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)

The cutaneous signs of anorexia nervosa (AN) and bulimia nervosa (BN) have been described previously in adult patients. For the first time, we present here dermatologic findings in children and adolescents suffering from eating disorders. Thirty consecutive young anorexic and bulimic inpatients (8 to 17 years of age, mean 15.1 years) underwent a standardized dermatologic examination. Patients were checked for abnormalities of the skin including atopic stigmata, dermographism, hair, nails, and oral cavity. Serum was obtained for hemoglobin, iron, zinc, GPT, thyroid, and sex-hormone levels. In 13 patients, the total serum IgE was determined, and a prick test was carried out with defined type I allergens. Findings in order of frequency included xerosis of the skin, white dermographism, diffuse hypertrichosis, acrocyanosis, scars, diffuse effluvium, artifacts, brittle nails, and onychophagia. Significant co-relations were found between the presence of hypertrichosis and the existence of amenorrhea or a body mass index of less than 16. In 22 patients a low T3 level was found. In summary, children and adolescents suffering from AN or BN show dermatologic features similar to those reported in older patients. Special findings in this age group are extensive lanugo hair and signs of autoaggressive behavior.
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PMID:Dermatologic findings in anorexia and bulimia nervosa of childhood and adolescence. 1033 69

An 82-year-old male patient was admitted for liver dysfunction. Laboratory test showed the following data; aspartate aminotransferase (AST) 79 IU/l, alanine aminotransferase (ALT) 28 IU/l, total bilirubin (T. Bil) 0.9 U, zinc sulfate turbidity test (ZTT) 48.9 U, gamma-globulin 4.9 g/dl, immunoglobulin G (IgG) 5,046 mg/dl, anti-nuclear antibodies x 320, anti-mitochondrial antibodies (-), hepatitis B virus surface antigen (HBsAg) (-), HBcAb (-), anti-hepatitis C virus (anti-HCV) (-), hepatitis C virus (HCV-RNA) (-), anti-hepatitis G virus (anti-HGV) (-), alpha-fetoprotein 306.8 ng/ml, carcinoembryonic antigen (CEA) 2.3 ng/ml, carbohydrate antigen (CA) 19-9 77.2 U/ml. Abdominal ultrasonography and computed tomography showed a large mass occupying most of the right lobe and portal thrombosis in the liver. Liver biopsy revealed cirrhosis with inactive hepatitis in the nontumorous lesion and well-differentiated hepatocellular carcinoma in the tumorous lesion. We report a rare case of an aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma.
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PMID:An aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma. 1039 80

The aim of this study was to identify apolar aldehydes in liver homogenates from rats with CCl4-induced cirrhosis and, as a corollary, the antioxidant effect of zinc administration. The study was performed in five control rats and in ten cirrhotic rats which were further sub-divided into two groups to receive either a standard diet or one supplemented with zinc. The percentage of hepatic fibrosis, plasma malondialdehyde concentration and alanine aminotransferase activity were measured as well as the following aldehydes: hexanal, octanal, decanal, 2-hexenal, 2-octenal, 2-nonenal, 2,4-heptadienal and 2,4-decadienal. Of the 10 cirrhotic rats, 4 had elevated concentrations of the highly toxic 2,4-dialkenals which coincided with a higher percentage of fibrosis and plasma alanine aminotransferase activity. These aldehydes were not observed in the control group. Zinc administration was associated with a reduction of the hepatic malondialdehyde concentration and an amelioration on the degree of hepatic injury. In conclusion, this study demonstrates the presence of the highly toxic 2,4-dialkenals in hepatic tissue of rats whith CCl4-induced cirrhosis. Results obtained would suggest that these particular aldehydes may be related to the severity of the hepatic injury.
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PMID:Hepatic production of apolar aldehydes in rats with carbon tetrachloride-induced cirrhosis. 1049 78

Doxorubicin produces clinically useful responses in a variety of human cancers. However, the toxicity of doxorubicin has limited its usefulness. This side effect is mainly due to the doxorubicin-mediated free radical formation. Administration of doxorubicin (10 mg/kg body weight) to rats intravenously induces heme oxygenase-1 (HO-1) in the liver. The levels of HO-1 protein were first detected at 6 hours and peaked at about 18 to 24 hours after the injection. It is known that HO-1 plays a protective role against the oxidative injury. Therefore, we have examined the protective effect of doxorubicin preconditioning against the hepatic ischemia-reperfusion injury. Partial hepatic ischemia was produced in the left and medium lobes for 45 minutes followed by 120 minutes reperfusion. When low doses of doxorubicin (1 mg/kg body weight) was intravenously administered to rats 2 days before the ischemia, the serum alanine transaminase (ALT) levels in the preconditioning rat were clearly improved compared with those in the rat without preconditioning. Under this situation, zinc-protoporphyrin IX, a specific inhibitor of HO-1, was injected subcutaneously to rats at 3 and 16 hours before the ischemia, the ALT levels were not improved by doxorubicin preconditioning. Histopathologic examination also supported these results. Although the HO-1 protein level was fairly low 2 days after the doxorubicin administration, significant amounts of HO-1 protein were detected. Our results indicated that the induction of HO-1 played a protective role against hepatic ischemia-reperfusion injury and that doxorubicin preconditioning is more clinically useful than other preconditioning methods.
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PMID:Doxorubicin preconditioning: a protection against rat hepatic ischemia-reperfusion injury. 1065 83

