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 relationship between plasma protein bound iodine (PBI) level and creatine kinase (CK) activity was investigated in 143 males and 528 females suspected of various thyroid disorders; there was significant negative correlation between low PBI level and raised CK activity. CK, aldolase, lactate dehydrogenase (LD), aspartate transaminase (AST), and alanine transaminase (ALT) activities were determined in plasma from patients with reduced PBI levels; apart from CK, LD was the only enzyme increased in an appreciable number of cases. A further series of specimens was collected from 66 patients with low PBI levels and the CK isoenzymes investigated. In all of these MM was the main form present; a trace of MB was found in 6. These findings do not explain the elevation of CK in hypothyroidism which may be a non-specific effect.
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PMID:An investigation into creatine kinase and other plasma enzymes in thyroid disorders. 7 98

The paper presents further investigations for a critical survey on the influences of drugs on laboratory methods. In controversion to the meanings you can find in the literature that ascorbic acid is most one of the important drugs to interfere with laboratory results we couldn't see in our systematical experimental investigation such results. Only in very extremly cases it seems to be right. Selected parameters of clinical chemistry (glucose, lactic dehydrogenase, aspartal-aminotransferase, alanine aminotransferase, alkaline phosphatase, protein, albumine, creatinine, butanol extractable iodine, ferrum) show under therapeutic conditions no influences of ascorbic acid, which can lead to diagnostic or therapeutic false interpretations. Above all the often mentioned example that glucose estimations in blood (reduction methods) can disturb if ascorbic acid is present, is abstracted in an uncritical manner how our experimental results may show.
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PMID:[The effect of drugs on laboratory diagnosis. The effect of ascorbic acid on selected automatic laboratory methods]. 54 78

The author carried out on 35 cats a study on the protein content, potasium and sodium. aldolase, GOT, GPT and LDH of the uterine muscle. The animals were divided into three groups: first-15 nonpregnant cats, second-10 pregnant cats at the first half of pregnancy and third-10 pregnant cats at the second half of pregnancy. He used a piece of uterine muscle from which proteins were extracted by solutions of potasium iodide with various strength. The total protein was determined by the method of Loury, but the sarcoplasmic proteins were examined electrophoretically. Electrolytes were estimated by flame photometer. The enzyme activity was examined by the reagents of "Boehringer". There was an increase of the amount of myosin and of the enzyme active sarcoplasmic protein fraction in the myometrium of pregnant animals. Potasium was increased in the uterine muscle during pregnancy, but sodium decreased. Enxyme activity of ALD, GOT and GPT was the highest in animals from the second group, but that of LDH-in the third group.
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PMID:[Biochemical changes in the myometrium of pregnant cats]. 124 Aug 2

The effect of three anticancer agents, cisplatin, doxorubicin, and mitomycin, on liver regeneration after 70% partial hepatectomy in rats was investigated by total DNA content of the liver and flow cytometric analysis of hepatocyte nuclei using two-color staining of anti-bromodeoxyuridine monoclonal antibody and propidium iodide. Total DNA content of regenerating liver 7 days after hepatectomy showed significant suppression of regeneration by these agents (P less than 0.01). The inhibitory effects of the agents on the cell cycle of hepatocytes by flow cytometric analysis were (1) a delay of the peak or a decrease in the proportion of S phase nuclei and/or (2) polyploidization of the nuclei, demonstrated by accumulation of 8c and occasionally 16c nuclei, of which the DNA contents were four and eight times as much as that of diploid (2c) cell nuclei, respectively. The former (1) suggests G0 or G1 phase block, and the latter (2) G2 phase block. In terms of total DNA content of regenerating liver, the inhibitory effect was most prominent in the cisplatin-administered groups. The polyploidization of nuclei was most remarkable in the mitomycin-administered groups. Although the total DNA content recovered to the level of control at 6 weeks after hepatectomy, the polyploidization effect persisted in the drug-administered groups. These agents had no cytocidal action on proliferating hepatocytes as can be seen from the aspartate aminotransferase and alanine aminotransferase serum levels. We conclude that in a short-term observation, the anti-cancer agents significantly inhibit liver regeneration, although the inhibitory effect on DNA synthesis does not last long.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of anticancer agents on cell cycle of regenerating hepatocytes in rats. 152 46

