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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ornithine decarboxylase (ODC) activity, the rate limiting enzyme in polyamine biosynthesis, was determined after 12-O-tetradecanoylphorbol 13-acetate (TPA) administration to female Sprague-Dawley rats. The extent of induction depended on the dose, exposure, time and route of administration. The most effective dose for ODC induction by the intraperitoneal route was 40 ug TPA/kg which caused 3-5 fold ODC induction. Maximal ODC induction occurred in a narrow time band 5 hours after TPA administration. TPA had no adverse effects on hepatic DNA (measured by alkaline elution), cytochrome P-450 content and reduced glutathione content or serum alanine aminotransferase (SGPT) activity.
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PMID:Dose, time and route dependency of the induction of rat hepatic ornithine decarboxylase by 12-tetradecanoylphorbol 13-acetate. 155 24

A 26 year-old man, who was treated for meningitis in our hospital previously, was rehospitalized 1 year later because he developed disturbance of consciousness, gait disturbance and urinary incontinence. Blood examination revealed accelerated ESR, elevated GPT, slight elevation of serum Ca, strong positive CRP, and a decrease in PHA and Con A. ACE was within normal range and tuberculin reaction was negative. Lumbar puncture revealed that the initial pressure was 310 mmH2O, cells were 152/3, and protein was 343 mg/dl. Bilateral hilar lymphadenopathy was absent in chest X ray film. Head CT revealed enlarged lateral ventricles and irregularly enhancing nodular lesions in the anterior half of the falx cerebri, and abnormally strong enhancement of the choroid plexus. Ventriculoperitoneal shunt was performed. As a diagnosis was difficult to obtain from the clinical data, biopsy of the nodular lesions was performed. The histopathologic diagnosis was sarcoidosis. Steroid hormone was administered thereafter, and the nodular lesions of the falx disappeared in the follow-up. In the literature, only 8 cases of sarcoidosis of the dura mater have been reported. Since intracranial sarcoidosis is a part of systemic sarcoidosis, its diagnosis is not difficult in most cases. However, in cases difficult to diagnose as in our case, biopsy may be necessary. When nodular lesion occurs in the dura mater, sarcoidosis must be included as a possibility in the differential diagnosis in addition to the usual meningioma, lymphoma, and metastatic brain tumor.
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PMID:[A case of dural sarcoidosis]. 160 81

Lead markedly augments the lethality of endotoxin lipopolysaccharide (LPS) in rats. In this model of LPS toxicity, the liver is severely injured. Much of the tissue injury produced by LPS is thought to be mediated by the cytokine tumor necrosis factor (TNF). Tumor necrosis factor recently has been speculated to be a mediator of several models of liver injury such as that produced by galactosamine. To investigate the possible role of TNF in the lead-enhanced LPS toxicity model, we administered doses of lead acetate (15 mg/kg), LPS (100 micrograms/kg), or TNF (6.25 x 10(6) U/kg) that produced minimal changes in liver enzymes. However, when lead was administered simultaneously with either LPS or TNF, serum aspartate transaminase, alanine transaminase, alkaline phosphatase, glutamyl transpeptidase, and plasma triglyceride levels were markedly increased. Lead + LPS treatment increased both peak serum TNF concentrations and TNF "area under the curve" as compared with LPS alone. We conclude that lead not only enhances LPS lethality but also LPS liver injury. Furthermore, lead enhances TNF liver injury and increases LPS-stimulated serum TNF levels. These data suggest that the lead-enhanced LPS model offers a system for studying TNF-induced liver injury.
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PMID:Lead enhances lipopolysaccharide and tumor necrosis factor liver injury. 167 39

Milk production of dairy cows in six herds was increased by approximately 15% by the administration of recombinantly derived bST in a sustained-release vehicle (somidobove, Eli Lilly/Elanco, Indianapolis, IN) at 28-d intervals, which commenced at 52 to 104 d postpartum. Milk composition, acidity, flavor, and growth of commercial lactic acid starter cultures were unaffected by somidobove treatment. No adverse effect upon health (metabolic diseases, mastitis) and reproduction was noted. Blood glucose, FFA, aspartate aminotransferase, alanine aminotransferase, Ca, Na, and K were unaffected by the application of somidobove. Somidobove did not affect the appearance of the organs of cows at slaughter; however, somidobove-treated cows had less subcutaneous and omental adipose tissue than controls. Cultured explants of subcutaneous adipose tissue of treated cows showed significantly lower lipogenesis from acetate than controls. The release of FFA was not affected by treatment. Recombinantly derived somidobove has been judged in Czechoslovakia to be effective and safe for cows and the environment. Edible products from the treated cows are safe for human consumption.
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PMID:Impact of bovine somatotropin on dairying in eastern Europe. 179 65

