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  • Author or Editor: Mark S. Kuhlenschmidt x
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SUMMARY

Corticosteroid-induced alkaline phosphatase (calp) and intestinal alkaline phosphatase (ialp) from dogs were purified to homogeneity, as determined by polyacrylamide gel electrophoresis. Purification involved an uninterrupted system using deae-cellulose, concanavalin Aagarose, and monoclonal antibody affinity columns. The monoclonal antibody was prepared by use of ialp as the antigen. The 2 isoenzymes were compared, using molecular weight determinations, amino acid analyses, peptide mapping, N-terminal sequencing of the first 10 amino acids, carbohydrate analyses, and recognition by anti-ialp)monoclonal antibody. The data indicated that canine ialp and (calp are identical with regard to recognition by monoclonal antibody and N-terminal amino acid sequence, nearly identical in amino acid content and peptide maps, but different in carbohydrate content. It was concluded that (calp is a product of the same gene as ialp and that differences in glycosyl transferase activities between liver and intestines or the presence of glycosidase activities in or around the intestinal mucosae result in the marked difference in carbohydrate content.

Free access
in American Journal of Veterinary Research

Summary

High serum alkaline phosphatase (alp) activity is considered a sensitive marker of cholestasis in most mammalian species, including dogs. Induction of high serum alp activity in association with cholestasis is dependent on high hepatic bile acids concentrations. Treatment of dogs with glucocorticoids also results in high serum alp activity. The possible causal relation between serum alp activity and bile acids concentration was investigated in dogs treated with glucocorticoids. The relation of glucocorticoid treatment to changes in the activity of individual alp isoenzymes, alanine transaminase (alt) and γ-glutamyltransferase (ggt) also was investigated.

Eight conditioned dogs were given 4 mg of prednisone/kg of body weight, im, daily for 10 days. Blood samples were taken prior to treatment and on treatment days 3, 5, 7, and 10. Liver tissue was then taken from each dog. Serum total alp activity was significantly (P < 0.05) high at day 3 in prednisone-treated dogs. Isoenzyme analysis indicated that this increase was attributable to an increase in the liver alp isoenzyme (LALP). Significant increases in serum corticosteroid-induced alp (calp) and bone alp were first observed on days 7 and 10, respectively. Serum alt and ggt activities were significantly increased by day 5. Increased serum or hepatic tissue bile acids concentrations were not observed in prednisonetreated dogs, compared with values in 8 clinically normal (control) dogs, but were high in 3 dogs with complete bile duct ligation.

Hepatic activities of LALP, calp, and ggt were higher in prednisone-treated dogs than values in controls, indicating probable increased hepatic synthesis of these enzymes. Hepatic alt activity was not increased. The ratio of serum to tissue lalp activity was increased in prednisone-treated dogs, compared with values in controls, indicating that lalp may have been preferentially released into serum. There was no difference in the ratio of serum to liver ggt activity between prednisone-treated dogs and controls. The lalp and ggt ratios were increased in bile duct-obstruction dogs.

It was concluded that, although lalp is the principal alp isoenzyme in serum during the first 10 days of prednisone treatment, hepatic bile acid concentrations are not increased and, therefore, are not likely to be responsible for induction and release of alp into serum. Prednisone may, therefore, be directly responsible for induction of alp activity in dogs treated thusly.

Free access
in American Journal of Veterinary Research