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 effects of ingesting a glucose polymer solution (GP) or water (W) on plasma pyridoxal 5'-phosphate (PLP) and pyridoxal (PL) concentrations were compared in six men (age: 30 +/- 2 y; VO2max: 57.4 +/- 3.2 mL.kg-1.min-1) under running (R) and control (C) conditions. Subjects ran for 2 h at 60-65% of VO2max for R and remained standing for C. For both R and C, 200 mL W or GP was ingested before (0-time) and every 30 min while running (30, 60, and 90 min). Plasma PLP decreased to 95% and 87% of 0-time at 180 min for WC and GPC and increased to 126% and 119% at 90 min and to 124% and 119% at 120 min for WR and GPR. By 60 min postrun, plasma PLP was 98% (WR) and 101% (GPR) of 0-time. There were no significant differences between W and GP conditions. Changes in PLP were not related to plasma volume or blood glucose, free fatty acids, lactate, alkaline phosphatase, aspartate aminotransferase, or alanine aminotransferase. No significant changes in plasma PL were noted. Exercise induces an increase in plasma PLP, perhaps due to transfer of B-6 vitamers from liver to skeletal muscle.
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PMID:Plasma pyridoxal and pyridoxal 5'-phosphate concentrations in response to ingestion of water or glucose polymer during a 2-h run. 198 51

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

Twenty of 320 patients with Wilson's disease initially presented with chemical and laboratory features of chronic active hepatitis, confirmed histologically in 17. When first seen, cirrhosis was present in all 20 and was complicated by ascites and/or jaundice in 11. Within 1 week to 8 years of the onset of over liver disease the diagnosis of Wilson's disease was established, and treatment with D-penicillamine was promptly initiated in 19 patients. One man refused treatment and died 4 months later. Treated patients received D-penicillamine or trientine for a total of 264 patient-years (median, 14 patient-years). Abnormal water retention, for which salt restriction and diuretics were added to penicillamine or trientine, disappeared in all but 1 of the patients so affected. Symptomatic improvement and virtually normal levels of serum albumin, bilirubin, aspartate aminotransferase, and alanine aminotransferase followed within 1 year in the majority of subjects. One woman died after 9 months of treatment. Two patients, who became noncompliant with the therapeutic regimen after 9 and 17 years of successful pharmacological treatment, required liver transplants. These results indicate that the prognosis of specifically treated Wilsonian chronic active hepatitis is very good in spite of the presence of cirrhosis.
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PMID:Prognosis of Wilsonian chronic active hepatitis. 199 98

Acetone potentiation of liver injury is greater when corn oil is given with acetone 18 h prior to a challenge with CCl4. This study aimed to further characterize the effects of the vehicle used to administer acetone on the severity of acetone-potentiated CCl4-induced liver injury. The more severe acetone-potentiated liver injury observed when corn oil was the vehicle does not seem to be due to greater liver acetone concentrations. When corn oil was used as the vehicle to administer acetone, liver and blood CCl4 concentrations were not significantly different from those where water was the vehicle. Therefore the relationship between blood or liver acetone concentration and plasma ALT activity for orally-administered acetone was modified by corn oil. Liver triglyceride concentration measured 18 h after a gavage of corn oil was significantly higher than that for the water-treated group. A direct effect of corn oil on liver, in particular a promotion of the propagation phase in the lipid peroxidation process induced by CCl4, is proposed to explain the increase in acetone-potentiated CCl4-induced liver injury.
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PMID:Inhalation versus oral administration of acetone: effect of the vehicle on the potentiation of CCl4-induced liver injury. 204 61

The subchronic toxicity of an aqueous extract of Viscum cruciatum Sieber, a parasite of Prunus amygdalus Stokes, was studied in Wistar rats. The extract at dosage-levels of 30, 120 and 480 mg/kg body weight/day was administered in the drinking water during 12 weeks; checks being carried out after 4 and 8 weeks of treatment. No apparent symptoms of toxicity were observed, except for a slight apathy and reduced mobility in the batch receiving the highest dose. A slight leukopenia and a moderate increase in glycemia, uremia and plasma GPT activity was observed. No modifications occurred in the other constants studied. Histopathological analysis of the spleen, lung, kidney and liver were found to occur at the highest dosage-level, while in the other organs slight lesions of a reversible nature were observed. A certain degree of recovery was observed in the case the spleen at the end of the experiment. In all, it can be said that no manifest signs of toxicity were found in animals receiving the intermediate and higher dosages, though these were not found to be related to sex. Taken together all these observations indicate that the aqueous extract of Viscum cruciatum Sieber has a low toxicity within the conditions of our experiment.
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PMID:[Subchronic toxicity of Viscum cruciatum Sieber]. 208 Aug 35

