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)

Slc/ddY mice (10 male, 10 female per group) were given a single p.o. intubation of tris (1,3-dichloro-2-propyl) phosphate (TDCPP) in olive oil and were observed for 14 days. LD50 values of male and female mice were 2.67 (2.52 approximately 2.83) and 2.25 2.25 (2.12 approximately 2.39) g/kg, respectively. The animals revealed ataxic gait, hyperactivity, and convulsion. Slc/ddY mice (12 male, 12 female er group) were administered diet containing 1.33, 0.42, 0.13, 0.04, and 0.01% of TDCPP for 3 months. Male and female mice of the 1.33% group showed emaciation, rough hair, and tremor; and all animals died within one month. Hematological studies showed slight anemia in males of the 0.42% group and females of the 0.42% and 0.13% groups. They also exhibited a tendency to increase ALP and GPT levels. The animals of the 0.42%, 0.13% and 0.04% groups exhibited tendency to increase liver weights and kidney weights in both sexes. Histopathologically, very slight focal necrosis was recognized in the liver in only 2 females of the 0.42% group. The NOEL under this condition is 0.01% in the diet of tris (1,3-dichloro-2-propyl) phosphate (male: 13.2 mg/kg/day, female: 15.3 mg/kg/day).
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PMID:[Acute and subacute toxicity studies of tris (1,3-dichloro-2-propyl) phosphate on mice]. 263 31

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

The estimation of plasma alanine aminotransferase (ALT) has been proposed as a surrogate test to identify potential non-A, non-B hepatitis carriers in blood donor populations. This report describes an ALT screening procedure which uses wells of microtitration trays as reactant vessels. The method utilizes a rate reading photometer, is economical and conveniently fits into the routine workflow. Within-batch and between-batch precision was 4.1% and 6.3% at enzyme concentrations of 49 IU/I. Results of testing 29,675 healthy blood donors gave values which ranged between 1.0 IU/I and 214 IU/I. A study of 762 donations showed a significant difference in mean ALT values between males and females (p less than 0.01). When a cut-off value of 46 IU/I was used, 2.5 percent of donations were considered unsuitable for transfusion. The medico-legal implications that may arise from the introduction of this screening test into the routine work flow are discussed.
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PMID:Surrogate testing for non-A, non-B hepatitis in Queensland, Australia: an ALT microtitre tray method for screening blood donors. 314

Acute toxicity of cefodizime sodium (THR-221) was examined in mice of both sexes, rats of both sexes (including 5-day-old young), and male dogs. The LD50 values of THR-221 (mg/kg) were as follows: (1) mice: intravenous, 7200 for males and 5000 for females; intraperitoneal, 10500 for males and 11000 for females; subcutaneous, 17500 for males and 16500 for females; and oral, 28000 for males and 29000 for females. (2) rats (adult): intravenous, 7000 for males and 8200 for females; intraperitoneal, 9500 for males and 8800 for females; subcutaneous, 17000 for males and 15500 for females; oral, more than 20000 for both sexes; and intramuscular, more than 3200 for both sexes. (3) 5-day-old rats: subcutaneous, 5278 for males and 5314 for females. (4) male dogs: intravenous, more than 5000. Major changes in general conditions observed in mice and rats were decreased spontaneous activity, lying prone, respiratory changes, staggering gait, clonic or clonic-tonic convulsions, and cyanosis, and in the animals dosed orally, diarrhea or salivation was also noted. The changes in 5-day-old rats were respiratory changes, agony, loss of reflex to an external stimulus, and congestion at the injection site, and those in dogs were vomiting, dryness of the nose, and soft or mucous stools. Autopsies on the mice and rats which died revealed hemorrhage on the brain surface. In addition, the following were seen: intraperitoneal retention of fluid and dark red spots on the abdominal wall (i.p.), subcutaneous retention of fluid or jellylike material and hemorrhage at the injection site (s.c.), and retention of fluid and dark red spots on the mucosa in the digestive tract (mice p.o.). In 5-day-old rats which died, the subcutaneous tissue at the injection site showed hemorrhage macroscopically and inflammatory changes microscopically. Hematological and blood chemical tests performed in dogs showed an increase in white blood cells and changes suggesting anemia, increases in GOT, LDH and ALP activities, and slight changes in urea nitrogen and inorganic phosphorus. In one animal given a low dose of 2500 mg/kg, an increase in GPT activity was also seen. However, these changes were all transient. Microscopic findings in dogs were slight inflammatory changes in the subcutaneous tissue around the injection site.
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PMID:[Acute toxicity study of cefodizime sodium]. 317 86