A prospective, double-blind clinical study has been carried out in 90 chinese women with postmenopausal period covering 0.5 to 21 years by administering a synthetic long-acting estriol derivative-nylestriol in the regimen of 2 mg every 2 weeks for 1 year (49 treated and 41 placebo). The result were: Total cholesterol (TC) and triglyceride (TG) remained unchangeable (P greater than 0.05), while high-density-lipoprotein cholesterol (HDL-C) increased after 6 months, low-density lipoprotein cholesterol (LDL-C) and TC/HDL-C,LDL-C/HDL-C ratios decreased after 3 months of medication (P less than 0.05); FSH were restrained (P less than 0.05), but LH did not change significantly (P greater than 0.05). One third of the women with intact uterus had spotting withdraw bleeding and another one third had moderate amount after the addition of medroxyprogesterone acetate 6 mg daily for 7 days at the end of the 12 months treatment. Side effects included breakthrough bleeding (10.3%), breast tenderness (11.8%), leukorrhagia (29.4). None showed abnormal liver function (GPT).
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PMID:[A prospective study of nylestriol on plasma lipids in postmenopausal women]. 180 5

Previously we have reported on the pigmentary lithogenic action of vitamin A in the form of retinol acetate. In the present work the possible lithogenic action of retinoic acid was tested, since this differs from retinol in several metabolic aspects, which can contribute to the understanding of the pathogenesis of the pigment cholelithiasis produced by vitamin A. Two experiments were performed in which the lithogenicity of retinol acetate added to a colony chow at the level of 25,000 IU%, was compared with that of 3 dietetic levels of all-trans retinoic acid. In the first experiment seric triglycerides were determined in order to establish whether there is a relation between the hypertriglyceridemic effect of retinoids and their lithogenicity; in the second experiment GPT and GOT were determined as indicators of hepatotoxicity. The results showed that the retinoic acid at levels of 24,000 and 35,000 IU% of diet, produced a cholelithiasis incidence similar to that of 25,000 IU% of retinol acetate, whereas the retinoic acid level of 12,000 IU% was not lithogenic. The dietetic retinoic acid produced a reduction of hepatic vitamin A, that was directly proportional to the level supplied. There was no relation between the hypertriglyceridemic effect of retinoids and its lithogenicity. The retinoids produced a light increase in GPT, which was higher with retinol acetate, whereas GOT had not significative changes. It is concluded that all-trans retinoic acid produces pigment gallstones in the hamster, with an incidence similar to that produced by retinol acetate.
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PMID:Gallstones in the golden hamster. XXXVI. Pigment cholelithiasis produced by retinoic acid. 181 96

The author studied the characteristics of ACE inhibitor-induced cough in 41 non-smoking hypertensive patients. For at least 6 months, 20 patients (10 males and 10 females) were treated with enalapril, and 21 (11 males and 10 females) with aracepril. The results were as follows. 1) ACE inhibitor-induced cough was induced in 7 cases (1 male and 6 females). The incident rate of cough was 17.1%. ACE inhibitor-induced cough was not significantly related to past allergic history or to the beta-adrenergic blocker therapy. The laboratory findings of the cough sufferers--such as eosinophil percent in venous blood, serum GOT and GPT, urea nitrogen, creatinine, renal function (PSP excretion test and creatinine clearance), and pulmonary function (%FVC, FEV1.0% and %V25)--were not significantly different from those of the non-coughers. 2) Inhibitory effects of ipratropium bromide inhalation of ACE inhibitor-induced cough were noted in 83.3% of the patients, but their coughs did not completely disappear. From these findings, the pathogenesis of this cough may be related to be as follows. The cough seems to be related to the release of acetylcholine from vagal nerve terminals or to the stimulation of irritant receptors and vagal reflex. 3) Chronic persistent cough or bronchial asthma did not occur after stopping the treatment with ACE inhibitors. The mean follow-up period was 15.6 months.
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PMID:[Angiotensin converting enzyme (ACE) inhibitor-induced cough in non-smoking hypertensive patients]. 183 7

