Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytoplasmic (c) and mitochondrial (m) isoenzymes of aspartate aminotransferase (AAT, EC 2.6.1.1.) were isolated from rat heart extracts by electrophoresis in agar gel. Their pH optima and Km values were estimated; optimal conditions for estimation of the enzymatic activities are reported. Isadrine activated and adrenaline inhibited the cAAT activity. Noradrenaline did not affect the activity of both isoenzymes. Phentolamine, as contrary to obsidane which decreased the activity of both isoenzyme, activated the isoenzymes; the effect was partially decreased by obsidane. Phentolamine did not alter the noradrenaline effect on either mAAT or cAAT; it decreased significantly the free form of the mAAT activity only. Results of the experiments with administration of adrenomimetic drugs suggested that adrenaline and noradrenaline-isadrine had different sites of attachment through which they mediated their action on aspartate aminotransferase in rat heart mitochondria.
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PMID:[Role of adrenoreceptors in regulating aspartate aminotransferase isoenzyme activity in albino rat hearts]. 2 53

A cardioselective parameter has been available for about 2 years since the development by KATUS of an immunoassay for cardiac Troponin T (TnT). The major advantages of this TnT assay are its cardiospecificity and its sensitivity. The parameters usually determined in toxicity studies in rats to detect alterations in the myocardial cells, e.g. aspartate aminotransferase (ASAT), creatinine kinase (CK) and lactate dehydrogenase (LDH), are either of low sensitivity in this species or give falsely high results as the consequence of stress or haemolysis. We therefore investigated in the present study how well Troponin T, determined with the ELISA Troponin T from Boehringer Mannheim, can detect experimentally induced myocardial lesions in rats. In order to achieve hypoxic damage of the cardiomyocytes in these experiments in rats, male Sprague-Dawley rats were given two doses of 4 mg/kg isoprenaline each (Aludrin from Boehringer Ingelheim, FRG) subcutaneously. The second dose was given 7 h after the start of the experiment. Serum samples were analysed for Troponin T (TnT) levels and, for comparison, aspartate aminotransferase (ASAT), creatine kinase (CK), and lactate dehydrogenase (LDH). Histological examinations of the heart muscle were performed 24 and 96 h after the first injection. As expected, histological examinations of the isoprenaline-treated animals revealed marked myofibrillic degeneration of the myocardium 24 h after the first injection. Markedly elevated serum TnT levels (up to 7.9 ng/ml) were already evident in these animals after 6 h. TnT values decreased with time, but were still statistically significant after 48 h. Of the well-established indicators for diagnosing myocardial infarction, only ASAT showed transient statistically significant increases over 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic efficiency of troponin T measurements in rats with experimental myocardial cell damage. 758 98

The aim of the paper is to present a case of self-poisoning with paracetamol, overdosed just before a delivery. A 21-year-old woman was admitted to Obstetric and Gynecology Ward of local hospital in the second stage of physiological delivery, more than 6 hours after she had ingested 19 g of acetaminophen for self-poisoning. She delivered a normal infant weighing 3520 g who had Apgar scores of 10, and then both infant and mother were sent in an emergency ambulance to the nearest poison centre. Blood samples for toxicological examination were taken on admission to toxicological intensive care unit i.e. 11 hours post maternal ingestion. Acetaminophen levels of both patients were above the acetaminophen overdose nomogram line and the antidote treatment, i.v. N-acetylcysteine was administered according to the protocol: the mother within 11 hours post-ingestion and approximately 4 hours after a delivery; the neonate within 11 hours post maternal ingestion and 4 hours of life. Higher paracetamol concentration in the blood of infant compared to the mother's was noted in the first and then control toxicological examination performed within 35 hours post maternal ingestion. Peak maternal aspartate aminotransferase (AST) activity was 326 U/L within 35 hours and alanine aminotransferase (ALT) activity was 262 U/L within 56 hours post-ingestion. The highest neonatal enzyme activity was noted within 11 hours post maternal ingestion of paracetamol, and the elevation was not high. Except moderate anaemia in the mother, no clinical or biochemical symptoms of renal, cardiovascular or CNS injury were stated in the mother or infant. Normalisation in the maternal enzymes activity was stated within 226 hours, while in the neonatal within 58 hours post maternal ingestion. The woman recovered without sequelae and was discharged from hospital on the 11th day following paracetamol overdosing. No evidence of the liver injury was found in the infant either.
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PMID:Suicidal paracetamol poisoning of a pregnant woman just before a delivery. 1046 99

