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)

Zinc deficiency (ZD) is teratogenic in rats, and fetal skeletal defects are prominent. To elucidate further the effects of maternal ZD in the fetal skeleton, we performed a morphological and histochemical study of tibial growth plate (GP) in ZD rat fetuses. The histochemical study included the identification of calcium, of hydrolytic enzymes associated with the process of calcification, and of oxidative enzymes related to energy production and to the synthesis of proteoglycans. Pregnant Sprague-Dawley rats were fed (1) a control diet (76.4 micrograms Zn/g diet) ad libitum (group C), (2) a zinc-deficient diet (0 micrograms/g) ad libitum (group ZD), or (3) the control diet pair-fed to the ZD rats (group PF). On day 21 of gestation, laparotomies were performed, the fetuses were removed, and fetal tibiae obtained. Specimens were stained with hematoxylin-eosin (H&E) and Masson Trichrome and were processed for identification of alkaline phosphatase, adenosine triphosphatase, succinic dehydrogenase, NADH dehydrogenase, and calcium. The morphologic patterns found in ZD fetal tibiae indicated defects in various cell types implicated in bone metabolism. Staining for hydrolytic enzymes revealed alterations in the size and distribution of matrix vesicles and a weaker staining for ATPase in ZD fetuses. Staining for oxidative enzymes was overall more intense in ZD fetal tibiae. ZD fetuses also presented irregular and defective calcification. These findings indicate that severe maternal ZD in the rat results in structural and functional alterations in the GP of fetal bone, leading to a defective endochondral ossification.
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PMID:Changes in the fetal tibial growth plate secondary to maternal zinc deficiency in the rat: a histological and histochemical study. 196 89

Zinc deficiency and cadmium toxicity have both been implicated in hypertension during pregnancy. The goals of this study were twofold: first, to assess the different zinc indices (plasma, red blood cell zinc, heat-labile alkaline phosphatase, and placental zinc) in normotensive and hypertensive parturients to determine whether they are altered in the different types of hypertension that occur during pregnancy; second, to assess whole-blood cadmium and placental cadmium with regard to hypertension and zinc status. Patients were diagnosed as having chronic hypertension or preeclamptic toxemia and were then further divided into groups on the basis of smoking status. Each patient was matched with a normal control subject based on age, parity, and smoking status. Forty-three hypertensive patients and their matched control subjects were studied. No differences were found in the various zinc indices between chronic hypertensive parturients and normal control subjects. However, in parturients with preeclamptic toxemia, the plasma zinc level was 19% lower than in control subjects (p less than 0.02); these patients had the lowest plasma zinc level of the three groups. Placental zinc was also 12% lower in patients with preeclamptic toxemia than in control subjects (p less than 0.04). Whole-blood cadmium and placental cadmium levels did not differ between control subjects or hypertensive patients. However, a significant positive correlation was found between whole-blood cadmium and plasma zinc levels in preeclamptic toxemia (r = 0.53; p less than 0.05). The results support a marginal zinc deficiency in parturients with preeclamptic toxemia but not in those with chronic hypertension. The role of cadmium in the cause of preeclamptic toxemia remains unclear.
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PMID:Zinc, cadmium, and hypertension in parturient women. 237 50

The influence of alimentary zinc deficiency on duration of skin allograft functioning was studied in experiments on guinea pigs. Feeding the animals with a ration deprived of zinc results in significant prolongation of the skin graft functioning period. Thus, in the test group animals that received the ration deprived of zinc the mean time of the graft functioning comprised 24.0 +/- 1.4 days, while in the guinea pigs of the control group that were fed with full value ration, this parameter was 9.9 +/- 0.42 days. At the same time the number of circulating lymphocytes was decreased and their capacity for spontaneous rosette-formation was suppressed in the peripheral blood of the test group animals, as well as manifest inhibition of zinc-dependent enzymes (lactate dehydrogenase, alkaline phosphatase, carbonic anhydrase) in the blood was recorded. Zinc deficiency in the ration induces significant diminution of this trace element content in the muscles, bones, liver, skin and blood, under conditions of its daily negative balance in the body.
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PMID:[Effect of exogenous zinc deficiency on the duration of skin graft functioning]. 329 91

1. Zinc deficiency was produced experimentally in guinea-pigs fed on a diet containing 1.25 mg Zn/kg diet over a period of 60 d. In addition, the response of the Zn-deficient (ZnD) animals to Zn supplementation was studied for 15 d. 2. In the ZnD group a significant reduction was found in serum Zn and protein concentrations and in alkaline phosphatase (EC 3.1.3.1; AP) activity from day 24 onwards. 3. Paper electrophoretic studies on serum revealed a significant decrease in relative values, as well as absolute values, of albumin and gamma-globulin and an increase in beta-globulin. 4. Albumin:globulin increased on day 24 but decreased significantly from day 48 onwards. 5. The kidney and testis of the ZnD group showed a reduction in Zn and protein contents, and AP activity. 6. Zn supplementation of the previously ZnD group resulted in marked although incomplete improvement in the biochemical indices studied.
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PMID:Experimental zinc deficiency in guinea-pigs: biochemical changes. 367 79

