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- Gustafson-Svärd, Christina, et al.
(författare)
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Phospholipase activation and arachidonic acid release in intestinal epithelial cells from patients with Crohn´s disease
- 1990
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Ingår i: Scandinavian Journal of Gastroenterology. - 0036-5521 .- 1502-7708. ; 25:11, s. 1151-1160
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Tidskriftsartikel (refereegranskat)abstract
- A method for studying the mobilization of free arachidonic acid (AA) in viable isolated human intestinal epithelial cells has been developed and applied to the study of patients with Crohn's disease. Cells were isolated from morphologically unaffected parts of the distal ileum and incubated with 14C-AA; most of the incorporated 14C-AA was then found in phospholipids (mainly phosphatidylcholine) and in a pool of neutral lipids (mainly triacylglycerols). Cells from patients with Crohn's disease incorporated more 14C-AA into their neutral lipids than did cells from control patients. When the labeled cells were stimulated with phospholipase C from Clos-tridium perfringens or with the calcium ionophore A23187, they released significant amounts of AA, mainly from phosphatidylcholine. There was no difference between cells from Crohn patients and controls in the 14C-AA amounts released, but unstimu-lated and phospholipase C-stimulated cells from prednisolone-treated Crohn patients released less AA than cells from control patients. The A23187-stimuiated AA release was completely inhibited by the phospholipase A2 inhibitor 4-bromophenacyl bromide, whereas the phospholipase C-stimulated release was not. These findings suggest that AA release in human small-intestinal epithelial cells may be caused by calcium-mediated phospholipase A2 activation or by products of microbial phospholipase C activity and that prednisolone reduces the mobilization of free AA in intestinal epithelial cells. They also illustrate the potential use of isolated epithelial cells for revealing mechanisms underlying AA release in the intestinal mucosa in different disease states.
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- Gustafson-Svärd, Christina, et al.
(författare)
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Phospholipase C from Clostridium perfringens stimulates formation of platelet-activating factor (PAF-acether) in cultured intestinal epithelial cells (INT 407)
- 1991
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 26:10, s. 1000-1006
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Tidskriftsartikel (refereegranskat)abstract
- This study demonstrates the ability of phospholipase C from Clostridium perfringens to stimulate the generation of platelet-activating factor (PAF-acether) in cultured intestinal epithelial cells (INT 407). Cells were exposed to phospholipase C for up to 60 min, and the content of PAF-acether within the cells and in the extracellular medium was determined. Phospholipase C caused a time-dependent formation of PAF-acether within the cells and also release of PAF-acether to the medium. In contrast, phospholipase C did not affect the cellular acetylhydrolase activity or the ability of the cells to metabolize extracellularly added C-14-PAF-acether. These findings suggest the possibility that intestinal epithelial cells, when stimulated with a naturally occurring intestinal bacterial toxin, generate and release PAF-acether. The possibility that this might contribute to the pathophysiology of inflammatory bowel disease is discussed.
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- Lapointe, Line, et al.
(författare)
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Resistance to low temperature photoinhibition is not associated with isolated thylakoid membranes of winter rye.
- 1991
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Ingår i: Plant Physiology. - : Oxford University Press (OUP). - 0032-0889 .- 1532-2548. ; 97:2, s. 804-810
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Tidskriftsartikel (refereegranskat)abstract
- In vivo measurements of chlorophyll a fluorescence indicate that cold-hardened winter rye (Secale cereale L. cv Musketeer) develops a resistance to low temperature-induced photoinhibition compared with nonhardened rye. After 7.2 hours at 5 degrees C and 1550 micromoles per square meter per second, the ratio of variable fluorescence/maximum fluorescence was depressed by only 23% in cold-hardened rye compared with 46% in nonhardened rye. We have tested the hypothesis that the principal site of this resistance to photoinhibition resides at the level of rye thylakoid membranes. Thylakoids were isolated from cold-hardened and nonhardened rye and exposed to high irradiance (1000-2600 micromoles per square meter per second) at either 5 or 20 degrees C. The photoinhibitory response measured by room temperature fluorescence induction, photosystem II electron transport, photoacoustic spectroscopy, or [(14)C]atrazine binding indicates that the differential resistance to low temperature-induced photoinhibition in vivo is not observed in isolated thylakoids. Similar results were obtained whether isolated rye thylakoids were photoinhibited or thylakoids were isolated from rye leaves preexposed to a photoinhibitory treatment. Thus, we conclude that increased resistance to low temperature-induced photoinhibition is not a property of thylakoid membranes but is associated with a higher level of cellular organization.
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