Wang J, Dudman N P, Wilcken D E
Department of Medicine, Prince Henry Hospital, University of New South Wales, Little Bay Sydney, Australia.
Thromb Haemost. 1993 Dec 20;70(6):1047-52.
Elevated plasma homocysteine is associated with an increased risk of intravascular thrombosis. Platelet aggregation and thrombosis are inhibited by prostacyclin produced by the vascular endothelium. Our aim was to investigate whether homocysteine and related metabolites inhibit endothelial prostacyclin production. We used a radioimmunoassay for 6-ketoprostaglandin-F1 alpha to assay medium which had been in contact with confluent cultured endothelial cells. In medium containing 20% human serum, endothelial prostacyclin production was not specifically inhibited by homocysteine, S-adenosylhomocysteine or protein-bound homocysteine. Further, there was no consistent difference in prostacyclin production by cells cultured in medium containing sera from homocystinuria patients, compared with medium containing normal healthy sera. We conclude that vascular disorder in homocystinuria is unlikely to result from effects of homocysteine or related metabolites on endothelial prostacyclin production. By contrast, S-adenosylhomocysteine and protein-bound homocysteine specifically inhibited prostacyclin production by cells cultured in medium containing 20% fetal calf serum.
血浆同型半胱氨酸水平升高与血管内血栓形成风险增加相关。血小板聚集和血栓形成受到血管内皮产生的前列环素的抑制。我们的目的是研究同型半胱氨酸及其相关代谢产物是否会抑制内皮细胞前列环素的产生。我们使用放射免疫分析法检测与汇合培养的内皮细胞接触过的培养基中的6-酮前列腺素F1α。在含有20%人血清的培养基中，同型半胱氨酸、S-腺苷同型半胱氨酸或与蛋白结合的同型半胱氨酸并未特异性抑制内皮细胞前列环素的产生。此外，与含有正常健康血清的培养基相比，在含有同型胱氨酸尿症患者血清的培养基中培养的细胞，其前列环素产生没有一致的差异。我们得出结论，同型胱氨酸尿症中的血管紊乱不太可能是由同型半胱氨酸或其相关代谢产物对内皮细胞前列环素产生的影响所致。相比之下，S-腺苷同型半胱氨酸和与蛋白结合的同型半胱氨酸特异性抑制了在含有20%胎牛血清的培养基中培养的细胞的前列环素产生。