The effect of zinc deficiency on bone collagenase activity and collagen turnover was studied in the chick. Zinc deficiency symptoms, evident after 8 days on the low zinc diet, included tibia deformities and decreased alkaline phosphatase. Bone collagen metabolism was markedly altered, with a significant reduction in collagen synthesis and turnover. Half-turnover time for tibia collagen was 13 days in the control and 35 days in the zinc-deficient chicks. Tibia collagenase activity was reduced by 40-80% in the zinc-deficient as compared to the control chicks. Heparin markedly increased collagenase activity in the zinc-deficient tibias elevating activity to control levels. But commercially available heparin was found high in zinc content which may explain this effect entirely. These data show that zinc deficiency decreases bone collagen turnover and probably accounts for the leg deformities seen in zinc-deficient chicks.
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PMID:Effect of zinc deficiency on bone collagenase and collagen turnover. 625 4

During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc deficiency in human subjects. 636 78

A zinc deficient diet which is not semi-synthetic was tried on 20 male Limousin X Romanoff three and a half month-old sheep weighing 36 kg on average. This diet was composed of strawy hay sprayed with caramel containing urea and minerals. Compared to hay alone this diet is more appetizing to lambs and more equilibrated as to energy level and soluble nitrogen utilization. The deficiency appeared within a week in zinc plasma and progressed clinically within 100 days. The plasmic free zinc and alkaline phosphatase were not better criteria for the deficiency diagnosis than total plasmic zinc. Supplementing the diet to 50 or even 100 mg Zn/kg DM was insufficient to suppress the deficiency. Zinc injection, by contrast, restored zincemia to normal in ten days. Zinc deficiency treatment by oral route should be reconsidered.
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PMID:A zinc-deficient diet for ruminants: diagnosis and treatment of deficiency. 668 25

Three premature infants with zinc deficiency who had an unusual presentation with generalized edema and hypoproteinemia between 5 and 9 weeks of age are described. The infants were fed their own mother's milk, supplemented with a proprietary formula after the first 2 to 3 weeks of life. None of the infants had diarrhea, liver disease, or urinary protein loss. Treatment with oral zinc supplements led to rapid resolution of the edema, with an increase in values for serum proteins, alkaline phosphatase, and zinc. There was no recurrence of symptoms following discontinuation of zinc therapy 1 month later. At 1-year follow-up, all infants were doing well and had normal growth and development. As zinc plays a critical role in nucleic acid and protein synthesis, it is postulated that dietary zinc deficiency in the phase of rapid postnatal growth precipitated edema and hypoproteinemia in these infants. Zinc deficiency should be included in the list of causes of generalized edema in the low-birth-weight infant.
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PMID:Edema, hypoproteinemia, and zinc deficiency in low-birth-weight infants. 670 Oct 56

1. Zinc deficiency in young rats reduced both the total alkaline phosphatase (EC 3.1.3.1) activity and Zn concentration in serum, kidney, small intestine and femur. 2. Addition of 0.01 mM-exogenous Zn had no greater activating effect with extracts of kidney, small intestine and femur from Zn-deficient than control rats, indicating that the main effect of the deficiency was on the amount of enzyme present rather than the efficiency of its operation. Exogenous Zn increased the activity of enzyme in serum Zn-deficient rats, but it was still lower than in the serum of control animals. 3. Electrophoresis on polyacrylamide gel separated the alkaline phosphatase activity from all tissues into two bands. The bands had similar electrophoretic mobilities and appeared to be qualitatively identical in corresponding tissues from Zn-deficient and control rats. 4. Zn deficiency eliminated the first band found in serum from control rats and it had selective effects on the activity of individual bands in other tissues. The major inhibitory effect was on the first bands of enzyme activity in kidney and femur, but in small intestine only the second band was affected. In liver the activity of the first band was increased and that of the second band decreased by similar amounts.
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PMID:The effect of zinc deficiency on alkaline phosphatase (EC 3.1.3.1) and its isoenzymes. 741 97

It is generally believed that the zinc metalloenzyme alkaline phosphatase is required to hydrolyze phosphorylated forms of vitamin B-6 prior to their use. To test this hypothesis, rats were fed a liquid diet containing either adequate or moderately low zinc during gestation and lactation. Zinc deficiency was produced in dams evidenced by significant reductions in zinc concentration of plasma (49%), liver (25%), and femur (24%), and plasma alkaline phosphatase activity (48%). Plasma pyridoxal-5'-phosphate (PLP), which significantly increased (61%) in these same rats, was negatively correlated (r = -0.74, P < 0.02) with plasma alkaline phosphatase activity. Maternal liver PLP concentration was unaffected by zinc status. The zinc and vitamin B-6 relationship seen in dams was less observable in offspring. Stimulation of erythrocyte alanine aminotransferase activity by exogenously added PLP in vitro tended to be higher in both moderately zinc-deficient mothers and their offspring, but the difference was not significant. Our results support the hypothesis that alkaline phosphatase activity is required for the hydrolysis of plasma PLP. Our results also suggest that zinc status as alkaline phosphatase activity should be defined in an individual if plasma PLP is to be used as an indicator of vitamin B-6 status.
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PMID:Increased plasma pyridoxal-5'-phosphate when alkaline phosphatase activity is reduced in moderately zinc-deficient rats. 750 77


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