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

Xenopus laevis (Daudin) adult specimens were submitted to hypophysectomy. Although the operation resulted subtotal, it served the purpose of removing the prolactin-producing cells, whereby the involvement of endogenous prolactin in osmoregulation phenomena was excluded. In the operated animals treated with ovine prolactin the following metabolic parameters, which are closely dependent upon interrenal activity, were estimated: 1) intestine alkaline phosphomonoesterase activity (E.C. 3.1.3.1); 2) liver glycogen level; 3) glucose-6-phosphatase (E.C. 3.1.3.9.) and phosphoenolpyruvate carboxykinase (E.C. 4.1.1.32.) in the liver; 4) blood glucose level; 5) blood ammonia and urea levels; 6) carbamoylphosphate synthetase activity in the liver (E.C. 2.7.2.a); 7) muscle sodium and potassium levels. The above metabolic parameters were found to be pressed by subtotal hypophysectomy and after subsequent prolactin treatment showed the tendency to go back to values similar to those of control animals.
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PMID:Biochemical data on subtotally hypophysectomized Xenopus laevis (Daudin) adult specimens treated or not with prolactin. 21 25

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

The aim of the present study was to determine whether the level of dietary protein would influence the onset of zinc deficiency in rats because zinc-deprived rats have problems metabolizing dietary protein. Young male Sprague-Dawley rats were fed isoenergetic Zn-deficient diets (0.8 mg Zn/kg diet) or control diets substituted with zinc sulfate (54 mg Zn/kg diet) and protein levels of 2, 5, 8, 10, 15, 20 or 25 g/100 g for 21 d to determine whether changing the protein level of Zn-deficient diets affects the Zn status of the rats. In rats fed low dietary protein levels of 2 and 5%, feed intake, growth and appearance did not differ between the Zn-deficient rats and the control rats because the low zinc requirement was met by mobilization of zinc from the skeleton. At higher dietary protein levels, the Zn-depleted rats developed marked signs of Zn deficiency and had reduced feed intake, growth, alkaline phosphatase activity in the serum and Zn concentrations in serum and femur compared with the control rats. The reduced feed intakes and decreased growth of Zn-depleted rats fed high dietary protein levels (20 and 25%) compared with control rats may be due to disturbed protein synthesis, as demonstrated by the increased activities of alanine aminotransferase, glutamate dehydrogenase and carbamoylphosphate synthetase in the liver. Zinc as an essential component of the diet is thus vital for the efficient utilization of dietary protein.
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PMID:Development of alimentary zinc deficiency in growing rats is retarded at low dietary protein levels. 1284 Jan 96