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)

Correlation between pyruvate and lactate contents as well as between enzymes participating in turnover of the substrates (pyruvate- and lactate dehydrogenases, alanine aminotransferase, pyruvate kinase) were studied in rat liver tissue simultaneously with tumor growth and intensive thiaminotherapy. Thiamine, administered into rats carrying carcinosarcoma Woker-256 at a daily dose 12.5 mg/kg body weight, exhibited the normalizing effect on activity of enzymes studied, on quantitative content of LDH isoenzymes and on content of lactate in blood and of pyruvate in liver tissue. Possible effect of thiamine on pyruvate metabolism in tumoral impairment is discussed.
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PMID:[Thiamine and pyruvate metabolism in tumor-bearing rats]. 66 48

In vivo studies with L-[13N]glutamate in the Walker 256 carcinosarcoma implanted under the renal capsule of female Sprague-Dawley rats demonstrate that uptake of glutamate and the rate of incorporation of the nitrogen label from this amino acid into metabolites is slower in the tumor than in nontumorous kidney tissue. Glutamate dehydrogenase, glutaminase, and alanine aminotransferase activities are significantly lower within the tumor than within the adjoining kidney. However, the tumor expresses high levels of aspartate aminotransferase, attesting to the importance of this enzyme in the metabolism of glutamate. Indeed, high performance liquid chromatographic analysis showed that the principal metabolic fate of label derived from L-[13N]glutamate in the tumor is incorporation into aspartate. Measurement of specific activity ratios of glutamate to aspartate shows that the transfer of nitrogen from glutamate to aspartate is rapid and that equilibration of label among components of the aspartate aminotransferase reaction is attained within minutes after tumor uptake. Analyses of the nontumorous portion of the implanted kidney also showed that aspartate is the major recipient of glutamate nitrogen. However, high performance liquid chromatographic analyses of deproteinized tissue revealed that glutamine and ammonia are also significant 13N-labeled metabolites formed from L-[13N]glutamate within the kidney. Proportionately lower amounts of these labeled metabolites were found in the tumor.
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PMID:Short-term metabolic fate of L-[13N]glutamate in the Walker 256 carcinosarcoma in vivo. 197 67

The antitumor-active bis-beta-diketonato metal complexes dichlorobis(1-phenylbutane-1,3-dionato)titanium (IV) and diethoxybis(1-phenylbutane-1,3-dionato)titanium (IV) (prop. INN: budotitane) are active against several transplantable tumors. Activity was demonstrated by treating the intramusculary, subcutaneously and intraperitoneally transplanted sarcoma 180 tumor and against the Walker 256 Carcinosarcoma as well. In these models an increase in survival time up to T/C-values of 200 to 300% (T/C = (median survival time of treated animals to that of controls) X 100) and reduction of tumor weight to 30 or 0%, compared with the untreated control animals, was demonstrated. The therapy of the leukemias P 388 and L 1210 turned out to be statistically significant but only marginal in terms of increase in survival time (T/C approximately 130%). The toxicological experiments demonstrate single doses up to 40 mg/kg, given intravenously in female SD-rats, as to be well tolerable. The dose 80 mg/kg caused lethality in the range between 14 and 50% in 3 independent experiments. The spontaneously dying animals showed haemorrhagic pleural effusions and haemorrhagic oedematous areas of the lung. Histopathologically hyperemia and multiple focal necroses of the liver were found. The described lung toxicity was found only in high, single and lethal doses. Chronic doses of 10 to 20 mg/kg caused only mild liver toxicity. The laboratory parameters were increased in the values of the enzymes GOT, GPT and LDH. No evidence of myelosuppression was found in the peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preclinical evaluation of dichlorobis(1-phenylbutane-1,3-dionato)titanium (IV) and budotitane. Two representatives of the new class of antitumor-active bis-beta-diketonato metal complexes. 356 44

