Weckbecker G, Keppler D O
Eur J Biochem. 1986 Feb 3;154(3):559-62. doi: 10.1111/j.1432-1033.1986.tb09435.x.
Uptake and metabolism of the cysteinyl leukotrienes C4 and E4 (LTC4 and LTE4) were studied in AS-30D hepatoma cell suspensions and compared with rat hepatocytes. The hepatoma cells were deficient in the uptake of [3H]LTC4 and [3H]LTE4 but took up, in control experiments, L-[14C]glutamine and [14C]adenosine in a time-dependent manner. By contrast, isolated hepatocyte suspensions incubated under the same conditions took up [3H]LTC4 and [3H]LTE4 as well as L-[14C]glutamine and [14C]adenosine. The hepatoma cells deficient in the uptake of cysteinyl leukotrienes metabolized extracellular [3H]LTC4 to [3H]LTD4 and to [3H]LTE4. Addition of acivicin, an inhibitor of gamma-glutamyltransferase, largely prevented metabolism of [3H]LTC4 by the hepatoma cells. Sonication of the cells did not enhance the formation of [3H]LTD4 and [3H]LTE4 from [3H]LTC4. We conclude that ectoenzymes of AS-30D hepatoma cells catalyze the conversion of LTC4 to LTE4 via LTD4. As compared to hepatocytes, these neoplastic cells have lost the uptake system for cysteinyl leukotrienes and may serve in studies on leukotriene metabolism by cell-surface enzymes.
在AS-30D肝癌细胞悬液中研究了半胱氨酰白三烯C4和E4（LTC4和LTE4）的摄取和代谢，并与大鼠肝细胞进行了比较。肝癌细胞对[3H]LTC4和[3H]LTE4的摄取存在缺陷，但在对照实验中，能以时间依赖性方式摄取L-[14C]谷氨酰胺和[14C]腺苷。相比之下，在相同条件下孵育的分离肝细胞悬液能摄取[3H]LTC4、[3H]LTE4以及L-[14C]谷氨酰胺和[14C]腺苷。摄取半胱氨酰白三烯存在缺陷的肝癌细胞将细胞外的[3H]LTC4代谢为[3H]LTD4和[3H]LTE4。添加γ-谷氨酰转移酶抑制剂阿西维辛可在很大程度上阻止肝癌细胞对[3H]LTC4的代谢。细胞超声处理并未增强[3H]LTC4生成[3H]LTD4和[3H]LTE4的过程。我们得出结论，AS-30D肝癌细胞的胞外酶催化LTC4经LTD4转化为LTE4。与肝细胞相比，这些肿瘤细胞已丧失半胱氨酰白三烯的摄取系统，可用于研究细胞表面酶对白三烯的代谢。
