A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases.
01 Jul 1957-American Journal of Clinical Pathology (AMERICAN JOURNAL OF CLINICAL PATHOLOGY)-Vol. 28, Iss: 1, pp 56-63
About: This article is published in American Journal of Clinical Pathology.The article was published on 1957-07-01. It has received 9424 citations till now.
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TL;DR: Side effects were generally mild and included hepatic dysfunction, elevation in serum amylase and blood ammonia, and mild depression and lethargy (in 4 patients with elevated blood ammonia levels).
Abstract: Summary Escherichia colil-asparaginase was administered to 29 children with leukemia in dosage schedules of 200 i.u./kg/day for a minimum of 7 days or 5000 i.u./kg twice weekly for a minimum of 2 weeks. A complete remission was achieved in 7 patients (20%) by l-asparaginase alone and in 2 further patients by a combination of l-asparaginase and prednisone. Remission was maintained with p. o. methotrexate (30 mg/sq m twice weekly) with a median duration of 90 days. Reinduction, generally with the original form of therapy, was possible in 2 out of 6 patients. Hypocellularity of the bone marrow was encountered in 2 patients. Twelve patients with a variety of solid tumors failed to show any response to different dosage schedules. The most serious side effect was hypersensitivity affecting 13 patients; in 2, the blood pressure was unobtainable for several minutes. A serum sickness-like reaction occurred in 1 patient, pulmonary edema occurred in 2 patients, and diabetic ketoacidosis occurred in 1 patient. Other side effects were generally mild and included hepatic dysfunction, elevation in serum amylase and blood ammonia (27 out of 28 patients), and mild depression and lethargy (in 4 patients with elevated blood ammonia levels). Pancreatitis and renal failure were not observed. There were no fatalities.
70 citations
TL;DR: Twenty men and one woman with porphyria cutanea tarda were treated with oral chloroquine, 125 mg twice weekly to treat nausea and vomiting.
Abstract: SUMMARY
Twenty men and one woman with porphyria cutanea tarda were treated with oral chloroquine, 125 mg twice weekly.
In nineteen of the patients chloroquine was taken for 8–5 months on average before complete clinical and biochemical remission occurred. Initially, treatment led to a considerable increase in urinary uroporphyrin and a mild increase in serum transaminases, but no adverse clinical reactions were observed. As the mechanism of chloroquine action in porphyria cutanea tarda has not yet been clarified, special caution must be observed when it is used therapeutically.
70 citations
TL;DR: It is suggested that acetylbergenin has hepatoprotective effects against GalN-induced hepatotoxicity by inhibiting lipid peroxidation and maintaining an adequate level of GSH for the detoxification of xenobiotics as underlying hepatoprotsective mechanisms.
70 citations
TL;DR: The regulation of glycogen meta- bolism in these tissues is a matter of delicate equili-brium between a number of enzyme systems, defects in which may cause profound alterations in the amount and structure of the glycogen.
Abstract: Glycogen is found in almost every tissue in the body, but is especially abundant in the liver where the content is very variable, and in skeletal muscle where the content is relatively constant except during prolonged exertion. The regulation of glycogen metabolism in these tissues is a matter of delicate equilibrium between a number of enzyme systems, defects in which may cause profound alterations in the amount and structure of the glycogen. The clinical results of such alterations have been known for many years as diseases of glycogen storage, or better, as the glycogenoses. The first cases, affecting liver and kidneys, were recognized by von Gierke in 1929. Since then other types of glycogenosis have been described and elucidated, including some which involve skeletal muscle. This study deals with the clinical, histological, and biochemical identification of two dissimilar cases of skeletal muscle glycogenosis. One, in a 48-year-old man, is the fourth of its type to be formally elucidated; the other, in a 4-year-old boy, is the second case reported and the first to be fully described.
70 citations
TL;DR: The administration of aspartame alone or in the presence of mild systemic inflammatory response increases oxidative stress and inflammation in the brain, but not in the liver, and causes dose-dependent inhibition of brain serotonin, noradrenaline, and dopamine.
Abstract: This study aimed at investigating the effect of the sweetener aspartame on oxidative stress and brain monoamines in normal circumstances and after intraperitoneal (i.p.) administration of lipopolysaccharide (LPS; 100 μg/kg) in mice. Aspartame (0.625–45 mg/kg) was given via subcutaneous route at the time of endotoxin administration. Mice were euthanized 4 h later. Reduced glutathione (GSH), lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), and nitrite concentrations were measured in brain and liver. Tumor necrosis factor-alpha (TNF-α) and glucose were determined in brain. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in liver. The administration of only aspartame (22.5 and 45 mg/kg) increased brain TBARS by 17.7–32.8%, decreased GSH by 25.6–31.6%, and increased TNF-α by 16.7–44%. Aspartame caused dose-dependent inhibition of brain serotonin, noradrenaline, and dopamine. Aspartame did not alter liver TBARS, nitrite, GSH, AST, ALT, or ALP. The administration of LPS increased nitrite in brain and liver by 26.8 and 37.1%, respectively; decreased GSH in brain and liver by 21.6 and 31.1%, respectively; increased brain TNF-α by 340.4%, and glucose by 39.9%, and caused marked increase in brain monoamines. LPS increased AST, ALT, and ALP in liver tissue by 84.4, 173.7, and 258.9%, respectively. Aspartame given to LPS-treated mice at 11.25 and 22.5 mg/kg increased brain TBARS by 15.5–16.9%, nitrite by 12.6–20.1%, and mitigated the increase in monoamines. Aspartame did not alter liver TBARS, nitrite, GSH, ALT, AST, or ALP. Thus, the administration of aspartame alone or in the presence of mild systemic inflammatory response increases oxidative stress and inflammation in the brain, but not in the liver.
70 citations
Cites methods from "A colorimetric method for the deter..."
...Tissue AST (Aspartate Aminotransferase) and ALT (Alanine Aminotransferase) activities were determined using kits provided by Stanbio Laboratory (USA) according to Reitman and Frankel (1957)....
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