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)

A study of the various biological parameters of the blood in the genetically obese Zucker rat, the nonobese Zucker rat, and the Wistar rat has revealed great similarity between the two latter types of animals. On the other hand, in genetically obese Zucker rats as compared with the nonobese ones, (1) the blood mass per unit of weight was lower; (2) the level of nitrogenous degradation compounds was the same; (3) the lipase activity was lower; (4) the levels of substances for which liver plays a crucial role--all lipid and protein fractions, glucose, and the enzyme GPT--were higher; (5) the levels of Ca, Zn, Fe, Cu and Pi were high; (6) the blood and bone-marrow cells were unremarkable.
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PMID:Biological parameters of the blood in the genetically obese Zucker rat. 9 25

1. The activities of lysozyme, acid and alkaline phosphatases, beta-glucuronidase, amylase, lipase, glutamate-oxalacetate transaminase, and glutamate-pyruvate transaminase in the whole hemolymph and 4000 g pellets and supernatants of Mya arenaria were determined. 2. All of these enzymes, except for amylase, occurred in whole hemolymph as well as in the 4000 g pellet and supernatant. 3. Based on earlier observations, these enzymes are believed to be of cellular origin within hemolymph cells. 4. In the case of amylase, it only occurred in the whole hemolymph and/or serum and is believed to have originated from the crystalline style.
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PMID:Selected enzyme activities in Mya arenaria hemolymph. 9 92

In rats, shortly after ligation of superior mesenteric artery serum enzyme activities are found significantly altered. Those changes concern aspartate aminotransferase (GOT), alanine aminotransferase (GPT), lipase, alpha amylase, and isocitrate dehydrogenase as well as glutamate dehydrogenase. The causes are discussed. The authors emphasize that the assessment of serum enzymes possibly gives some help in diagnosing acute intestinal ischemias in early stages.
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PMID:[Behavior of various serum enzymes following ligation of the superior mesenteric artery in the rat (preliminary report)]. 60 23

The development of toxicity to 4'-demethylepipodophyllotoxin-9-(4,6,-O-thenylidene-beta-glucopyranoside) an epipodophyllotoxin with oncolytic activity, was characterized in mice treated three times at 3-day intervals with 10 mg of drug i.p. per kg of body weight. Changes in organ function and general metabolism were determined by measuring 18 constituents of blood for up to 10 weeks after drug administration. The results indicate three distinct phases of toxicity to 4'-demethylepipodophyllotoxin 9-(4,6-O-2-thenylidene-beta-glucopyranoside). Acute toxicity developed within the first 10 days and was expressed by a depressed hematocrit and elevated plasma levels of glutamate-pyruvate transaminase, glutamate-oxaloacetate transaminase, lactic dehydrogenase, amylase, lipase, and uric acid. By 4 weeks, levels ahd returned to normal. The acute phase was followed by a chronic phase, which was characterized by progressive decreases in plasma levels of glucose, cholesterol, albumin, and total protein. Finally, about 7 weeks after treatment, a terminal phase indicated by correlated increases in glutamate-pyruvate transaminase, glutamate-oxaloacetate transaminase, lactic dehydrogenase, and blood urea nitrogen became apparent. Plasma levels of creatine phosphokinase, calcium, inorganic phosphate, total bilirubin, ketones, and alkaline phosphatase did not change. Although the pancreas liver and marrow were all affected during acute toxicity, boserved changes in blood components during the chronic and terminal phases correlate best with continued hepatotoxicity. The present evidence on delayed toxicity to 4'-demethylepipodophyllotoxin 9-(4,6-o-2-thenylidene-beta-D-glucopyranoside) is most compatible with irreversible hepatotoxocity which leads to metabolic deficiencies and terminates in death of mice.
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PMID:Acute, chronic and terminal toxicity to 4'-demethylepipodophyllotoxin thenylidene glucoside (VM26) in mice. 113 30

