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)

Eight otherwise healthy insulin-dependent diabetic patients were subjected to controlled, symptomatic hypoglycaemia for 20 min (median glucose concentration 1.7 mmol/l, range 1.0-2.6 mmol/l). Concentrations of plasma adrenaline and plasma vasopressin were significantly increased, indicating normal counter-regulatory responses for these hormones. Plasma activities of the hepatic enzymes AST, ALT, LDH, GGT, and CK did not increase during or following the period of hypoglycaemia. Thus, abnormal plasma enzyme activities noted after clinical hypoglycaemia should be fully investigated, and not disregarded as due to the hypoglycaemic episode.
 ...
PMID:A rise in the plasma activities of hepatic enzymes is not a common consequence of hypoglycaemia. 289 67

16, 16 Dimethyl prostaglandin E2 (dmPGE2), a known cytoprotective agent, was examined for its ability to alter the course of fulminant hepatitis in an experimental model of fulminant viral hepatitis, murine hepatitis murine hepatitis type 3 (MHV-3). Fully susceptible BALB/cJ mice, infected with 100 50% lethal doses (LD50) of MHV-3 developed histologic and biochemical evidence of fulminant hepatitis, as evidenced by massive hepatic necrosis with hypoglycemia, metabolic acidosis, and a markedly elevated serum alanine aminotransferase (ALT) (mean, 1,402 +/- 619 IU/liter). In contrast, animals treated with dmPGE2 either before or after infection (up to 48 h) demonstrated a marked reduction in both histologic and biochemical evidence of liver damage as characterized by normal blood glucose, total CO2, and ALT determinations (mean ALT, 63 +/- 40 IU/liter). Treatment of infected mice with PGF2 alpha demonstrated no cytoprotective effects. High titers of infectious virus were recovered from the livers of both dmPGE2-treated and -untreated animals throughout the course of infection. In a parallel in vitro study, dmPGE2 (10(-4)-10(-8) M) demonstrated a similar cytoprotective effect on monolayers of isolated cultured hepatocytes from fully susceptible BALB/cJ mice infected at a multiplicity of infection of 0.1, 1.0, and 10.0. In addition, splenic macrophages recovered from infected and untreated BALB/cJ mice demonstrated a marked augmentation in procoagulant activity (PCA) from a basal 10 +/- 5 mU/10(6) splenic macrophages to a maximum of 615 +/- 102 mU/10(6) splenic macrophages, whereas no increase in macrophage PCA was detected in infected animals treated with dmPGE2. These results suggest that dmPGE2, without detectably altering viral replication or infectivity in vivo, confers a marked cytoprotective effect on hepatocytes both in vivo and in vitro, and prevents the induction of macrophage PCA in vivo in fully susceptible BALB/cJ mice after murine hepatitis virus type 3 infection.
 ...
PMID:16, 16 Dimethyl prostaglandin E2 prevents the development of fulminant hepatitis and blocks the induction of monocyte/macrophage procoagulant activity after murine hepatitis virus strain 3 infection. 362 90

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
 ...
PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

The animals examined were 30 sows after eleven or more farrowings (pluriparous sows) and 26 primiparous sows. The pluriparous animals were 75.1 months old on the average and had farrowed an average of 13.23 litters. The mean age of the primiparous sows was 12.8 months. The blood sera of pluriparous sows had higher concentrations of total protein and urea and lower levels of 11-hydroxycorticosteroids (11-OHCS) and lower aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase activities than those of primiparous sows. The pluriparous sows showed mild hypoglycaemia and hypocholesterolaemia. When insulin was injected i.m. in the dose of 1 I.U. per kg body mass, a decrease in blood serum glucose, total protein and potassium levels was recorded 60 min later in both pluriparous and primiparous sows; a significant rise in 11-OHCS concentration occurred only in the primiparous sows. It was concluded that the response of the hypothalamo-pituitary-adrenal axis in pluriparous sows to an insulin load is reduced. Studies of pluriparous sows contribute to a better understanding of the ontogenetic development of pigs throughout their postnatal development.
 ...
PMID:Biochemical changes in sows after eleven or more farrowings. 670 30

