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)

The present study investigated the effects of piriprost (U-60,257B; an inhibitor of LT synthesis) and various LTs on alkaline phosphatase (ALP) activity of rat endometrial stromal cells in vitro. Mature ovariectomized rats were pretreated with hormones to sensitize their uteri for the decidual cell reaction. Endometrial stromal cells were isolated and cultured for up to 72 hr with various treatments. The ALP activity in all experiments was significantly (p less than 0.01) higher at 72 hr than at 24 hr, irrespective of treatment. We examined the effects of 100 microM piriprost, with or without 1 microM LTB4, 0.01 microM LTC4, 0.1 microM LTD4 or 0.001 microM LTE4 on ALP activity. At 72 hr, as indicated by analyses of variance, there were significant interactions (p less than 0.01) between the effects of piriprost and the LTs. Piriprost by itself increased (p less than 0.01) ALP activity in all experiments, and a further increase (p less than 0.01) in ALP activity was observed when either LTB4, LTC4, LTD4 or LTE4 was added with piriprost. LTB4, LTD4, or LTE4 alone had inhibitory effects (p less than 0.01) while LTC4 alone had no effect. These studies suggest LTs may be involved in decidualization which, in vitro, is accompanied by an increase in endometrial ALP activity. However the exact role of LTs is still unclear.
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PMID:Effects of piriprost (U-60, 257B) and leukotrienes on alkaline phosphatase activity of rat endometrial stromal cells in vitro. 166 40

Previously, piriprost (U-60,257B; an inhibitor of leukotriene (LT) synthesis) was shown to increase alkaline phosphatase (ALP) activity in cultured endometrial stromal cells (1). The present study investigated the mechanism of action of piriprost in this system. Sensitized rat endometrial stromal cells were isolated and cultured for up to 72 hr with various treatments. Piriprost (100 microM) was found to decrease 5-hydroxyeicosatetraenoic acid (a 5-lipoxygenase product) by 53% after 72 hr which provided evidence that 5-lipoxygenase was being inhibited by piriprost. Lactate dehydrogenase (LDH) activity confirmed that piriprost was not toxic to the cells. The possibility of piriprost acting in an analogous manner with that of PGs was examined. Three microM PGE2 or 20 microM carba-prostacyclin (CP), an analogue of PGI2, maximally increased (p less than 0.01) ALP activity at 72 hr and the further addition of 100 microM piriprost to PGE2 or CP caused an additional, additive increase in ALP activity. This indicated that the mechanism of action of piriprost was probably different from that of PGE2 or PGI2. The possibility that piriprost was shunting arachidonic acid into PG production was examined. Ten microM indomethacin (an inhibitor of PG synthesis) caused a decrease (p less than 0.01) in ALP activity and a 99% reduction in PGE2 at 72 hr. The effects of the combination of 100 microM piriprost and 10 microM IM were statistically additive, suggesting that the effects of piriprost were not due to an increase in PG production. These studies suggest that the effects piriprost on possible in vitro decidualization may be due to inhibition of 5-lipoxygenase.
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PMID:Examination of the effects of piriprost (U-60,257B) on alkaline phosphatase activity of rat endometrial stromal cells in vitro. 177 38