Alkaline phosphatases occurrence

The frequent occurrence of sialylated enzymes, or even of multiple forms, which are sometimes tissue-dependent, with a varying number of sialyl residues as, for example, in y-glutamyltranspeptida.se (EC 2.3.2.2),456,457 is not yet fully understood. Although the activity of most of these enzymes is not influenced by removal of sialic acid,454 the activity of monoamine oxidase A (EC 1.4.3.4) of outer mitochondrial membranes of rat liver has been shown to be destroyed by treatment with sialidase438 the substrate specificity of acetylcholinesterase (EC 3.1.1.7) is altered,459 the kinetic properties of human acid and alkaline phosphatases (EC 3.1.3.1 and 3.1.3.2) are changed, and the stability of a-D-galactosidase (EC 3.2.1.22) is drastically lowered.415 In these cases, an influence of sialyl residues on the conformation of the enzyme is assumed, but awaits firm evidence. 

Alginates 170,178 Alkali metal ions 206 Alkaline phosphatases 645 active site of 645 occurrence 645 Alkane(s) 382 Alkenes, hydration of 683 Alkyl shift, rearrangements with 527 Alkyl cobalt 867 Alkyl ethers 382 Alkyl cobalamms... 

Neither the occurrence of a constant value of Vmax or a constant product ratio is sufficient proof of the presence of an intermediate. It was seen for alkaline phosphatase that a constant value for Vmax is an artifact, and also that there is no a priori reason why the attack of acceptors on a Michaelis complex should not also give constant product ratios. In order for partitioning experiments to provide a satisfactory proof of the presence of an intermediate, they must be linked with rate measurements. When the rate measurements are restricted to steady state kinetics, the most favorable situation is when the intermediate accumulates. If the kinetics of equations 7.5 to 7.7 hold, it may be concluded beyond a reasonable doubt that an intermediate occurs. The ideal situation is a combination of partitioning experiments with pre-steady state studies, as described for chymotrypsin and amides. 

Goldstein DJ, Rogers C, Harris H (1982) A search for trace expression of placental-Uke alkaline phosphatase in non-malignant human tissues demonstration of its occurrence in lung, cervix, testis and thymus. Clin Chim Acta 125 63-75... 

Fishman L, Miyayama H, Driscoll SG et al (1976) Developmental phase-specific alkaline phosphatase isoenzymes of human placenta and their occurrence in human cancer. Cancer Res 36 2268-2273... 

The biochemical response of patients with Paget s disease to other therapeutic agents is similar to that detailed for calcitonin except for the occurrence of the escape phenomenon, which has been observed only with calcitonin therapy. During mithramycin therapy, serum alkaline phosphatase declines more rapidly than during calcitonin therapy (L7)... 

While unexplained hyperphosphatasemia is sometimes found in otherwise healthy patients (see Section 5), this is a relatively uncommon occurrence. Hence, serum alkaline phosphatase elevation, unless clearly due to a rise in nonhepatic enzyme, calls for thorough investigation of the hepatobiliary system. 

A18. Asanti, R., Hultin, H., and Visakopi, J. K., Serum alkaline phosphatase in healthy infants. Occurrence of abnormally high values without known cause. Ann. Paediatr. Fenn. 12, 139-142 (1966). 

The most prominent signs of chronic hypervitaminosis A are cutaneous, including dryness of the mucous membranes. Laboratory abnormalities include radiologically detected bone changes in children, increased serum alkaline phosphatase, increased serum calcium, increased cerebrospinal fluid pressure, and disturbed blood clotting. Adverse effects associated with chronic hypervitaminosis A, in decreasing order of occurrence, are presented in Table V. 

Functional differences, such as variations in the occurrence of certain enzymes, may exist between different vascular beds. In brain capillary endothelial cells, the distribution of alkaline phosphatase and Na , K ATPase differs between the luminal and antiluminal cytoplasmic membranes. Cadmium is known to inhibit several SH-containing enzymes and it might be speculated that the content and subcellular distribution of enzymes in ganglionic endothelial cells are of importance for the preferential occurrence of cadmium-induced vascular injury in ganglia. A similar theory has been proposed to explain the vascular damage caused by cadmium in the testis. Thus, Aoki and Hoffer suggested that a cadmium-sensitive testicular isoenzyme of carbonic anhydrase may in some way be associated with the capillary endothelial cells. 

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