Under certain circumstances, segmented neutrophils (PMNs) injure extrahepatic tissue by releasing toxic oxygen species and degradative enzymes. The authors used an isolated, perfused rat liver preparation to determine whether PMNs might injure the liver. Livers from fasted rats were perfused with Krebs-Ringer bicarbonate buffer (pH 7.4) containing 3% bovine serum albumin (BSA) in a recirculating system. Rat peritoneal PMNs (4 x 10(8] or vehicle (Hank's balanced salt solution [HBSS], pH 7.35) were added, and liver injury was assessed 90 minutes later by release of alanine aminotransferase (ALT) into the perfusion medium and histopathologic analysis of liver sections. Perfusion of livers receiving only HBSS for 90 minutes resulted in a small increase in ALT activity in the perfusion medium but did not significantly alter histologic features of liver sections. Addition of unstimulated PMNs did not increase further the ALT activity and, with the exception of vascular neutrophilia, did not significantly change the histomorphology compared with controls. When PMNs activated with a combination of phorbol myristate acetate (PMA, 31 ng/ml) and lithocholate (100 mumol/l [micromolar]) were added to the perfusion system, however, livers released greater amounts of ALT than those perfused with PMA, lithocholate, and HBSS. Activated PMNs caused a transient reduction in flow of perfusion medium that lasted approximately 5 to 15 minutes. Liver sections had multifocal to coalescing foci of moderate to severe, acute hepatocellular necrosis associated with the areas of intense sinusoidal neutrophilia. In addition a second type of lesion was observed and was characterized by triangular foci of necrosis located adjacent to periportal regions of sinusoids or portal veins containing neutrophilic thrombi. These lesions were void of PMNs and were consistent with infarcts. A combination of superoxide dismutase and catalase added to the perfusion medium (500 U/ml each) prevented the elevation in ALT activity but not the transient reduction in flow. These results indicate that activated PMNs may cause liver injury by an oxygen radical-dependent mechanism. It is unclear whether PMN-derived oxygen radicals, hepatocellular-derived oxygen species resulting from reduced tissue perfusion and reperfusion, or both are involved in the pathogenesis.
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PMID:Activated neutrophils injure the isolated, perfused rat liver by an oxygen radical-dependent mechanism. 195 24

Lipid peroxidation (LPO) and alterations in cellular systems protecting against oxidative damage were determined in the liver, kidney and skeletal muscle of male F344/NCr rats, 1 h to 3 days after a single intraperitoneal (i.p.) injection of 107 mumol nickel(II)acetate per kg body weight. At 3 h, when tissue nickel concentrations were highest, the following significant (at least, P less than 0.05) effects were observed: in kidney, increased LPO (by 43%), increased renal iron (by 24%), decreased catalase (CAT) and glutathione peroxidase (GSH-Px) activities (both by 15%), decreased glutathione (GSH) concentration (by 20%), decreased glutathione reductase (GSSG-R) activity (by 10%), and increased glutathione-S-transferase (GST) activity (by 44%); the activity of superoxide dismutase (SOD) and gamma-glutamyl transferase (GGT), as well as copper concentration, were not affected. In the liver, nickel effects included increased LPO (by 30%), decreased CAT and GSH-Px activities (both by 15%), decreased GSH level (by 33%), decreased GSSG-R activity (by 10%) and decreased GST activity (by 35%); SOD, GGT, copper, and iron remained unchanged. In muscle, nickel treatment decreased copper content (by 43%) and the SOD activity (by 30%) with no effects on other parameters. In blood, nickel had no effect on CAT and GSH-Px, but increased the activities of alanine-(ALT) and aspartate-(AST) transaminases to 330% and 240% of the background level, respectively. In conclusion, nickel treatment caused profound cell damage as indicated by increased LPO in liver and kidney and leakage of intracellular enzymes, ALT and AST to the blood. The time pattern of the resulting renal and hepatic LPO indicated a possible contribution to its magnitude from an increased concentration of nickel and concurrent inhibition of CAT, GSH-Px and GSSG-R, but not from increased iron or copper levels. The oxidative damage expressed as LPO was highest in the kidney and lowest in the muscle, which concurs with the corresponding ranking of nickel uptake by these tissues.
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PMID:Nickel induced lipid peroxidation in the rat: correlation with nickel effect on antioxidant defense systems. 197 9

The hormonal and biochemical effects of danazol (600 mg a day) and high-dose medroxyprogesterone acetate (MPA; 100 mg a day) were studied in a placebo-controlled, 6-month trial. Serum gonadotrophins and prolactin levels did not change during danazol and MPA treatments, whereas oestradiol and progesterone levels decreased significantly in relation to placebo without any difference between danazol and MPA. Both drugs significantly suppressed the sex hormone-binding globulin level (SHBG), and consequently, the free-androgen index (serum total testosterone nmol/l per SHBG nmol/l x 100) as compared with placebo, the effect of danazol being significantly stronger than that of MPA. Danazol, but not MPA, significantly increased serum aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and haemoglobin levels, and also thrombocyte counts, whereas MPA, but not danazol, increased the serum concentration of albumin in relation to placebo. Serum total bilirubin, conjugated bilirubin, gamma-glutamyl transferase, creatinine, alkaline phosphatase, sodium and potassium levels and leucocyte counts remained unchanged during both treatments. Danazol and high-dose MPA did not differ from each other in their ovarian and anterior pituitary effects, while the increase in androgenic activity induced by danazol was greater than that achieved with MPA. Danazol also had more biochemical effects than MPA. It interfered with the functions of the liver and the production of thrombocytes and haemoglobin, whereas MPA affected only albumin synthesis/release.
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PMID:Placebo-controlled comparison of hormonal and biochemical effects of danazol and high-dose medroxyprogesterone acetate. 214 9


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