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)

Small intestinal mucosal function and structure was investigated in 13 patients with pernicious anemia prior to and after treatment with vitamin B12. Histological abnormalities of the jejunal mucosa were shortening of villi of varying degree, increased infiltrate of the lamina propria with monocytes and plasma cells and megalocytosis of the absorptive epithelial cell. Malabsorption of d-xylose occurred in 45%, fat in 30%, vitamin B12-IF complex in 69%, hypocarotinemia in 23% and hypoalbuminemia in 30% of the patients. By contrast, digestive brush border enzymes, i.e. disaccharidases, alkaline phosphatase and leucyl-naphthylamidase were not altered in pernicious anemia. Patients with significant jejunal mucosal abnormalities and decrease of the absorptive surface demonstrated malabsorption of one or more nutrients. Morphological and functional abnormalities were restored to normal after treatment with vitamin B12, suggesting that small intestinal changes in pernicious anemia constitute primary systemic manifestations.
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PMID:Functional and morphological abnormalities of the small intestinal mucosa in pernicious anemia--a prospective study. 69 8

Progressive changes in serum enzyme activity and liver histologic features were monitored in calves fed tansy ragwort (Senecio jacobaea)-contaminated pellets. The experiments were designed to simulate natural intoxicant ingestion conditions in relationship to the dose and duration of exposure to the toxic plant to correlate early laboratory diagnostic changes with the natural progression of the disease, thereby facilitating early diagnosis and intervention by veterinary clinicians. Eight calves were fed tansy ragwort and 4 additional calves served as controls. In group 1, 4 calves were continuously fed dried tansy ragwort mixed in a pelleted feed at a 5% concentration by dry weight until terminal liver disease developed. Serum liver enzyme (alkaline phosphatase, glutamate dehydrogenase, and gamma-glutamyltransferase) activities were monitored at weekly intervals in these calves and in the 2 controls. In group 2, 4 calves were fed the same contaminated feed for only 60 days, with return to normal feed for the duration of the trial. Two additional calves served as controls. Their liver enzyme activities were monitored every other week in conjunction with percutaneous liver biopsies. All 8 calves fed tansy ragwort-contaminated pellets developed terminal hepatopathy in either a chronic pattern (n = 6) or a chronic-delayed pattern (n = 2), with the onset of a moribund state or sudden death at 11 to 17 weeks and 27 to 51 weeks, respectively. The calves were euthanatized when classic terminal signs of hepatic encephalopathy first became evident. The clinicopathologic patterns of chronic and chronic-delayed toxicoses were typical of over 5,000 cases of field tansy toxicosis diagnosed at the diagnostic laboratory. Serum glutamate dehydrogenase was the first enzyme to increase in most animals, with a short-term increase to peak values followed by a rapid return to normal. This enzyme change was followed by increases in alkaline phosphatase and gamma-glutamyltransferase. Serum enzyme changes preceded development of recognizable histologic lesions. Vacuolar changes in hepatocyte nuclei, biliary hyperplasia, and fibrosis sequentially developed in liver biopsy specimens from each animal, whereas megalocytosis was not a predominant feature until necropsy. On the basis of our findings, we suggest that the optimal tests for diagnosis of pyrrolizidine alkaloid intoxication should consist of liver biopsy and determination of concurrent serum liver-enzyme activities.
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PMID:Serum liver enzyme and histopathologic changes in calves with chronic and chronic-delayed Senecio jacobaea toxicosis. 168 78

Experimental liver injury was provoked in test rats with intraperitoneal injections of D-galactosamine. Traumatized rats received further intraperitoneal injections of Hepasor, a protoberberine alkaloid mixture from Enantia chlorantha (Annonaceae). Biochemical assays from blood plasma, serum alanine transferase, serum alkaline phosphatase, serum creatinine, serum hydroxyproline and serum calcium were done and liver and kidney samples for histological processing were taken. The biochemical results obtained indicate a marked influence by Hepasor on the serum alanine transferase activities and serum hydroxyproline values in female rats, but more accidental ones in male rats. A reduction in serum alkaline phosphatase activity and the serum creatinine values was also found, being also dependent on sex. The histological findings in the liver sections of female rats show that 1 week Hepasor therapy greatly furthers the healing process in a D-galactosamine-pretraumatized liver, eliminating megalocytosis, contraction of chromatines and other disorders in the cell architecture. The inhibitory effect of Hepasor on proceeded traumatization caused by D-galactosamine was nearly complete.
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PMID:Regeneration of D-galactosamine-traumatized rat liver with natural protoberberine alkaloids from Enantia chlorantha. 341 61

Eupatorium adenophorum (Crofton weed), a native of Central America. has appeared as a major weed in several areas in different parts of the world. Horses that eat this plant are poisoned on prolonged exposure. Toxicity due to consumption of this plant by other grazing animals is not clear. Administration of freeze-dried leaf powder to mice results in hepatotoxicity. Earlier attempts to produce toxicity in rats using the leaves of this plant were not successful. In the present study, administration of oven-dried E. adenophorum leaves collected at the flowering stage elicited hepatotoxicity in rats. The affected animals had a marked increase in the concentration of plasma bilirubin and in the activities of 5'-nucleotidase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase. There were no significant differences in plasma creatinine, urea or total protein values in the affected animals compared to controls. The livers of the affected animals had focal areas of necrosis throughout the parenchyma and hepatocytes showed megalocytosis. The bile ducts were dilated and the epithelium showed degenerative to necrotic changes. The alterations in bilirubin, enzymes and histopathological changes imply cholestasis and liver injury.
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PMID:Biochemical alterations in the blood plasma of rats associated with hepatotoxicity induced by Eupatorium adenophorum. 1158 83

We studied the hepatocellular alterations induced by sub-lethal concentrations (0.50 muM) of arsenic in Indian catfish Clarias batrachus L. Sub-lethal arsenic exposure altered serum aspartate aminotransferase and alkaline phosphatase levels and brought about significant changes in different serum biochemical parameters. Arsenic exposure reduced total hepatocyte protein content and suppressed the proliferation of hepatocytes in a time-dependent manner. Routine histological studies on liver documented arsenic-induced changes characterized by dilated sinusoids, formation of intracellular edema, megalocytosis, vacuolation and appearance of hepatic cells with distorted nuclei. Transmission electron microscopy of hepatocytes further revealed hyperplasia and hypertrophy of mitochondria, development of dilated rough endoplasmic reticulum and changes in peroxisome size with duration of arsenic exposure. Degeneration of mitochondrial cristae and condensation of chromatin was also evident in arsenic-exposed hepatocytes. A significant number of hepatocytes isolated from arsenic-exposed fish stained with annexin V and demonstrated DNA ladder characteristic of apoptosis. Single-cell gel electrophoresis of exposed hepatocytes also revealed the development of comets usually seen in apoptotic cells. Using specific inhibitors it was determined that the arsenic-induced apoptosis of hepatocytes was caspase-mediated, involving the caspase 3 pathway.
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PMID:Sub-lethal concentration of arsenic interferes with the proliferation of hepatocytes and induces in vivo apoptosis in Clarias batrachus L. 1733 63