A male born to first cousins presented at 12 months with hypocalcemic convulsions, rickets, epistaxis due to vitamin K deficiency, and extremely low serum levels of beta-carotene and vitamin A. Liver function was altered moderately (glutamic-oxaloacetic transaminase, 55 U/L; glutamic-pyruvic transaminase, 37 U/L; lactate dehydrogenase, 255 U/L; alkaline phosphatase, 437 U/L). To correct the deficiencies, 8,000 IU vitamin D/day, 10,000 IU vitamin A/day, and intramuscular administration of vitamin K1 were required. At 9 years, he presented signs of neuromuscular affection, and the serum vitamin E level (measured for the first time) was extremely low. Classic lipid malabsorption syndromes (abetalipoproteinemia, chronic cholestasis, mucoviscidosis, coeliac disease, Whipple's disease) were excluded by appropriate examinations. Composition of duodenal bile acids was characterized by undetectable levels of cholic acid metabolites, and only chenodeoxycholic acid metabolites were present. Serum total bile acid concentration was normal, with an atypical low cholic acid/chenodeoxycholic acid ratio and abnormal presence of 3 beta-OH-delta 5-cholenic acid and 6-OH-bile acids. Urinary bile acid composition was also characterized by elevated 6-OH-bile acids. Known enzymopathies of the bile acid synthetic pathway were excluded (cerebrotendinous xanthomatosis, cerebro-hepato-renal syndrome of Zellweger, coprostanic acidemia). Bile acid pool sizes were determined by using stable isotopes: cholic acid pool size [2.90 (N, 32 +/- 16) microM/kg] and chenodeoxycholic acid pool size [10.8 (N, 32.6 +/- 9.9) microM/kg] were extremely low; fractional turnover rates of both bile acids were in a normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malabsorption of liposoluble vitamins in a child with bile acid deficiency. 379 31

Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.
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PMID:Acute experimentally induced aflatoxicosis in the weanling pony. 613 67

The acute oral toxicity (LD50) of chlorfenvinphos (Chl) showed no significant difference between Wistar rats (males and females) aged 42 days kept for 30 days on 4.5% or 26%-protein diet, but a twofold difference appeared after 60 days on these diets (LD50 was lower in low-protein rats) showing that a longer period of protein deficiency more increases the susceptibility of rats to the lethal action of Chl. During acute poisoning produced by intragastric administration of single convulsive dose of Chl (30 mg/kg body weight) to rats kept for 30 days on low-protein or optimal-protein diet, changes were observed in the activity of some enzymes in the serum and brain. Protein deficient diet increased the Chl-produced inhibition of acetylcholinesterase (AChE) activity in the brain; the augmented activity of aspartate aminotransferase (AspAT) and alanine aminotransferase (AlaAT) and glucosephosphate isomerase (PHI) appeared only in the serum of low-protein rats--these changes were more marked in females. Other enzymatic alterations caused by Chl were similar independently of the diets and also more evident in females; for comparison the rats received also standard Murigran diet. Activity of the brain aromatic amino acids aminotransferases (AAA) showed a decreasing trend in Chl-poisoned rats, while in the liver the activity of these enzymes rose, but chiefly in the rats receiving previously the diet with 26% of protein or standard diet. In the rats surviving the acute Chl poisoning, with the evidently seen convulsions, the activity of nearly all enzymes was normal after 14 days.
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PMID:Relationship between dietary protein level and enzymatic changes in acute poisoning of rats with chlorfenvinphos. 651 1

