Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), ornithine carbamoyltransferase (OCT), sorbitol dehydrogenase (SDH), gamma-glutamyl transferase (GGT), alkaline phosphatase (AP), lactate dehydrogenase (LDH) and creatine kinase (CK), were determined in eight organs of 10 healthy male blue foxes. OCT was absolutely liver specific and ALT was also found to be liver specific. SDH was also found primarily in the liver but its activity was relatively low. GGT was found almost exclusively in the kidneys. The highest levels of AP were observed in the kidneys and in the intestines. LDH together with AST was present in high activities in all the tissues tested. CK activity was highest in skeletal and cardiac muscles.
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PMID:Activities of some enzymes in the tissues of the blue fox (Alopex lagopus). 613 May 87

The toxicity and the distribution of polybrominated biphenyls (PBB) were investigated by feeding rations containing different concentrations of PBB to sows during pregnancy and lactation. Sows and newborn pigs were clinically unaffected. Mortality was increased among pigs nursing sows fed rations containing PBB. Although transplacental passage of PBB resulted in an appreciable amount of PBB in tissues of newborn pigs, far more PBB were transferred to the pigs through the milk. On a body-weight basis, nursing pigs consumed PBB in concentrations similar to the concentrations given to the sows. The highest tissue concentrations of PBB (fat basis) were found in the liver, followed by the adipose tissue, kidney, and brain. Dietary concentrations of 10 mg of PBB/kg of feed increased serum concentrations of alkaline phosphatase, alanine aminotransferase, and thyroid hormones of pigs, whereas dietary concentrations of 100 or 200 mg of PBB/kg of feed caused those values to decrease. Gross pathologic changes consisted of increased weight of the thyroid gland of newborn pigs and increased weight of the liver of 4-week-old pigs. Histologically, thyroid glands of newborn pigs were slightly hyperplastic, and the colloid was scant and vacuolated. In the liver, lesions consisted of fatty change and centrolobular necrosis; changes were more severe in the sows than in the pigs nursing those sows. Measuring serum concentrations of ornithine carbamoyltransferase was the most effective clinical test in assessing the degree of liver damage in the pigs.
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PMID:Toxicosis in sows and their pigs caused by feeding rations containing polybrominated biphenyls to sows during pregnancy and lactation. 626 87

Influence of alimentary zinc deficiency on nitrogen elimination and activities of urea cycle enzymes This study was conducted to investigate whether the hyperammonaemia shown in earlier zinc-deficiency experiments was the result of disturbed enzyme activities of the urea cycle. For this study 36 male Sprague-Dawley rats with an average body weight of 85 g were divided into three experimental groups of 12 animals each. Group 1 received the semisynthetic zinc-deficient diet (AIN-93G; 1.2 mg Zn/kg DM) ad libitum over 33 experimental days. Group 2 received the zinc-sulphate-supplemented control diet (60 mg Zn/kg DM) ad libitum and group 3 received the same diet matched to the feed intake of the zinc-deficient rats. Alimentary zinc deficiency reduced the zinc concentration and the activity of the alkaline phosphatase in serum by 75 and 67%, respectively. The activity of the glutamate dehydrogenase and the concentrations of ammonia and urea in the serum of the zinc-deficient rats showed no significant differences compared with pair-fed control rats. On the other hand the hepatic activity of the mitochondrial localized glutamate dehydrogenase of the zinc-deficient rats was significantly increased and the carbamoylphosphate synthetase and ornithine carbamoyltransferase were reduced about half in comparison with both control groups. The activities of the cytosolic liver enzymes such as argininosuccinate synthetase, argininosuccinase and arginase were again significantly increased in zinc-deficient rats compared with both control groups. The increased hepatic activity of the glutamate dehydrogenase possibly led to an enhanced NH(3) elimination in addition to urea synthesis. The typical reduction of feed intake in consequence of zinc deficiency is therefore not the cause of hyperammonaemia due to disturbed urea synthesis, as has been hypothesized in earlier studies.
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PMID:[Influence of alimentary zinc deficiency on nitrogen elimination and enzyme activities of the urea cycle]. 1168 72

The aim of this investigation was to determine if the hyperammonaemia shown in previous zinc-deficiency experiments was the result of disturbed enzyme activities for urea synthesis caused by zinc deficiency per se or was a secondary effect of the reduced feed intake accompanying energy and protein deficiency. For this, 24 male Sprague-Dawley rats with an average body weight of 109 g were divided into two groups of 12 animals each. Both groups were force fed by intragastric tube four times daily over 11 experimental days. Group 1 received a zinc-deficient diet (1.3 mg Zn/kg diet) in a total amount of 11.6 g/day/animal. Group 2 received the zinc sulphate-supplemented control diet (25 mg Zn/kg diet) in the same amount. This technique made it possible to supply even the zinc-deficient rats with sufficient nutrients over the whole experimental period in the same manner as for the control rats, at the same time and with the same dietary amounts. At the end of the experiment, the serum zinc concentration and the alkaline phosphatase activity were significantly reduced in the zinc-deficient rats by 59 and 37%, respectively, in comparison with control animals. This showed a severe alimentary zinc-deficiency status of the animals. The concentrations of ammonia and urea, as well as the activity of glutamate dehydrogenase in serum, were not influenced by the zinc-deficient nutrition within the experimental time. Likewise, the mitochondrial activities of glutamate dehydrogenase and carbamoylphosphate synthetase in the liver were not affected by the alimentary zinc concentration. On the contrary, the activities of ornithine carbamoyltransferase and cytosolic liver enzymes argininosuccinate synthetase, argininosuccinase and arginase were significantly increased in comparison with control rats. In the case of a sufficient supply of nutrients, alimentary zinc deficiency did not cause hyperammonaemia owing to disturbed urea synthesis, as previously hypothesized.
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PMID:[Nitrogen detoxification in artificially-fed zinc-deficient rats]. 1168 84


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