538), and concentrations of urinary parameters, such as vanilmandelic acid (r = 0.429) and free cortisol (r = 0.437). The subjects showing prominent leucocytosis over 9500 cells.microliters-1 exhibited a lower concentration of serum cholinesterase than those who showed milder leucocytosis. The serum Mn-SOD concentration was closely correlated with the serial changes in serum concentrations of AST, ALT, LD and CK, indicating exercise-induced muscle and liver damage. The change in peripheral leucocyte number was assumed to be diagnostically informative and may be a prognostic marker, reflecting organ damage and restoration after strenuous physical exercise.
...
PMID:Leucocytosis as a marker of organ damage induced by chronic strenuous physical exercise. 878 93

Bleomycin-induced 6-thioguanine-resistant mutants pretreated with or without TRIEN (triethylenetetramine), a superoxide dismutase (SOD) inhibitor, or TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl), an SOD mimic, were analyzed by polymerase chain reaction (PCR)-based deletion screening in a Chinese hamster ovary (CHO) clone K1-BH4 and its derivative AS52 cells. As we proposed earlier, TRIEN would decrease and TEMPOL would increase the intracellular level of hydroxyl radical leading to a higher and lower recovery of deletion mutants. We found that the proportion of the deletion mutants induced by bleomycin at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus in K1-BH4 cells was 45.5% (25/55). The proportion of deletion HPRT- mutants induced by bleomycin pretreated with TRIEN was 31.0% (9/29) and with TEMPOL was 50.0% (14/28). The proportion of deletion mutants induced by bleomycin on the xanthine-guanine phosphoribosyltransferase (gpt) gene in AS52 cells was 61.0% (36/59). The proportion of deletion GPT- mutants induced by bleomycin pretreated with TRIEN was 56.8% (21/37) and with TEMPOL was 61.4% (27/44). The trend of the change of the proportion of bleomycin-induced deletion mutants as affected by TRIEN and by TEMPOL provides molecular evidence for the involvement of reactive oxygen species (ROS) in bleomycin mutagenesis in mammalian cells, in which deletion is a major type of induced mutation.
...
PMID:Polymerase chain reaction-based deletion screening of bleomycin induced 6-thioguanine-resistant mutants in Chinese hamster ovary cells: the effects of an inhibitor and a mimic of superoxide dismutase. 769 Aug 90

The effects of autonomic nervous system on liver damage induced by carbon tetrachloride (CCl4) and repair were investigated morphologically and biochemically in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). After repetition of CCl4 treatment twice a week for 4 weeks, the SHR showed liver cirrhosis histologically. In WKY, however, only fibrosis was observed. Biochemically, the serum glutamate-pyruvate transaminase (GPT), liver lipid peroxidation (LPO) and superoxide dismutase (SOD) activities were measured. CCl4 increased the activities of GPT and LPO but decreased that of SOD in SHR more than in WKY. These findings indicate that liver damage induced by CCl4 was more severe in the sympathetic hyperactive SHR than in the normally active WKY. In induced cirrhotic liver of SHR and fibrotic liver of WKY, diffuse serotonin particles and numerous mast cells were observed in the fibrotic matrix, and some neovascular adrenergic fibers were found in these areas. These results indicate that the sympathetic nerve can exacerbate the liver damage, and both mast cells or serotonin particles and sympathetic nerve participate at some stages in the repair of liver damage.
...
PMID:The role of the autonomic nervous system in chemically-induced liver damage and repair--using the essential hypertensive animal model (SHR). 773 87

A normocalcemic animal model of vitamin D (vit. D)-deficiency has been successfully developed by feeding a high calcium (Ca2+) diet to vit. D.-deficient rats. The modulating role of Ca2+ on the hepatic antioxidant defence system and lipid peroxidation has been evaluated in this model. Partial restoration of liver function was noted in these rats following extra Ca2+ feeding. Serum alkaline phosphatase and alanine aminotransferase reverted to a normal level. The reduced levels of hepatic SOD and glutathione peroxidase in vit. D.-deficient rats, were also increased after extra Ca2+ supplementation. Even elevated lipid peroxidation due to vit. D.-deficiency was reduced after feeding the extra Ca(2+)-supplemented diet. However, catalase activity remained at the control level throughout the study. The results provide important evidence that normocalcemia is essential for maintaining the hepatic antioxidant defence and controlling lipid peroxidation in the in vivo milieu.
...
PMID:The role of calcium in the modulation of the hepatic anti-oxidant defence system. 821 47

