Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, the protective effect of PGE2 on intestinal damage in indomethacin-treated adult rats was investigated. Ileal integrity was evaluated making use of different biochemical and histological parameters: activities of sucrase, maltase and diamine oxidase; concentrations of DNA, putrescine, spermidine and spermine; incorporation of 3H-thymidine into DNA; mitotic index and mucosal thickness. Results expressed per g of mucosal weight, showed that: maltase and diamine oxidase activities as well as DNA, spermidine and spermine concentrations decreased markedly in indomethacin-treated rats when compared to control rats; the decrease of maltase activity as well as DNA, spermidine and spermine concentration was less pronounced in PGE2-treated rats when compared to indomethacin-treated rats; 3H-thymidine incorporation into DNA and mitotic index values showed no significant variation in the course of different treatments; mucosal thickness increased strongly, in PGE2-protected rats. We suggest that PGE2 could protect the rat's intestinal mucosa against the effects of indomethacin through a trophic action on intestinal villi.
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PMID:Effect of prostaglandin E2 on the small intestine of indomethacin-treated rats. 311 78

Prostaglandins have been reported to exert trophic effects on gastrointestinal tissues. To determine whether there is a direct interaction with enterocytes, prostaglandins PGE2, PGF2 alpha, PGA2, PGB2 and the stable PGE2 derivative suleprost as well as the prostacyclin derivative nileprost were tested in rabbit ileal mucosa under organ culture conditions. At concentrations between 10(-9) and 10(-5) M, none of the prostaglandins significantly affected biopsy DNA or protein content, or the activity of the brush border enzymes alkaline phosphatase, lactase, sucrase or maltase. The inhibition of endogenous prostaglandin synthesis with indomethacin also failed to alter these parameters. Moreover, the growth rate of a rat duodenal crypt cell line was unaffected when cultured in the presence of PGE2, PGF2 alpha or indomethacin. Thus, there was no evidence for a direct effect of exogenous or endogenous prostaglandins or their deficiency on the differentiation or growth in cultured small intestinal cells.
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PMID:Prostaglandins are not involved in the differentiation or growth of cultured small intestinal cells. 381 31

High doses of 16,16-dimethyl prostaglandin E2 (dmPGE) are trophic to the small bowel of adult and suckling rats. In suckling rats this effect is paralleled by an increase in brush border enzyme activities, possibly indicating accelerated mucosal maturation. To investigate the possible physiological significance of this phenomenon, we examined whether this induction of intestinal enzyme activities can be reproduced in adult rats and whether cell growth and enzyme activity might be suppressed by indomethacin. Treatment twice daily for 2 weeks with 100 micrograms/kg dmPGE by intragastric instillation increased villus length in the proximal and distal small bowel by 36% and 40%, respectively, while 2 mg/kg indomethacin by subcutaneous injection had no effect. Maltase, trehalase, lactase, and sucrase activities were unchanged after dmPGE or indomethacin. [3H]-thymidine incorporation into DNA was not significantly influenced for up to 24 h after a single dose of both 100 micrograms/kg PGE intragastrically or 10 mg/kg indomethacin subcutaneously. These studies confirm that in adult rats large doses of 16,16-dm PGE2 increase the volume of the small-bowel mucosa. In contrast to the situation in suckling rats, the activity of hydrolytic brush border enzymes is not increased. There is thus no evidence that endogenous prostaglandins are trophic or influence brush border enzymes in the adult rat.
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PMID:Influence of 16,16-dimethyl prostaglandin E2 on morphology and brush border enzymes of small-bowel mucosa. Differences in reactivity between adult and suckling rats. 392 42

Several markers of growth and biochemical development in the rat were studied after administration of prostacyclin (PGI2) and 16, 16-dimethyl prostaglandin E2 (16, 16DM PGE2). Intermittent administration of PGI2 for 3 days to 10- and 19-day-old animals, with subsequent sacrifice at 14 and 23 days, resulted in significant dose related decreases in growth at 23 days. Total sucrase and maltase (glucoamylase) activities were elevated compared to controls at 14 days. Total activities of these enzymes were decreased in postweaned 23-day-old animals, but specific activities per mg intestinal protein were not significantly different. 16, 16DM PGE2 administered continuously between day 10-16 of life caused alterations in growth as well as increases in sucrase and maltase (glucoamylase) activities. Exogenously administered prostaglandins, therefore, are associated with altered growth and markers of biochemical development in the rat.
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PMID:Prostaglandin-mediated effects on growth and markers of biochemical development in the rat. 641 40