Mice were fed with high zinc diet (15 g/kg) for 3 weeks. High zinc could cause liver toxicity: 1. inhibiting the activity of GOT and GPT in liver homogenate, reducing GSH and glycogen contents. 2. increasing the activity of aniline hydroxylase and inhibiting the activities of NADPH-cytochrome C reducease, benzo-phytamine-N-demethylase and glutathione S-transferase. The activities of cytochrome P450 and cytochrome b5 were not obviously changed 3. increasing microsomal membrane fluidity in the superficial layers, but not in the deep layers.
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PMID:[Effects of high dietary zinc on liver function, hepatic drug metabolism enzymes and membrane fluidity in mice]. 1068 26

The ability of chromium (Cr) salts to increase metallothionein (MT) levels in rat liver, kidney and pancreas, and its relationship with the presence of toxic effects are reported here. Rats were injected subcutaneously with 0, 10, 20, 30, 40, or 50 mg K2Cr2O7/kg and sacrificed 24 h later. Total Cr accumulation followed a dose-dependent pattern, levels in kidney being higher than those in liver or pancreas, suggesting different tissue bioavailabilities and accumulation patterns. Cr(IV) administration resulted in a tissue-specific MT induction: pancreas and liver showed five- and 3.5-fold MT increases, respectively; no increase was observed in the kidney. A positive correlation was observed between zinc and MT concentrations in liver, and between total Cr and MT concentrations in pancreas. Serum alpha-amylase activity showed a dose-dependent increase starting from 20 mg/kg, whereas serum glucose levels increased at doses higher than 30 mg/kg. Serum aspartate aminotransferase and alanine aminotransferase activities were increased in a dose-dependent manner, from 20 and 30 mg/kg, respectively. Our results showed that treatment with Cr(VI) can induce MT synthesis in pancreas and suggests a subsequent binding of Cr to MT. Also, pancreas is a target organ for Cr toxicity, and the usefulness of alpha-amylase activity as a sensitive biomarker of Cr toxicity in human exposed populations merits further study.
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PMID:Chromium increases pancreatic metallothionein in the rat. 1068 10

In previous trials, the orally active iron chelator deferiprone (L1) has been associated with sporadic agranulocytosis, milder forms of neutropenia and other side-effects. To determine the incidence of these events, we performed a multicentre prospective study of the chelator. Blood counts were performed weekly, and confirmed neutropenia mandated discontinuation of therapy. Among 187 patients with thalassaemia major, the incidence of agranulocytosis (neutrophils < 0.5 x 109/l) was 0.6/100 patient-years, and the incidence of milder forms of neutropenia (neutrophils 0.5-1.5 x 109/l) was 5.4/100 patient-years. All cases of neutropenia resolved after interruption of therapy. Neutropenia occurred predominantly in non-splenectomized patients. Nausea and/or vomiting occurred early in therapy, was usually transient and caused discontinuation of deferiprone in three patients. Mild to moderate joint pain and/or swelling did not require permanent cessation of deferiprone and occurred more commonly in patients with higher ferritin levels. Mean alanine transaminase (ALT) levels rose during therapy. Increased ALT levels were generally transient and occurred more commonly in patients with hepatitis C. Persistent changes in immunological studies were infrequent, although sporadic abnormalities occurred commonly. Mean zinc levels decreased during therapy. Ferritin levels did not change in the overall group but decreased in those patients with baseline levels > 2500 microgram/l. This study characterized the safety profile of deferiprone, and, under the specific conditions of monitoring, demonstrated that agranulocytosis is less common than previously predicted.
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PMID:Safety profile of the oral iron chelator deferiprone: a multicentre study. 1069 60