Isoproterenol, upon oxidation, produces quinones which react with oxygen to produce superoxide anions (O2.-) and H2O2. In the present study, isoproterenol was administered to rats in two doses so as to evaluate its beta adrenergic and toxicological action in terms of lipid peroxidation (LPO) and antioxidant enzymes in erythrocytes. Isoproterenol (30 mg/100 g body wt.) was administered to rats and the animals were followed up to 7 days after administration. Some of these animals were treated with a second dose of isoproterenol 24 h after the first dose and the animals were followed up to 12 h. The result showed increased lipid peroxidation (LPO) and superoxide dismutase (SOD) activity in erythrocytes in response to isoproterenol. Catalase (CAT) activity in erythrocytes decreased with isoproterenol between day 2-7 as compared to control. The second injection of isoproterenol showed increased CAT activity in erythrocytes which decreased at 12 h as compared to control. The erythrocyte GSH content and glutathione-S-transferase (GST) activity decreased with isoproterenol treatment as compared to control. However, erythrocyte GSH content as well as GST activity both recovered towards control with time. Elevated serum lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and glutamate oxaloacetate transaminase (GOT) activity was observed after isoproterenol treatment. The results show increased LPO and altered antioxidant system in erythrocytes in response to isoproterenol induced oxidative stress.
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PMID:Lipid peroxidation and antioxidant enzymes in isoproterenol induced oxidative stress in rat erythrocytes. 1084 29

Isoproterenol (ISPH) induced myocardial infarction was confirmed by disturbances in serum and heart tissue marker enzymes such as lactate dehydrogenase (LDH), creatine phospho kinase (CPK), aspartate transaminase (AST) and alanine transaminase (ALT), increased level of lipid peroxidation and histopathological changes in the heart of ISPH administered rats. Pretreatment with mangiferin (10 mg/100 g body weight) for 28 days was found to ameliorate the effect of ISPH-induced pathological changes, reduced the lipid peroxide formation and retained the myocardial marker enzyme activities at near normal level. The above results indicate the cardioprotective effect of mangiferin against ISPH-induced myocardial infarction in rats.
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PMID:Cardioprotective effect of mangiferin on isoproterenol induced myocardial infarction in rats. 1653 59

A 21-year-old woman of Romany origin, in the third trimester of her fourth pregnancy, was admitted to the hospital because of a generalized erythematous and pustular eruption and desquamation involving her face, neck, trunk, and extremities. The skin changes were accompanied by fever (100.4 degrees F [38 degrees C]) and malaise. The patient was convinced that the dermatitis was induced by the consumption of "spoilt" pork sausage (bad smell, changed taste) approximately 24 hours earlier. Clinical examination revealed a woman with phototype III skin, black eyes, and black hair, in good general health. Widespread, symmetrical, moderately intense erythema and isolated or coalescing targetoid lesions studded with discrete, pinhead-sized, nonfollicular pustules in the center or at the periphery were distributed over her face, trunk, groins, and upper and lower extremities (Figures 1). On the neck and abdomen, lamellar desquamation was observed (Figure 2). Palms, soles, scalp, mucous membranes, hair, and nails were not affected. Nikolsky's sign was negative. The patient complained of very slight skin burning and itching. The pregnancy was proceeding without any complications and her obstetric status was normal. The woman had neither any accompanying diseases, nor previous personal or family history of psoriasis, nor any known allergies. She had taken no systemic medication (not even vitamins). She had three pregnancies; two ended with the delivery of healthy babies and one of them was aborted at her will. Laboratory studies revealed leukocytosis (13.2 x 109/L), neutrophilia (8 x 109/L), anemia (hemoglobin, 108 g/L), and an elevated erythrocyte sedimentation rate (68-110 mm/h). The results from the following investigations were normal: urinalysis, renal and hepatic function, serum albumin, Ca, Na, K, aspartate aminotransferase titer, cryoprotein, hepatitis B surface antigen, and serum markers for syphilis. Bacterial and fungal cultures of pustular content were sterile. A skin biopsy specimen of lesional skin revealed subcorneal pustules containing leukocytes and necrotic keratinocytes and a mixed perivascular inflammatory infiltrate with isolated eosinophils in the dermis (Figure 3). The patient was treated with systemic methylprednisolone in gradually reduced doses, fluocinonide cream 0.05%, and emollients. As a result, her fever disappeared and her erythema faded. Frequent obstetric examination and cardiotocography were normal and showed no evidence of placental insufficiency. At 40 weeks' gestation, the patient spontaneously gave birth without any complications to a healthy boy. She was discharged with complete resolution of the skin lesions, preceded by massive desquamation of the epidermis. The 1-year follow-up of the patient revealed no relapses or new pustular eruptions.
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PMID:Food-induced acute generalized exanthematous pustulosis in a pregnant woman. 1685 16