A Phase II study of vindesine was carried out by the Vindesine Study Group in 130 patients with hematological malignancies: mainly 3 mg/body (about 2 mg/m2) of vindesine was administered once weekly by bolus injection. In 122 evaluable patients who had been heavily pretreated with vincristine and/or others, remissions were observed in patients with acute lymphocytic leukemia, blastic crisis of chronic myeloid leukemia, malignant lymphoma and other leukemias. The overall response rate was 39.3% including 20 complete and 28 partial remissions. No remissions were obtained in acute nonlymphocytic leukemia and multiple myeloma. All patients were evaluable for toxicity: Leukopenia occurred in 64.9%; peripheral neuropathy in 24.6%; GPT and GOT elevation in 20.7% and in 10.8%; alopecia in 11.5%; gastrointestinal disturbance in 10.8%; and fever in 5.4%. The treatment with vindesine was generally well tolerated, although in five out of 130 patients (3.8%) the treatment was discontinued due to convulsion, feeling of abdominal distention plus constipation, paralytic ileus, dysuria plus constipation, or interstitial pneumonia. Leukopenia and peripheral neuropathy appeared to be dose-limiting factors.
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PMID:[Phase II study of vindesine in hematological malignancies]. 658 Aug 41

Five patients with HSE were treated with adenine arabinoside and one additional patient with cytosine arabinoside. The diagnosis of HSE was confirmed in retrospect by the rising CF titers and the Enzyme-Linked Immunosorbent Assay (ELISA) levels in CSF (Table 2). Brain biopsy was not performed. The treatment was started promptly when HSE was strongly suspected by symptoms and signs, EEG, CT and CSF findings before the specific laboratory data were available. The clinical and laboratory data on the 6 patients were shown in Table 1. All the 5 patients of HSE treated with adenine arabinoside survived: 3 returned to normal daily life, including one having no neurological deficits, and the other 2 had mild to moderate memory disturbances. Improvement of CT abnormalities indicated a good prognosis. Age or sex did not have influence on the prognosis. The patient treated with cytosine arabinoside died of complications after being in a state of apallic syndrome for 1 year and 8 months. On the basis of the analysis of our patients, one of the crucial factors in the treatment of HSE seems to be the earliest possible use of adenine arabinoside: in our patients on the 2nd up to 9th day of onset, although there was no correlation between the day the medication was started and the morbidity. The other important factor includes the management of acute stage of HSE: the treatment of cerebral edema and generalized convulsions. The major side effects of adenine arabinoside included diarrhea (one case), elevation of GOT, GPT or LDH (one case) which all improved after the treatment. Adenine arabinoside could be an effective drug for HSE reducing the mortality and morbidity with few side effects.
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PMID:[Early adenine arabinoside therapy in herpes simplex encephalitis (HSE)]. 713

Changes in serum biochemical and hematological parameters were studied in 20 male rhesus monkeys following acute poisoning by the organophosphate nerve agent cyclohexylmethylphosphonofluoridate (CMPF or GF). Animals were challenged with 5 x LD50 GF (233 micrograms/kg, IM) following pretreatment with pyridostigmine (0.3-0.7 mg/kg per 24 h) and treated with atropine (0.4 mg/kg, IM) and either 2-PAM (25.7 mg/kg, IM) or H16 (37.8 mg/kg, IM) at the onset of clinical signs or at 1 min after exposure. Muscle fasciculations, tremors, or convulsions occurred in 19 of 20 animals. Serum biochemical and hematologic parameters were analyzed 2 days and 7 days after exposure and compared to pre-exposure baseline values. Significant increases in creatine kinase (CK), lactate dehydrogenase (LD), aspartate transaminase (AST), alanine transaminase (ALT) and potassium ion (K+), associated with damage to striated muscle and metabolic acidosis, occurred in both oxime-treated groups 2 days after exposure. Total protein, albumin, red blood cell (RBC) count, hemoglobin concentration (Hb) and hematocrit (Hct), were decreased in both oxime-treated groups at 7 days. The results demonstrate that animals exposed to a single high dose of GF and treated with standard therapy exhibit changes in serum biochemical and hematological indices directly and indirectly associated with their clinical presentations.
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PMID:Acute toxicity of cyclohexylmethylphosphonofluoridate (CMPF) in rhesus monkeys: serum biochemical and hematologic changes. 749 75


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