The influence of sodium fluoride on the course of repair process in the mechanically injured rat bone was studied. Thirty six male Wistar rats aged 5 months, weighing 460-540 g were investigated. The animals lived under standard conditions and were fed ad libidum with the standard LSM food including 0.7 mg/kg of fluorine on the average. The animals randomly divided into 3 groups that comprised study and control groups, 6 rats each. The rats in the first group were given water with 20 mg (1.05 mmol) of sodium fluoride per kg of body weight for 24 h over a period of 2 weeks--group Ia. In the second group--IIa--animals were given water with sodium fluoride at a dose of 1.5 mmol/kg b.w./24 h for a period of 4 weeks. In the third group--IIIa--the animals were given sodium fluoride in a dose of 1.5 mmol/kg b.w./24 h for a period of 6 weeks. The rats from the control groups I, II and III were given water without sodium fluoride for the period of 2, 4 and 6 weeks, respectively. At the beginning of the experiment a hole was drilled in both femoral bones in rat under barbiturate anaesthesia. According to the protocol the rats underwent ether euthanasia after 2, 4 and 6 weeks after surgery and the following samples were collected: blood from the heart for biochemical studies and both femoral bones for biochemical and histological studies. The following parameters were evaluated in blood serum: fluorine, calcium, magnesium contents, serum concentrations of urea, creatinine, bilirubin and activity levels of enzymes: aspartate aminotransferase, alanine aminotransferase, cholinesterase, base phosphatase. Fluorine, calcium magnesium and zinc contents were estimated in bone samples. The concentration of fluorine ions in animal serum after 2, 4 and 6 weeks of experiment increased significantly as compared with the corresponding controls. The highest fluorine concentrations were observed in serum of rats supplemented with NaF for 6 weeks. The fluorine concentrations in the bone tissue and fresh and dried granulation tissues in all studied groups also revealed statistically significant increase as compared to the controls. The rats fed with sodium fluoride for the period of 6 weeks revealed statistically significant increase of serum magnesium concentration as compared to the remaining study groups. Bone magnesium concentrations in animals fed with NaF for the period of 2 and 6 weeks were higher as compared to the corresponding control groups, with the highest differences observed after 6 weeks of experiment. Animals fed with sodium fluoride for the period of 6 weeks revealed increased serum calcium concentrations as compared to the study groups after 2 and 4 weeks of experiment. Similar results were achieved in bone tissue samples (Fig. 1 and 2, Tab. 1-6). Basing on the achieved results in biochemical studies and histological pictures it should be assumed that laboratory animals fed with sodium fluoride in doses recognised as non-toxic reveal intensified healing process within mechanically injured bones. The use of sodium fluoride led to accelerated chondrogenesis process in the area of insufficiently perfused bone, osteogenesis including temporary callus formation and mineralization of the new bone, as well as remodelling into mature lamellar bone. The greatest differences in the repair dynamics for both groups occurred between the second and fourth week of experiment. These results could be the base of clinical studies on application of the sodium fluoride in the acceleration of fracture healing.
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PMID:[Evaluation of the repair process in mechanically injured rat bone stimulated by sodium fluoride with non-toxic doses]. 1090 90

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.
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PMID:Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy. 1103 77

The toxicological literature is replete with studies attempting to explain the mechanism of action of organophosphorus (OP) insecticides to their anticholinesterase activities, but not much is known about the metabolism and detoxification of these compounds. The goal of this study was to ascertain the toxic effects of chlorpyrifos, one of the most widely used OPs, on the liver of male rats and also to evaluate the protective potential of zinc in mediating its toxic effects. It was observed that chlorpyrifos (13.5 mg/kg body weight) treatment resulted in significant inhibition (p < 0.001) of serum and hepatic acetylcholinesterase (AChE) activities after 8 wk. However, zinc-treated (227 mg/L drinking water) animals resulted in significant normalization of the inhibited AChE activities. Similarly, a significant increase in the levels of various serum and liver marker enzymes (viz. alkaline phosphatase, aspartate aminotransferase [AST], and alanine aminotransferase [ALT]) was observed following treatment with chlorpyrifos. However, coadministration of zinc to these animals restored these enzymes to within normal limits, even though some increase in the activity of serum ALT and hepatic alkaline phosphatase still persisted at the end of the study. Chlorpyrifos treatment diminished serum and hepatic zinc levels significantly (p < 0.01 to p < 0.001) compared to normal control animals. Serum iron concentrations also plummeted significantly following chlorpyrifos treatment. On the contrary, serum copper levels were significantly increased (p < 0.01) in chlorpyrifos-treated animals, but they were normalized following zinc supplementation to the rats in this group. Interestingly, chlorpyrifos treatment resulted in elevated hepatic levels of copper, iron, and selenium, but zinc treatment could only partially restore the raised elemental concentrations. These data clearly demonstrate the potential role of zinc in mediating the toxic effects of chlorpyrifos, presumably because of their antioxidant properties and also their possible interaction with other trace elements in maintaining the cellular harmony.
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PMID:Protective effects of zinc in chlorpyrifos induced hepatotoxicity: a biochemical and trace elemental study. 1105 90


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