Goustard-Langelier B, Alessandri J M, Raguenez G, Durand G, Courtois Y
Institut National de la Recherche Agronomique, Laboratoire de Nutrition et Sécurité Alimentaire, Jouy-en-Josas, France.
J Neurosci Res. 2000 Jun 1;60(5):678-85. doi: 10.1002/(SICI)1097-4547(20000601)60:5<678::AID-JNR13>3.0.CO;2-T.
The metabolic conversion of n-3 fatty acids was studied in the human Y79 retinoblastoma cell line. Cultured cells were exposed to increasing concentrations of either 18:3n-3, 22:5n-3, or 22:6n-3, and their phospholipid fatty acid composition was analyzed after 72 hr. Cells internalized the supplemental fatty acids and proceeded to their metabolic conversion. Supplemental 22:6n-3 was directly esterified into cell phospholipids, at levels typical for normal neural retinas (41% by weight of phosphatidylethanolamine fatty acids, and 24% of phosphatidylcholine fatty acids). In contrast, 18:3n-3 was mainly converted to 20:5n-3 and 22:5n-3, both of which appeared in cell phospholipids after exposure to low external concentrations of 18:3n-3 (10 microg/ml). Y79 cells can proceed to the metabolic conversion of 18:3n-3 through elongation and Delta6- and Delta5-desaturation. When cells were exposed to high external concentrations of 18:3n-3 (30 microg/ml), the supplemental fatty acid was directly incorporated, and its relative content increased in both phospholipid classes to the detriment of all other n-3 fatty acids. Cells cultured in the presence of 22:5n-3 did not incorporate 22:6n-3 into their phospholipids but did incorporate 20:5n-3 and 22:5n-3. The data suggest that Y79 cells can proceed to the microsomal steps of n-3 metabolism, involving elongation, desaturation, and chain shortening of 22C fatty acids. Although Y79 cells avidly used supplemental 22:6n-3 for phospholipid incorporation at levels typical for normal photoreceptor cells, they failed to match such levels through metabolic conversion of n-3 parent fatty acids. The terminal step of the very long-chain polyunsaturated fatty acid synthesis, consisting in Delta6-desaturation followed by peroxisomal chain shortening of 24C-fatty acids, could be rate-limiting in Y79 cells.
在人Y79视网膜母细胞瘤细胞系中研究了n-3脂肪酸的代谢转化。将培养的细胞暴露于浓度递增的18:3n-3、22:5n-3或22:6n-3中，72小时后分析其磷脂脂肪酸组成。细胞摄取了补充的脂肪酸并进行代谢转化。补充的22:6n-3直接酯化到细胞磷脂中，其水平为正常神经视网膜的典型水平（占磷脂酰乙醇胺脂肪酸重量的41%，占磷脂酰胆碱脂肪酸的24%）。相比之下，18:3n-3主要转化为20:5n-3和22:5n-3，在暴露于低外部浓度的18:3n-3（10微克/毫升）后，这两种脂肪酸都出现在细胞磷脂中。Y79细胞可以通过延长以及Δ6-和Δ5-去饱和作用进行18:3n-3的代谢转化。当细胞暴露于高外部浓度的18:3n-3（30微克/毫升）时，补充的脂肪酸被直接掺入，其相对含量在两种磷脂类别中均增加，损害了所有其他n-3脂肪酸。在22:5n-3存在的情况下培养的细胞没有将22:6n-3掺入其磷脂中，但确实掺入了20:5n-3和22:5n-3。数据表明，Y79细胞可以进行n-3代谢的微粒体步骤，包括22碳脂肪酸的延长、去饱和和链缩短。尽管Y79细胞积极地将补充的22:6n-3用于磷脂掺入，其水平为正常光感受器细胞的典型水平，但它们未能通过n-3母体脂肪酸的代谢转化达到该水平。超长链多不饱和脂肪酸合成的末端步骤，包括Δ6-去饱和，随后是24碳脂肪酸的过氧化物酶体链缩短，在Y79细胞中可能是限速步骤。