In risk assessments the various forms of iodine have been treated as if they were toxicologically equivalent. While iodide (I-) and iodate (IO3-) have been studied, no studies concerned with the subchronic toxicity of iodine (I2) have been conducted in experimental animals. This study examined toxicities associated with iodine. Rats were treated with 0, 1, 3, 10, and 100 mg/l of either iodine or iodide (as Nal) in the drinking water for 100 d. Treatment had no effect on body, brain, or heart weights in either sex, or on testes weights in male rats. Although differences in kidney and liver weights were noted, they did not appear to be treatment related. Thyroid weight in male rats was significantly increased with an increasing concentration of iodide in the water, but not iodine. In contrast, thyroid weight decreased at the highest dose of iodide in female rats. Hematocrit, hemoglobin, and blood urea nitrogen (BUN) values were relatively constant and did not vary with treatment. There were no significant differences in AST, ALT, cholesterol, and triglyceride values. After 10 d on treatment a dose-related trend in increased plasma T4 concentrations was observed in both sexes treated with iodine. Statistically significant increases in the T4/T3 ratio in both sexes was also noted with iodine treatment. This increase was maintained for 100 d of treatment. Iodide did not produce this effect at 10 d. Although there was a significant increase in T4/T3 ratios in female rats after 100 d of treatment with iodide, the magnitude of the changes was smaller than that observed with iodine treatments. The results of this study indicate that iodine and iodide affect thyroid hormone status in substantially different ways.
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PMID:Comparison of toxicity induced by iodine and iodide in male and female rats. 198 65

Excretion of urinary lactate dehydrogenase (LDH, EC 1.1.1.27), gamma-glutamyltransferase (gamma-GT, EC 2.3.2.2), alkaline phosphatase (ALP, EC 3.1.3.1), alanine aminopeptidase (AAP, EC 3.4.11.-), alanine aminotransferase (GPT, EC 2.6.1.2) and N-acetyl-beta-D-glucosaminidase (NAG, EC 3.2.1.30) was studied following a single i.v. application of 1 mg mercuric chloride/kg body weight or a radio contrast medium (SH H 340 AB) at a dose of 7.5 g iodine/kg body weight in rats. Measurements of urinary enzymes and serum urea nitrogen and creatinine were carried out on the second, third, fourth and ninth days after treatment. Histological examinations of kidneys were performed on day 9. A drastic increase in urinary LDH and moderate increase in gamma-GT, ALP and AAP and a very slight increase in GPT was observed in the first 18-h urine samples after mercuric chloride. This increase in enzymuria was associated with a drastic increase in serum urea nitrogen and creatinine, with a maximum on day 4. The radio contrast medium-treated animals showed a similar but less pronounced pattern of urinary enzymes excretion and only a slight increase of serum urea nitrogen on day 2. A good correlation was found between histological findings and enzymuria as well as serum urea nitrogen and creatinine. Thus, determination of only some urinary enzymes (LDH and gamma-GT) is valuable in predicting early nephrotoxicity and sufficient for the diagnosis of proximal tubule damage in rats.
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PMID:Value of enzyme determinations in urine for the diagnosis of nephrotoxicity in rats. 287 61

Povidone-iodine caused peritonitis with neutrophilic leukocytosis and a minimal left shift at the dosage rate of 3.5 ml/kg body weight. A dosage rate of 2 ml/kg only caused slight neutrophilic leukocytosis. There was a significant increase in the levels of creatinine (p = 0.049) and BUN (p = 0.020) in dogs that received the higher dose rate. Two dogs died from povidone-iodine toxicity with a marked increase in ALT, AP, SDH and conjugated bilirubin. It is concluded that povidone-iodine is unsafe for use in the peritoneal cavity of dogs.
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PMID:Haematology and serum biochemistry in the racing greyhound following intraperitoneal povidone-iodine. 317 40

We studied the effect of L-glutamine (Gln), the principal intestinal fuel, on proliferation of a porcine jejunal cell line, IPEC-J2. In cells synchronized by serum deprivation for 4 h, Gln stimulated ornithine decarboxylase (ODC; EC 4.1.1.17) in a dose- and time-dependent manner, with maximal effects at 10 mM in 3 h (P < 0.01). Similar effects were seen for the structurally related amino acid L-asparagine and serum. The Gln effect on ODC was specific, as isosmolar mannitol, glucose, methyl-beta-D-glucoside, L-phenylalanine, ammonia, and aminoisobutyric acid were ineffective. The alanine aminotransferase inhibitor aminooxyacetate (AO) inhibited the ODC stimulation by Gln in a dose-dependent manner (half-maximal inhibitory concentration = 0.5 mM). AO was not toxic to cells, as determined by propidium iodide uptake into nuclei. In addition, Gln stimulated a twofold increase of cellular 24-h [3H]thymidine incorporation above rates of control cells bathed in standard media (P < 0.01); this effect was also blocked by AO. Gln and phorbol 12-myristate 13-acetate stimulated ODC in a synergistic manner. The Na+/H+ exchange inhibitor methylisobutyl amiloride blocked the enhancement of ODC by Gln. Gln also induced the mRNA of the immediate-early gene c-jun. Gln stimulates proliferation in a porcine jejunal cell line through a mechanism requiring transamination and intact Na+/H+ exchange. This stimulation of enterocyte proliferation by Gln suggests that therapeutic Gln administration could facilitate epithelial recovery in the injured small intestine.
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PMID:L-glutamine and L-asparagine stimulate ODC activity and proliferation in a porcine jejunal enterocyte line. 748 12

