Detail of "1553-41-9"

Reference

Docosahexaenoic acid metabolism and effect on prostacyclin production in endothelial cells

Docosahexaenoic acid metabolism and effect on prostacyclin production in endothelial cells. Hadjiagapiou, Christos; Spector, Arthur A. (Dep. Biochem., Univ. Iowa, Iowa City, IA 52242, USA). Arch. Biochem. Biophys., 253(1), 1-12 (English) 1987. CODEN: ABBIA4. ISSN: 0003-9861. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Bovine aortic endothelial cultures readily take up docosahexaenoic acid (DHA) [2091-24-9]. Most of the DHA was incorporated into phospholipids, primarily in ethanolamine and choline phosphoglycerides, and plasmalogens accounted for 34% of the DHA contained in the ethanolamine fraction after a 24-h incubation. The retention of DHA in endothelial phospholipids was not greater than other polyunsatd. fatty acids and unlike arachidonic [506-32-1] and eicosapentaenoic acids [1553-41-9]. DHA did not continue to accumulate in the ethanolamine phosphoglycerides after the initial incorporation. About 15% of the [14C(U)]DHA uptake was retroconverted to docosapentaenoic [2234-74-4] and eicosapentaenoic acids in 24 h. Some of the newly incorporated [14C(U)]DHA was released when the cells were incubated subsequently in a medium contg. serum and albumin. The released radioactivity was in the form of free fatty acid and phospholipids and after 24 h, 11% was retroconverted to docosapentaenoic and eicosapentaenoic acids. Total DHA uptake was decreased only 10% by the presence of a 100 mM mixt. of physiol. fatty acids, but as little as 10 mM docosatetraenoic acid reduced DHA incorporation into phospholipids by 25%. DHA was not converted to prostaglandins or lipoxygenase products by the endothelial cultures. When DHA was available, however, less arachidonic acid was incorporated into endothelial phospholipids, and less was converted to PGI2 [35121-78-9]. Enrichment of the endothelial cells with DHA also reduced their capacity to subsequently produce PGI2. These findings indicate that endothelial cells can play a role in DHA metab. and like eicosapentaenoic acid, DHA can inhibit endothelial PGI2 prodn. when it is available in elevated amts.Except for chemicals metioned above, 506-32-1 and 2234-74-4 are also used. .

Effect of dietary fish oil on myocardial phospholipids and myocardial ischemic damage

Effect of dietary fish oil on myocardial phospholipids and myocardial ischemic damage. Hock, Carl E.; Holahan, Marie A.; Reibel, Diane K. (Sch. Osteopath. Med., Univ. Med. Dent. New Jersey, Camden, NJ 08103, USA). Am. J. Physiol., 252(3, Pt. 2), H554-H560 (English) 1987. CODEN: AJPHAP. ISSN: 0002-9513. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) The effect of dietary fish all on myocardial phospholipids and ischemic damage to the heart was studied in the rat. Four weeks of feeding 5% (i.e., 12% of energy) menhaden oil (MO)produced both profound changes in the fatty acyl compn. of phospholipids in myocardial membranes and significantly decreased the loss of creatine kinase [9001-15-4] following coronary artery ligation compared with feeding the same level of corn oil (CO). The MO diet did not change the content of either phospholipids or cholesterol in the heart. However, dietary MO significantly increased the percentage of satd. fatty acids, the n-3/n-6 ratio, and the double bond index in the total phospholipids. The changes varied for the phospholipid classes. Although the n-3/n-6 ratio was increased in each of the individual phospholipids examd., the major n-3 fatty acid incorporated (i.e., C [1553-41-9], C [2234-74-4], and C [2091-24-9]) differed for the major phospholipid classes. The percentage satd. fatty acids was elevated in phosphatidylcholine with no change in double-bond index; both percentage satd. fatty acids and double-bond index were elevated in phosphatidylethanolamine. Thus, dietary MO resulted in selective alterations in individual myocardial phospholipids. These membrane changes may be involved in the obsd. 2234-74-4 and 9001-15-4 are just another two chemicals used in this study. redn. of ischemic damage in the heart. .