Serum activities of alanine-aminotransferase (ALAT, EC 2.6.1.2), aspartate-aminotransferase (ASAT, EC 2.6.1.1), lactate dehydrogenase (LDH, EC 1.1.1.27), and alkaline phosphatase (AP, EC 3.1.3.1) were increased significantly after a dose of 0.16 g/kg/b. w. (ip.) carbon tetrachloride (tetrachloromethane) in rats pretreated with 10% (v/v) ethanol for one and 10 weeks in comparison with water/carbon tetrachloride-treated animals. At the end of 30 and 52 weeks of ethanol consumption these levels were very slightly increased or not detectable. Ethanol treatment alone did not cause an increase in serum enzyme activities or histological liver damage, but caused a diminished intake of fluid and food and in some cases also a reduction of weight gain in the animal body. Significant decrease in body weight after carbon tetrachloride was more evident in rats pretreated with ethanol (1 week greater than 10 greater than or equal to 52 weeks) than in water drinking animals, the lethality caused by carbon tetrachloride was also higher after one and 10 weeks than after 30 to 52 weeks of ethanol pretreatment. The results indicate a decrease of carbon tetrachloride toxicity with increased duration of ethanol pretreatment. This phenomenon could be attributed to reduced sensibility to those alcohol effects which are responsible for increase of carbon tetrachloride toxicity.
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PMID:Influence of ethanol pretreatment of differing duration on toxic effects of carbon tetrachloride in rats. 208 Sep 8

To assess the validity of determining the origin of plasma lactate from the ratio of lactate and glucose specific activities (SA) during infusion of labeled glucose, normal subjects received infusions of [6-3H]- and [6-14C]glucose for 4 h after a 12 h fast, and, on another day, cold glucose labeled with both tracers during 4-6 h of hyperinsulinemia (approximately 650 microU/ml). Basally, less lactate was derived from plasma glucose when measured with [6-3H]glucose (27 +/- 2%) than with [6-14C]glucose (40 +/- 2%, P less than 0.001). Insulin did not increase the percent of lactate derived from plasma glucose when measured with [6-3H]glucose (29 +/- 2%) but did increase when measured with [6-14C]glucose (60 +/- 4%). The arterialized blood (A) [3H]lactate SA was 30-40% higher (P less than 0.01) than deep venous blood (V) [3H]lactate SA, whereas A and V [14C]lactate SA were similar. During conversion of alanine to lactate with glutamic-pyruvic transaminase (GPT) and lactate dehydrogenase (LDH) in vitro, 32 +/- 2% of 3H in [3-3H]alanine was found in water and 68 +/- 2% in lactate. During infusion of [6-3H]- and [6-14C]glucose, the ratio of [14C]alanine to lactate SA (0.88 +/- 0.05) was less than the ratio of [3H]alanine to lactate SA (0.31 +/- 0.03, P less than 0.001). In conclusion 1) loss of 3H relative to 14C from position 6 in glucose occurs during lactate formation in extrahepatic tissues possibly due to the GPT reaction (alanine conversion to pyruvate), and 2) even under supraphysiologic hyperinsulinemic conditions not all of plasma lactate originates from plasma glucose.
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PMID:Measurement of lactate formation from glucose using [6-3H]- and [6-14C]glucose in humans. 220 8