The present study set out to investigate whether plasma phosphatidylcholine hydroperoxide (PCOOH) levels could accurately reflect lipid peroxidation linking to liver damage due to ischemia--reperfusion. PCOOH is a primary peroxidative product of phosphatidylcholine (PC), which is the most important functional lipid in the hepatocellular membrane, and may mediate oxidative stress. We quantified PCOOH and PC in the plasma and liver of rats subjected to hepatic ischemia-reperfusion by chemiluminescence detecting HPLC (CL-HPLC) method. Plasma PCOOH levels showed no significant rise in either the ischemia only group or in the sham-operation group, compared to controls (0.7 nmol/mL plasma). At 60 min subsequent to reperfusion, the PCOOH levels in plasma and liver, as well as the levels of several serum markers of liver injury [lactic dehydrogenase (LDH), glutamic-oxalacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT)] increased in proportion to the duration of ischemia (up to 60 min). During periods of reperfusion following 30 min of ischemia, plasma PCOOH increased biphasically (2 nmol/mL; 12-24 hr duration of reperfusion), and generally ran parallel to that in the liver after more than 60 min of reperfusion. Dose-dependent protective effects against warm ischemia (30 min)-reperfusion (12 hr) injury were clearly demonstrated in the groups treated with allopurinol, diclofenac Na, ascorbic acid (V.C), alpha-tocopherol and coenzyme Q10, but not in those treated with r-h-superoxide dismutase or betamethasone. The rises in plasma PCOOH and serum GOT, GPT and LDH of the ischemia-reperfused rats were ameliorated most in the group pretreated with diclofenac Na, and next most in the group pretreated with V.C. These results indicate that the plasma PCOOH levels are a useful index both for liver cell damage induced by oxygen free radicals generated during ischemia-reperfusion, and to investigate the efficacy of drugs against oxidative stress.
...
PMID:Effects of anti-free radical interventions on phosphatidylcholine hydroperoxide in plasma after ischemia-reperfusion in the liver of rats. 825 Sep 60

Ethanol administration to rats for 30 days and 90 days followed by paracetamol administration resulted in liver injury indicated by the significant increase in the serum GOT and GPT levels. The ethanol treatment to rats and the administration of paracetamol to the normal and alcoholic rats also caused a significant increase in the activity of serum acid and alkaline phosphatase. The hepatotoxicity of ethanol and paracetamol were indicated by the histological alterations in this study. The content of lipid peroxidation products-malondialdehyde, hydroperoxides and conjugated dienes were increased in the liver, heart, kidney and brain of the acute and chronic ethanol treated and paracetamol treated rats. The activities of the antiperoxidative enzymes-SOD and catalase decreased in the ethanol and paracetamol treated rats. The changes in the activities of the antiperoxidative enzymes in alcoholism and drug toxicity suggests increased peroxidation, increased synthesis of ecosonoids and increased damage to the tissues. The glutathione levels were decreased in the rats administered ethanol for 30 days, while the glutathione levels increased in the 90 days ethanol treated rats. The paracetamol treatment caused a decrease in the glutathione levels in the normals and the ethanol treated rats.
...
PMID:Role of lipid peroxides, glutathione and antiperoxidative enzymes in alcohol and drug toxicity. 835 54

The hepatotoxicity of 1,2-dichlorobenzene (1,2-DCB) was studied in Fischer-344 (F344) rats administered methyl palmitate (MP) to inhibit Kupffer cell function or superoxide dismutase (conjugated to polyethylene glycol, i.e., PEG-SOD) to scavenge superoxide anions. In rats not pretreated with phenobarbital (PB), administration of either MP or PEG-SOD dramatically reduced the severity of 1,2-DCB-induced liver injury. Both agents reduced the elevations in plasma ALT activities by 80%. PEG-SOD conferred protection when administered 2 hr before or 2 hr after 1,2-DCB. Light microscopic examination of H & E-stained liver sections confirmed that the reductions in plasma ALT activities reflected protection from hepatocellular injury. Interestingly, MP did not protect against 1,2-DCB-induced hepatotoxicity in PB-pretreated rats. The degree of inhibition of 1,2-DCB hepatotoxicity by PEG-SOD in PB-pretreated animals was also less than that in normal rats and was not significantly different. The lack of a significant inhibition of the PB-potentiated hepatotoxicity by both PEG-SOD and MP suggests that reactive oxygen species released from a nonparenchymal source were not as crucial to the 1,2-DCB hepatotoxicity in the PB-pretreated rats as in the normal rats. Our results using both MP and PEG-SOD support the hypothesis that reactive oxygen species released from Kupffer cells play a major role in the progression of 1,2-DCB hepatotoxicity in the F344 rat.
...
PMID:Modulation of 1,2-dichlorobenzene hepatotoxicity in the Fischer-344 rat by a scavenger of superoxide anions and an inhibitor of Kupffer cells. 838 65


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---