This study was designed to investigate the effect of oral curcumin pretreatment (200 mg/kg) on isoproterenol-induced myocardial injury in rats. Isoproterenol (85 mg/kg, s.c., in two divided doses at 24 h intervals) administration induced a statistically significant increase (P < 0.01) in serum lactate dehydrogenase, creatine kinase, aspartate transaminase, and alanine transaminase activities and significant increase (P < 0.01) in myocardial lipid peroxides levels as compared to vehicle control rats. Furthermore, significant depletion (P < 0.01) of myocardial endogenous antioxidants viz. superoxide dismutase, catalase, and tissue glutathione levels were also found in the pathogenic control group, that is, isoproterenol only treated animals. Curcumin (200 mg/kg) pretreatment for 20 days in isoproterenol treated rats significantly lowered (P < 0.01) the serum lactate dehydrogenase, creatine kinase, aspartate transaminase, alanine transaminase, and myocardial lipid peroxides levels and increased the levels of myocardial endogenous antioxidants (superoxide dismutase, catalase, and tissue glutathione) as compared to pathogenic control rats. Furthermore, histological examination of rat's heart section confirmed myocardial injury with isoproterenol administration and near normal pattern with curcumin pretreatment. The results of our study provide clear evidence that the curcumin pretreatment enhances the antioxidant defense against isoproterenol-induced oxidative myocardial injury in rats and exhibit cardioprotective property.
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PMID:Protective role of curcumin in myocardial oxidative damage induced by isoproterenol in rats. 1837 36

Hematological complications have been frequently associated with acute brucellosis, but pancytopenia is less frequently seen. Also, capillary leak syndrome has been rarely reported in the literature. In this report, we present a case of brucellosis with pancytopenia leading to capillary leak syndrome. A 21-year-old man was admitted to hospital with complaints of a one-month history of weakness, sweats, and fever and he had hepatosplenomegaly and edema over the pretibial areas. Hemogram revealed pancytopenia and biochemical tests revealed moderate hypoalbuminemia, elevations of lactate dehydrogenase and aspartate aminotransferase. He was diagnosed as brucellosis and capillary leak syndrome. He was given doxycycline and rifampicin. The patient's symptoms were resolved after treatment.
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PMID:The first documented case of brucellosis manifested with pancytopenia and capillary leak syndrome. 1845 81

We investigated the antioxidant preventive effect of betaine on isoprenaline-induced myocardial infarction in male albino rats. Isoprenaline induced myocardial infarction was manifested by a moderate elevation in the levels of diagnostic marker enzymes (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase) and homocysteine in plasma of experimental rats. Significant rise in the level of lipid peroxidation with a concomitant decline in the levels of myocardial non-enzymic (reduced glutathione) and enzymic antioxidants (glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase) was also observed. Oral pretreatment with betaine significantly prevented isoprenaline-induced alterations in the levels of diagnostic marker enzymes and homocysteine in plasma of experimental groups of rats. It counteracted the isoprenaline-induced lipid peroxidation and maintained the myocardial antioxidant defense system at near normal. Histopathological observations also confirmed the protective effect of betaine against isoprenaline-induced myocardial infarction. The results of the present investigation indicate that the protective effect of betaine is probably related to its ability to strengthen the myocardial membrane by its membrane stabilizing action or to a counteraction of free radicals by its antioxidant property.
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PMID:Antioxidant defense of betaine against isoprenaline-induced myocardial infarction in rats. 1928 77

The study aimed to evaluate the protective role of myricetin obtained from Vitis vinifera (Vitaceae) on heart rate, electrocardiographic (ECG) patterns, vascular reactivity to catecholamines, cardiac marker enzymes, antioxidant enzymes together with morphological and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats. Rats treated with isoproterenol (85 mg/kg, administered subcutaneously twice at an interval of 24 h) showed a significant increase in heart rate and ST elevation in ECG, and a significant increase in the levels of cardiac marker enzymes - lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in serum. Isoproterenol significantly reduced superoxide dismutase (SOD) and catalase (CAT) activity and increased vascular reactivity to various catecholamines. Pretreatment with myricetin (100 mg/kg, p.o. and 300 mg/kg, p.o.) for a period of 21 days significantly inhibited the effects of ISO on heart rate, levels of LDH, CK, AST, SOD, CAT, vascular reactivity changes and ECG patterns. Treatment with myricetin (100 mg/kg and 300 mg/kg) alone did not alter any of the parameters compared with vehicle treated Wistar rats. Myricetin treated animals showed a lesser degree of cellular infiltration in histopathological studies. Thus, myricetin (100 mg/kg and 300 mg/kg) ameliorates the cardiotoxic effects of isoproterenol and may be of value in the treatment of MI.
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PMID:Cardioprotective potential of myricetin in isoproterenol-induced myocardial infarction in Wistar rats. 1930 80


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