The toxicity of cadmium was examined in rats fed diets containing either tissue-incorporated cadmium or cadmium salt for 4 wk. The test diets contained 30 mg cadmium/kg either as cadmium chloride, or as cadmium incorporated in pigs' livers; the control group was fed a diet containing liver from a pig not treated with cadmium. Over 90% of the cadmium present in the pigs' livers was bound to metallothionein. Analysis of the diet and determination of the food consumption revealed that both cadmium-fed groups were exposed to similar dietary cadmium levels. There was no adverse effect on general health or survival. Feeding cadmium resulted in growth retardation and slightly decreased water intake. Moreover, both cadmium-treated groups showed clear signs of anaemia and increased plasma aspartate and alanine aminotransferase activities. For the group fed cadmium chloride, all of these effects were more pronounced than for the group fed cadmium incorporated in liver. Microscopic examination of the liver and kidneys, however, did not reveal any lesion that could be attributed to the cadmium treatment. After exposure to cadmium the spleen showed decreased extramedullary haematopoiesis, an effect that was also more pronounced after feeding of the cadmium chloride than after feeding liver-incorporated cadmium. The differences in the extent of the toxic effects between the inorganic and the tissue-incorporated cadmium were accompanied by differences in the cadmium concentrations in liver and kidneys: the feeding of cadmium incorporated in pigs' livers resulted in about half the accumulation of cadmium in the rats' livers that took place after intake of a diet containing cadmium chloride. In contrast a much less marked difference in cadmium accumulation was observed in the kidneys. Since humans are usually exposed to tissue-incorporated cadmium these findings deserve further investigation, with special attention to the observed difference in tissue accumulation.
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PMID:Comparison of the toxicity of inorganic and liver-incorporated cadmium: a 4-wk feeding study in rats. 221 May 16

A subchronic, toxicity study of lovastatin-acetaminophen combination in s/w mice is reported. Oral administration of lovastatin in corn oil 30 mg/kg three times a week and acetaminophen 0.75% w/v in drinking water for 13 weeks resulted in significant increase in SGPT (ALT) in both male and female mice. Histopathology of the liver revealed centrilobular hepatocyte swelling. These results provide evidence of hepatic injury in s/w mice when concomitantly exposed to lovastatin and acetaminophen.
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PMID:Lovastatin-acetaminophen subchronic toxicity in mice. 223 4

Aflatoxins B1, B2, G1 & G2 were administered in a low concentration (100 ppb of each aflatoxin (AN] in a mash offered to Baladi rabbits. An other group of rabbits were fed on the same contaminated mash in addition to 0.25% charcoal (CC). The two groups were compared to control animals fed on AN-free mash. Inclusion of AN in the diet decreased feed and water consumption, body weight and survival rate. Charcoal improved somewhat feed and water consumption and growth rate than AN-group. However, CC-group affected digestibility of organic matter more than AN-group. Relative weights of liver, kidneys, heart and adrenal glands were significantly higher in AN and CC groups than the control group. Blood haemoglobin content, packed cell volume percentage and sedimentation rate were lower in AN group. Although there were an increase in each of serum, calcium, inorganic phosphorus, cholesterol, phospholipids and glutamic-pyruvic transaminase in AN group, yet the serum nitrogen and glutamic-oxalacetic transaminase were reduced. Charcoal had alleviated AN-effects concerning N, GPT and phospholipids. Chemical analysis revealed elevation of water, ash and silica contents of liver and water content of muscles from AN-animals. On the other hand, fat content, GOT and vitamin A in the liver as well as muscles ash were reduced. Addition of CC to the diet reduced AN-effects on liver fat, ash and silica but resulted in a rise of the water content of liver and muscles and liver GPT activity. Charcoal also resulted in a sharp decrease in vitamin A content of the liver. Aflatoxin treatments (in AN and CC groups) reduced bone ash, silica and magnesium as well as bone volume. Charcoal administration increased Ca-content of bones. Aflatoxin feeding (in AN group) resulted in a high residual percentage of AN in muscles, serum, liver, heart and kidneys with relationships of 51 :24 : 3 :2 : 1, respectively. Only 1.42% of the fed AN was excreted in the faeces. Charcoal usage had a good effect as it prevented AN to accumulate in the organs. Aflatoxin contaminated diets (in AN and CC groups) resulted in paralysis, disorder of fat deposition, discolouration and haemorrhages of some organs. Scanning electron microscopic examination revealed no ill effect on the surface structure of the small intestine due to either AN or AN + CC. Pathological examination showed that the main affected organs were liver, heart and spleen, respectively. The changes include hepatic round cell infiltration, irregularities of lobular plats, focal necrosis and periportal fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of low level of dietary aflatoxins on baladi rabbits. 224 71


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