The reasons of fat embolism as well as the following fat embolism syndrome are most likely long bone fractures, especially if the femur is participated. On the other hand there are cases, where a severe concussion of the entire body caused fat embolism. But it is also supposed, that intramedullary reaming as well as the insertion of knee- and hip-prostheses could be a releasing factor, because the applicated pressure on the medullary canal can cause a fat release in the systemic blood system. The morbidity depends on age and fracture, which is on fractures between 0.9 and 2%. The most affected group are people between 18 and 28 years of age. The fat embolism is manifesting at 46-60% of the patients in the first 24 hours and over 90% of the patients are affected in the first three days. If you look at the metabolic changes, you will find shortly after the fracturing process a rapid increase of free fatty acids (FFA), as well as an increase of the plasmatic enzyme levels (lipase, GPT, GOT, GLDH, LDH, etc.), catecholamines and glucocorticoids. In order to discuss the pathogenesis in a fairly complete way, you have to take different theories into consideration, because several parallel running processes--which are influencing each other--are leading to the syndrome. Infloating theory: Proceeding on the assumption that contents of the bone marrow are floating out of the fracture gap into the venous system and are leading to fat embolism in the lungs. Lipase theory: You can diagnose in 50-70% of the fracture patients an increase of the lipase level, which is correlating with the manifestation of the fat embolism. The lipase releases fat from the body depositories in addition to the fat, who is coming out of the fracture gap. Shock and coagulation theory: During shock the microcirculation is decelerated, the blood viscosity is increased and the suspension stability of the cellular blood components is decreased, which is leading to the sludging phenomenon. So the capillaries of the lungs and the brain are a kind of sludge filter of the blood, that is changed in its suspensions stability. Free fatty acids theory: Primary existing capillary defects are reasonable caused by free fatty acids (FFA). They are hydrolyzed of the neutral fats and are histotoxic for the walls of the blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Fat embolism and fracture, a review of the literature]. 135 89

The serum hormone (T3, FT3, T4, FT4, TSH, hTG, a-hTG, GH, PTH, PRL, Cortisol) concentrations, the inorganic phosphate complexes (HPO2-4, H2PO-4, NaHPO-4, KHPO-4, CaHPO4, MgHPO4) and the enzyme activities (Amylase, Lipase, AP, ACE, GOT, GPT, psi-ChE, CK, gamma-GT, LDH) were investigated in 13 haemodialysed children, 7 kidney-transplanted children and in 15 healthy controls. This study confirmed that the kidney plays an important role in the metabolism of hormones. Prior to kidney transplantation 8 of the 11 tested hormone levels of haemodialysed children significantly differed from those of healthy controls, however, after kidney transplantation only two parameters did. The effect of dialysis is the least on the CaHPO4 complex among the different inorganic phosphate complexes. This may play a role in vascular calcification in chronic renal failure patients. The amylase and lipase activity were elevated in haemodialysed group, while in kidney-transplanted children the angiotensin converting enzyme (ACE) and alkaline phosphatase (AP) differed from those of the control group.
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PMID:The serum hormone levels, phosphate complex concentrations and enzyme activities in haemodialysed and kidney-transplanted children. 169 May 69

Eighty-three patients suffering from upper abdominal pain were studied to evaluate the contribution of commonly used biochemical markers in the diagnosis of acute pancreatitis. On admission to hospital, serum amylase, lipase, total bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transferase activities were measured. By stepwise logistic discrimination, only two determinations appeared to be of clinical value: lipase and alkaline phosphatase activities. A classification rule was established including these two measurements and its diagnostic performance evaluated by a jackknifed method amounted .83%. ROC curves were used to assess sensitivity and specificity. Our study clearly shows that serum lipase measurements should be preferred to amylase measurements, and that our two-test classification rule provides an efficient aid in clinical decision-making.
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PMID:Combined diagnostic value of biochemical markers in acute pancreatitis. 169 97

Seventeen serum markers (including 9 enzyme activities) for eventual tissue damage were studied after ESWL in 40 patients with unilateral kidney calculosis. No changes were established in the 8 non-enzymic parameters and the activities of amylase, lipase, AST (GOT), ALT (GPT) and CK-MB. A statistically significant increase was found in LDH, alpha-HBDH, CK (twice) and glutamate dehydrogenase (3 times). The slight elevation of LDH and alpha-HBDH could be due to haemolysis caused by the shock waves. Increased activity of CK suggested myolysis and that of GlDH a hepatocellular damage.
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PMID:Acute changes of serum markers for tissue damage after ESWL of kidney stones. 188 66