The levels of L-lactate and pyruvate as well as the enzymes of their conversion (lactate dehydrogenase in direct and reverse reactions, pyruvate dehydrogenase, pyruvate kinase, alanine transaminase) have been studied simultaneously in the liver and skeletal muscle of rats bearing carcinosarcoma Walker 256, control animals and after additional oxythiamine administration. Properties of oxythiamine independent of its anticoenzymic activity manifest themselves in the body of tumour-bearing animals to a greater extent. After the antivitamin administration there occur strong inhibition of pyruvate kinase, activation of alanine transaminase, normalization of the L-lactate level in the tissues.
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PMID:[Lactate and pyruvate metabolism in the tissues of rats with Walker carcinosarcoma injected with oxythiamine]. 651 Mar 36

We report a 61-year-old Japanese man who died of complications of esophagus cancer surgery. He was well until his 55 years of the age, when he had an onset of speech disturbance and hand writing. He was seen by a neurologist who prescribed Menesit 600 mg/day. His symptoms improved with this medication. In 1993, three years after the onset, he started to show gait disturbance and easy to fall. In 1995, he noted difficulty in eye opening. He visited our clinic on October 26, 1996. On examination, he showed vertical gaze paresis, masked face, nuchal rigidity, small step gait, freezing phenomena, and festination. His mental status was normal. He was treated with 800 mg/day of Menesit, 800 mg/day of L-dops, and 10 mg/day of bromocriptine with little improvement in his symptoms. Cranial CT scan revealed some dilatation of the third ventricle. Subsequent clinical course was one of the slow progression of his parkinsonism. In September of 1997, he noted difficulty in swallowing. He was admitted to the gastrointestinal service of our hospital on October 14, 1997. On admission, neurologic status was essentially similar to the previous one, but he showed more advanced state of his parkinsonism. Upper gastrointestinal series revealed a mass lesion of about 11.5 cm in length protruding into the lower esophagus lumen. Subtotal esophagus resection including the mass was performed on December 2, 1997. The stomach was elevated for anastomosis with the upper esophagus. No metastases were found in the mediastinum except for two lymph nodes in the para-esophageal region. The subsequent course was complicated by marked elevation of GOT, GPT, LDH, total bilirubin as well as direct bilirubin, alkaliphosphatase, and amylase starting in the evening of the surgery. On December 7, leukocytosis and pneumonic shadow were seen involving his right lung. On December 10, he developed cardiopulmonary arrest. He was once resuscitated; however, he developed cardiac arrest again seven hours later and pronounced dead. He was discussed in a neurologic CPC. The chief discussant arrived at the conclusion that the patient had PSP and the cause of the death was ascribed to circulatory disturbance to the liver. The discussant also thought that the terminal course was complicated by cholangitis or cholecystitis, sepsis, and pulmonary embolism. Surgical specimen of the esophagus tumor revealed carcinosarcoma. Postmortem examination revealed yellowish discoloration of the peritoneum and mesenterium, and accumulation of clouded ascites indicating the presence of peritonitis. Inflammatory change extended to the mediastinum. On microscopic examination, various kinds of bacilli and candida spores were seen. The liver was enlarged and a perforation was noted in the gallbladder causing biliary necrosis in the adjacent liver. An extensive infarct was seen in the left lobe of the liver; this was found to be due to obstruction of the hepatic artery at the site of the duodenohepatic mesenterium and obstruction of intrahepatic portal vein secondary to retrograde intrahepatic cholangitis in the left lobe. A piece of surgical threads was seen adjacent to the hepatic artery; foreign body granulomatous reaction was seen surrounding the surgical thread. The rupture of the gallbladder appeared to be due to the obstruction of the left branch of the hepatic artery. Neuropathologic examination revealed extensive degeneration of the pallidum, the substantia nigra, and the subthalamic nucleus and presence of neurofibrillary tangles in the remaining neurons. The neuropathologic findings were consistent with progressive supranuclear palsy, although the pathologic changes in the midbrain tegmentum was only mild gliosis.
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PMID:[A 61-year-old man with progressive gait disturbance, freezing, and vertical gaze paresis who developed esophagus cancer]. 986 33