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

The plasma levels of alpha-lipoproteins, triglycerides, cholesterol, bilirubin, ALT and AST were followed serially in a group of 10 patients with acute viral hepatitis. Hypertrygliceridaemia, low level of cholesterol and very low level of alpha band of the lipoproteins were found at the onset of the disease. Alpha-lipoprotein reappeared gradually during the course of the disease and was sensitive indices of improvement of liver function. A negative linear correlation was found between alpha-lipoprotein and total bilirubin and between alpha-lipoprotein and ALT.
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PMID:[Alpha-lipoproteins and viral hepatitis (author's transl)]. 22 Jun 61

Hepatic function of 80 children aged under 3 years with Plasmodium vivax malaria were studied during the acute attack and 6 weeks after antimalarial treatment. Raised levels of serum aspartate transaminase (serum AST; SGOT), serum alanine transaminase (serum ALT; SGPT), and alkaline phosphatase were observed in 68%, 39% and 46% of cases respectively. AST levels were higher than ALT ones and the mean level of both enzymes was much higher in patients with hepatomegaly. The hepatic dysfunction which these observations reflect is transient, as these enzymes were found to be at their normal levels 6 weeks after treatment. A transient derangement of liver function is thus a common feature of childhood malaria, and hepatic dysfunction takes place to a significant degree even in P. vivax malaria.
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PMID:Hepatic dysfunction in childhood malaria. 37 43

Twenty biochemical parameters have been studied in 94 athlets of Marcialonga in basic conditions and after 30 min from the end of the competition. Urea, uric acid, creatinin, total proteins, albumin, sodium, calcium, phosphorus and several enzymes (AST, ALT, LAD, CK and ALP) have shown statistically significant increasings. It is, above all, clear the increasing of CK. On the contrary triglycerides have undergone a significant decreasing. The AA. try to explain the results obtained, considering some pathogenetic theories.
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PMID:[A study of biochemical parameters in 94 athlets of Marcialonga (author's transl)]. 75 25

The authors studied the activity of acid phosphatase (AP), lactic dehydrogenase (LDH), aspartic and alanine-aminotranspherases (AST and ALT) in the serum of rats with intact and removed adrenal glands after a severe multifocal trauma induced according to Noble-Collip (300 rpt of the drum with the rotation speed of 37 rpt/min). Adrenalectomy showed practically no influence on the dynamics of the LDH and AP activity. An increase in the activity of the AST and especially of the ALT in the serum of adrenalectomized rats after the trauma was considerably less than in the animals with the intact adrenal glands.
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PMID:[The role of the adrenals in the development of hyperenzymemia in experimental multiple injuries]. 121 54

In previous studies, we reported that the age-dependent hepatotoxicity of galactosamine (GalN) was evident in hepatocytes maintained in primary cultures. Cellular proliferation and tissue repair are not manifested in response to injury in this in vitro system. Neonatal (5-day) rats have ongoing hepatocellular proliferation in contrast to adult (5-month) rats, and should be therefore resilient to GalN toxicity. Liver injury was assessed by serum transaminases (ALT, AST), 3H-thymidine (3H-T) incorporation into nuclear DNA, and content of hepatocellular nuclear DNA. While the dose of 400 mg/kg did not cause any significant liver injury in the neonates, it did produce significant liver injury in adult rats. At a dose of 800 mg/kg, GalN produced significant injury in the neonates. Because 400 mg/kg causes clearly demonstrable liver injury in the adult and no injury in the neonates, this dose was used for further studies. In addition to the above measures of injury, uracil nucleotides (UTP, UDP, and UMP), glycogen, histopathology, and autoradiographic examination of liver sections were used to assess the liver injury in neonatal and adult rats. In a time-course study, all of the above were measured at 0, 12, 24, 36, 48 and 72 h after GalN administration. Serum enzyme elevations as well as the appearance of necrotic and swollen hepatocytes were maximal at 24 h in the adults rats. In contrast to these observations in the adult rats, none of these measurements indicated significant liver injury in the neonates. 3H-T incorporation into nuclear DNA was much higher in the neonatal liver in comparison to the adults reflecting the difference in regeneration. Hepatocellular nuclear DNA was also higher in the neonate and was significantly decreased due to GalN treatment. In the adult rats, the quiescent normal level of 3H-T incorporation and nuclear DNA content were further decreased at 12 h, increased at 48 h and returned to normal low, quiescent levels at 72 h. In the neonates mitotic activity of hepatocytes was higher than in the adult rats. In the adult rats, mitotic activity was increased at 48 h after GalN administration and returned to normal at 72 h. In the neonates GalN did not alter the mitotic activity significantly. These findings demonstrate that in the presence of hepatocellular regeneration, galactosamine toxicity is minimal while in the absence of it, clear toxicity is manifested. In conclusion, while perturbation in uracil nucleotides and related biochemical events may explain the infliction of liver injury by GalN in an age-dependent fashion, the extent of tissue repair impacts decisively on the final outcome of injury.
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PMID:Ongoing hepatocellular regeneration and resiliency toward galactosamine hepatotoxicity. 129 Apr 5