The objective of the paper was to assess the occurrence of congenital struma in kids in relation to the clinical and biochemical finding in their mothers. Observations involved 46 imported goats of Saanen and Alpine breeds in the course of kidding and their kids. Thyroid gland hypertrophy (39 goats) and somewhat worse or even bad state of nutrition were dominant clinical findings in pregnant goats and in goats after kidding. Abortions in the last month of pregnancy were recorded in 14 goats, and 14 goats delivered stillborn kids. Eighteen goats delivered 26 liveborn kids, but 18 out of them died within 12 to 24 hours after birth. Dead kids were hairless, they had skin edema, and very shortened thoracic as well as pelvic limbs. The thyroid gland was well visible and palpable. Surviving kids lagged behind in their growth and often suffered from bronchopneumonia as an additional disease. Iodine concentration in the blood serum of goats (5.58 +/- 2.14 mumol/l) was significantly lower (P < 0.01) in comparison with kids (133.4 +/- 15.61 mumol/l). This state was characterized by adequate T3 and T4 concentrations in the blood serum of goats (1.78 +/- 0.59 and 4.53 +/- 4.44 nmol/l, resp.) and of kids (4.66 +/- 2.26 and 182.93 +/- 2.59 nmol/l, resp.). Iodine content in the thyroid gland of the seven kids that died was 1.86 +/- 0.96 mg/kg fresh tissue. Examination of indicators of the internal environment in the blood serum showed alternate statistical differences (P < 0.01) between adult goats and their kids in erythrocyte counts, hemoglobin, hematocrit value, leucocyte counts, activities of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, concentrations of total protein, albumin, total immunoglobulins, total lipids, cholesterol, phosphorus, copper, iron and zinc, while the explicit relation to disorders of iodine metabolism and thyroid hormones was not confirmed. The average content of iodine in the examined samples of soil (14.67 mg/kg) and alfalfa hay (0.1 mg/kg) demonstrated that primary deficiency of iodine in goats was the cause of congenital struma in kids.
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PMID:[Iodine deficiency in goats as a cause of congenital goiter in kids]. 869 66

Severe trauma may initiate a systemic inflammatory response, which in turn may result in remote organ injury. After limb ischemia/reperfusion (I/R), intravital fluorescence microscopy was applied to the livers of normotensive rats to investigate the initiation of remote injury to the liver. Additionally, we determined whether Kupffer cell activation and tumor necrosis factor-alpha (TNF-alpha) were involved, via perfusion deficits, in such injury. TNF-alpha, measured by immunoassay, peaked at 30 minutes of reperfusion, but returned to baseline within 60 minutes. Limb I/R resulted in significant increases to global hepatocellular injury measured by alanine transaminase (ALT) and lethal hepatocyte injury as seen with intravital fluorescence microscopy. Although the number of perfused sinusoids went unchanged, a significantly augmented perfusion heterogeneity was measured. After 1.5 hours of reperfusion, both TNF-alpha and Kupffer cells were shown to contribute to global hepatocellular injury (e.g., ALT). After 3 hours, TNF-alpha was no longer essential for this injury, suggesting that some other mechanism(s) activated Kupffer cells and initiated hepatocellular injury. Using propidium iodide and fluorescence microscopy, we found that both TNF-alpha and Kupffer cell activation were necessary to drive hepatocytes toward lethal injury. No additional benefits were observed with a combination of TNF-alpha inhibition and Kupffer cell suppression. These results not only implicate both Kupffer cells and TNF-alpha in the initiation of remote hepatic injury, but suggest that sinusoidal perfusion deficits are not essential for the initiation of such injury. Other mechanism(s) are likely involved in the pathogenesis of remote hepatic parenchymal injury.
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PMID:Initiation of remote hepatic injury in the rat: interactions between Kupffer cells, tumor necrosis factor-alpha, and microvascular perfusion. 1038 49


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