Clinically healthy silver foxes obtained from a closed colony were investigated for the purpose of establishing base-line data for this species. The anthropometry (body weight; body length; length and width of the head; width, depth, and circumference of the chest; length of the tail), anatomical measurements (weight; longitudinal and transverse length; thickness of the main organs) and serum biochemical assays (AST, ALT, ALP, LDH, CK, lipase, GGT, T-Cho, beta-Lipo, TG, Phos-Lip, Tp, T-Bil, UA, BUN, Crea, Glu, Ca, IP, Mg, Fe, Na, K, Cl, LDH and CK isoenzymes) were carried out. The data were presented as mean values with standard deviations, and compared with those of the dog. The coefficient of variation (CV) for each of the anthropometric parameters was low, except for that of female body weight for which the CV was 17%. The body size of the male was larger than the female, and the weights of the main organs, corresponding to body size, were greater than the female. The results were equivalent to those for a Beagle dog aged between 3 and 5 months. Significant differences between the sexes were detected in the following parameters: concentrations of BUN, beta-Lipo and T-Bil (p less than 0.01); concentration of Mg and Glu (p less than 0.05); activity of LDH and lipase (p less than 0.05). The biochemical data ware uniform with some exceptions. These were AST (142 IU/l) and ALP (122 IU/l) in a 5-year-old male fox, Glu (over 200 mg/dl) in four 2-year-old female foxes, CK (629 IU/l) in a 2-year-old female fox, and finally CK (366 IU/l) and lipase (428 IU/l) in an 8-year-old female fox, all of which were elevated. These data were similar to the reference values for the dog previously reported. The reference values presented in this report for the silver fox will be valuable as a guide for clinical diagnosis and research.
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PMID:Reference data on the anatomy and serum biochemistry of the silver fox. 195 49

The toxicity of L-canavanine was investigated because of its demonstrated potential as an antitumor drug. This natural product was only slightly toxic to Sprague-Dawley rats following a single sc injection: the LD50 was 5.9 +/- 1 8 g/kg in adult rats and 5.0 +/- 1.0 g/kg in 10-day-old rats. Following a single dose of 2.0 g/kg, the systemic clearance value for canavanine in adult rats was 0.114 liter/hr, the volume of distribution at steady state was 0.154 liter, and the half-life was 1.56 hr. Forty-eight percent of the dose was excreted unaltered in the urine following an iv injection, and 16% of a sc dose was recovered in the urine. Bioavailability of a 2.0 g/kg sc dose was 72%. Single oral doses of canavanine were less toxic to adult rats than sc injections. Bioavailability of a 2.0 g/kg po dose was 43%, and only 1% of the administered canavanine was recovered in the urine. Twenty-one percent of the administered canavanine remained in the gastrointestinal tract 24 hr after an oral dose. Less than 1% of a 2.0 g/kg dose of L-[guanidinooxy-14C]canavanine was incorporated into the proteins of adult and neonatal rats 4 or 24 hr following administration. Repeated sc administration of canavanine resulted in more severe toxicity. Weight loss and alopecia were observed in rats given daily sc canavanine injections for 7 days. Food intake was decreased by 80% in adult rats subjected to this dosing regimen, but returned to normal after canavanine injections were terminated. Histological studies of tissues from adult rats treated with 3.0 g/kg canavanine daily for 6 days revealed pancreatic acinar cell atrophy and fibrosis. Serum amylase and lipase levels were elevated following one sc injection of 2.0 g/kg canavanine; after three daily injections both serum enzymes were depleted. Elevations in serum glucose and urea nitrogen, and depletion of cholesterol, were observed. The most significant changes were severe attenuations of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activity.
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PMID:Toxicity and pharmacokinetics of the nonprotein amino acid L-canavanine in the rat. 244 82


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