Over a three-year-period, 310 babies with prolonged jaundice admitted to GHKL were studied, to determine the incidence of alpha-1-antitrypsin deficiency as a cause of the problem. Ninety-two babies (29.7%) were found to be alpha-1-antitrypsin deficient. The percentage incidence was found to be highest in Indians (33.3%), followed by Malays (31.9%) and Chinese (26.7%). There was a male preponderance with a M:F ratio of 1.6:1. Most of these babies presented at the hospital at the age of more than two weeks but less than one month. Apart from the problem of prolonged jaundice and alpha-1-antitrypsin deficiency, 2 had associated bleeding problems, 11 associated infections and 3 respiratory problems. Two babies had clinical features of Down's syndrome, 2 had G6PD deficiency and 1 had congenital hypothyroidism. AST, ALT and ALPO4 were high in 20, 26 and 3 babies respectively.
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PMID:Alpha-1-antitrypsin deficiency in babies with prolonged jaundice. 130 30

The influence of Ukrain on the activity of aminotransferases (ALT and AST) and on the serum total protein content was estimated in mice and rats of both sexes receiving single or repeated doses of the drug. It was found that one hour after intraperitoneal (i.p.) administration of Ukrain no characteristic changes were recorded in the activity of the investigated enzymes, or in the serum protein content of animals of either sex. Similar effects were observed after three months treatment with Ukrain in rats of either sex. Only in mice receiving Ukrain for three months was a rise in ALT and AST activity found. No particular changes were observed in the total serum protein level, except for a small decreases in the sera of male mice.
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PMID:Effect of single and three months treatment with Ukrain on aminotransferases (ALT and AST) and on the serum protein level in rodents. 130 51

It has been shown in experiments on white rats that chronic (for one month) intoxication with CCl4 and C2H5OH results in liver injury. It manifests by activation of aminotransferases (ALT, AST) and alkaline phosphatase in blood serum, initiation of lipid peroxidation, depletion of the liver pool of reduced glutathione, and suppression of bile production. The liver preparations (sirepar and vitohepat) reduce hepatotoxicity of the poisons in question. The use of vitohepat and sirepar in combination with carsil potentiated hepatoprotective and antioxidative activity of the liver preparations.
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PMID:[The efficacy of vitogepat and sirepar in combination with karsil in chronic liver lesions]. 130 40

The presence of antibody to the hepatitis C virus was determined in 254 alcoholic patients with non-B chronic hepatitis and a titre of antinuclear antibodies of 1/40 or lower. Alcoholic hepatitis was present in 12 patients, steatohepatitis in 20, active chronic hepatitis in 22, cirrhosis in 181, and hepatocarcinoma in 19. Twenty patients had previously received blood transfusion alone or during surgery, 49 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 4 patients were drug addicts, 41 had received blood transfusion after the diagnosis was made, and 128 presented with alcoholism alone. Anti-hepatitis C antibody was found in 20 out of 2,000 blood donors (1%) in our hospital. Anti-hepatitis C antibody was found in 87 patients (34.2%) in our series, a figure unaltered by past medical history. Patients with anti-HC antibody had higher levels of AST, ALT, total proteins, gamma-globulin, and IgG. The incidence of active chronic hepatitis was higher among patients with anti-HC antibody, whereas the incidence of steatohepatitis was higher among patients without anti-HC. Regarding findings on liver biopsy, the incidence of anti-HC was significantly higher (p less than 0.001) among patients with active chronic hepatitis (72.7%) than in any other group; no significant differences were found between patients with cirrhosis (33.3%), hepatocarcinoma (31.5%), steatohepatitis (15%), or alcoholic hepatitis (16.7%). Among HBsAg-negative patients, the incidence of anti-HC was similar between those with (39.7%) and without other serum markers of HB (32.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence and significance of the C virus antibody in chronic hepatopathy not related to B virus in alcoholics]. 131 33

The development of a serologic assay to detect antibodies directed at an antigen (C-100-3) of the hepatitis C virus (anti-HCV) has been a major breakthrough in the long search for causative agents of non-A, non-B (NANB) hepatitis. The frequency of HCV in those who have end-stage liver disease is not known. Moreover, the rate of recurrence after liver transplantation (OLTx) and the rate of acquisition of new HCV infection as a result of the OLTx experience is as yet unknown. This study was performed in an attempt to answer these questions. The prevalence of HCV in 372 patients undergoing OLTx at the University of Pittsburgh was determined. Those transplanted for HBV-related liver disease with hepatoma had the highest rate of HCV antibody positivity (45.4%) followed by those with metabolic liver disease (42.5%), putative NANB liver disease (41.4%), and cryptogenic cirrhosis (20.9%); those with cholestatic liver disease exhibited the lowest rate (16.2%). HCV antibody was positive in only 26.3% of patients with hepatoma. Of those patients who were negative prior to transplantation, 12.2% acquired HCV antibody post-OLTx. In the putative NANB group, no difference was detected in the AST and ALT prior to transplantation in either the HCV antibody-positive or -negative patients. In patients with cryptogenic cirrhosis, those who were positive for HCV antibody had higher transaminase levels prior to transplantation than did those patients who were HCV antibody negative.
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PMID:Prevalence of hepatitis C virus antibody in a liver transplantation population. 131 88


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