Sixteen athletes (11 men, 5 women), averaging 21 years of age, were studied before and after four weeks of daily exhaustive exercise (six days/week) during an endurance training course. In comparing blood chemistries before and after training, concentrations of blood glucose, total serum lipids, serum triglycerides, and serum cholesterol were significantly reduced; serum free fatty acid ( SFFA ) level was significantly increased; and serum protein and serum phospholipid concentrations remained unchanged. It was concluded that exhaustive training produces reduced blood glucose (but not clinically significant hypoglycemia) with increased fat utilization as a result of depletion of carbohydrate storage and that such training reduces the resting levels of serum cholesterol and serum triglycerides. The increased hematocrit, serum Na+, and serum K+ concentrations observed were presumably due to plasma water loss from excessive perspiration. Concentrations of blood urea nitrogen (BUN) and serum glutamic-oxaloacetic transaminase (SGOT) were increased significantly; serum glutamic-pyruvic transaminase (SGPT) and serum creatinine showed no significant changes. None of the athletes showed evidences of water-electrolyte deficiency syndrome, renal dysfunction, or liver cell damage, despite a persistent mild degree of dehydration and catabolic state noted after training.
 ...
PMID:Metabolic effects of exhaustive training of athletes. 674 92

In rats, i.v. administration of praseodymium, cerium and lanthanum (3 to 14 mg/kg) produced a dose-dependent increase in the serum activities of GOT, GPT and SDH. These dose-response curves of serum enzyme activities were shifted to the right by simultaneous treatment with silybin (75 mg/kg i.p.). Silybin also attenuated the increase of bromosulphthaleine retention and prevented the accumulation of liver triglycerides induced by praseodymium (7 mg/kg i.v.). Furthermore, silybin reduced the mortality rate of rats treated with high doses of the lanthanides. Rats treated with praseodymium (7 mg/kg i.v.) developed a pronounced hypoglycemia. On the 3rd day after praseodymium injection liver glycogen decreased to 4%, liver glutathione (GSH) to 82%, hepatic microsomal cytochrome P-450 content to 53%, aniline hydroxylase activity to 58% and aminophenazone demethylase activity to 40% of the control values. Silybin prevented praseodymium-induced hypoglycemia completely and the changes in the biochemical parameters of liver function partially but did not influence the decrease of liver GSH.
 ...
PMID:The influence of silybin on the hepatotoxic and hypoglycemic effects of praseodymium and other lanthanides. 719 8

Chlordecone (Kepone) amplification of CCl4 toxicity occurs at small, nontoxic levels of chlordecone and CCl4 and results in highly increased irreversible hepatotoxicity culminating in lethality. Although it is generally assumed that CCl4 lethality is due to hepatic failure, no definitive studies are available in the literature bridging massive liver failure and death. The present studies were designed to evaluate whether hepatic failure is the cause of the lethality during chlordecone-amplified CCl4 toxicity. Male Sprague-Dawley rats were maintained on control or a chlordecone (10 ppm) diet for 15 days and injected with CCl4 (100 microliters/kg, ip) on Day 16. Rats were killed at 0, 6, 12, 24, 36, and 48 hr after CCl4 challenge. Hepatic failure was evaluated by measuring plasma glucose, ammonia, bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), sorbitol dehydrogenase (SDH), hepatic ATP, glycogen, and by histological and histomorphometric analyses. Plasma creatinine, urea, and kidney histopathology were also assessed for possible renal injury. As expected CCl4 administration to chlordecone-pretreated rats resulted in 20% lethality by 36 hr, which progressed with time, and all rats died within 72 hr. A significant and progressive hypoglycemia was observed with a 60% reduction in plasma glucose at 48 hr. Hepatic glycogen content dropped precipitously. Similarly, hepatic ATP levels remained suppressed (80% of control) at all the time points studied. Plasma ammonia levels were significantly elevated, and by 48 hr, a threefold increase was observed. Plasma ALT, AST, SDH, and bilirubin increased progressively until the death of rats receiving the chlordecone + CCl4 combination.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hepatic failure leads to lethality of chlordecone-amplified hepatotoxicity of carbon tetrachloride. 750 40

The pharmacokinetics and toxicity of intravenous lonidamine were investigated in dogs receiving four cycles of lonidamine (400 or 800 mg/m2) +/- whole-body hyperthermia (WBH). Clearance and volume of distribution in dogs receiving lonidamine during WBH increased 1.6-2.3 and 1.9-3.5-fold respectively, relative to dogs receiving lonidamine under euthermic conditions (p < 0.02). In dogs receiving lonidamine under euthermic conditions or 400 mg/m2 + WBH, the area under the lonidamine concentration versus time curve (AUC) measured during the fourth treatment was 21-58% lower than the first treatment AUC. However, in dogs receiving 800 mg/m2 + WBH, the fourth treatment AUC was four-fold higher than the first treatment AUC (p < 0.02). This suggests repeated exposure to 800 mg/m2 lonidamine and WBH impairs lonidamine metabolism. Weakness, hypoglycaemia, and elevations in amylase, alanine aminotransferase, alkaline phosphatase and bilirubin were more severe or occurred exclusively in dogs receiving 800 mg/m2 + WBH. Since these changes were attributable to marked AUC increases, which occurred secondary to repeated exposure to 800 mg/m2 lonidamine during WBH, 400 mg/m2 was identified as the maximum tolerable dose to be administered intravenously to dogs during WBH.
 ...
PMID:Effect of whole-body hyperthermia on the pharmacokinetics and toxicity of lonidamine in dogs. 759 7

Megaesophagus was diagnosed in 9 adult ferrets. Clinical history of the ferrets included regurgitation, difficulty in swallowing, partial anorexia, and lethargy. Cachexia, dehydration, weakness, and ptyalism were observed on physical examination. Radiography revealed the esophagus of each ferret to be dilated in the thoracic and cervical regions. Of 4 ferrets that had lymphocytopenia, 2 had concurrent leukopenia. Serum biochemical analysis revealed high activity of alanine transaminase (4 ferrets) and aspartate transaminase (3), and hypoglycemia (4). Treatment included administration of fluid, antibiotics, and agents directed against possible primary causes of megaesophagus. Treatments were ineffective, and all of the ferrets died or were euthanatized. All 6 ferrets that were submitted for necropsy had bronchopneumonia, hepatic lipidosis, mild esophagitis, and gastritis. The etiopathogenesis of megaesophagus in the ferrets was not determined.
 ...
PMID:Megaesophagus in nine ferrets. 796 Oct 71

We reviewed 15 cases of poisoning from ingestion of yellow phosphorus-containing fireworks and analyzed its associated acute hepatotoxic effects. Two patients (13%) had no clinical or biochemical evidence of hepatic damage, four (27%) had subclinical hepatic injury, five (33%) manifested varying degrees of hepatocellular necrosis and cholestasis, and four (27%) had fulminant hepatic failure. Jaundice was not associated with mortality (p > 0.05), but it appeared to predict the length of hospital confinement. Early elevations in transaminase and alkaline phosphatase, a more than tenfold increase in alanine aminotransferase, and a severe derangement in prothrombin time all indicate poor prognosis. Metabolic acidosis and hypoglycemia were significantly associated with mortality (p < 0.01 and p < 0.05, respectively). The use of intravenous N-acetylcysteine did not significantly alter disease outcome (p > 0.05). Our mortality rate was 27%, confirming that yellow phosphorus is extremely lethal when ingested. Its indiscriminate use in the manufacture of fireworks should be eliminated.
 ...
PMID:Acute hepatotoxicity from ingestion of yellow phosphorus-containing fireworks. 858 80


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