三环抗抑郁药诱导成纤维细胞和神经母细胞瘤细胞培养鞘磷脂酶缺乏。

S Albouz, J J Hauw, Y Berwald-Netter, J M Boutry, R Bourdon, N Baumann
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引用次数: 0

摘要

三环抗抑郁药(丙咪嗪和地西帕明)在小鼠神经母细胞瘤和人成纤维细胞培养中引起鞘磷脂酶活性的显著降低。在细胞培养基中,终浓度为1或2 × 10(-5) M时,在1 ~ 2小时内发生。其他溶酶体酶如酸性脂肪酶、芳基磺化酶A和B和己糖氨酸酶未被修饰。鞘磷脂酶活性低可能与药物的两亲性有关:具有相同三环核心但缺乏两亲性所必需的侧链的亚氨基二苄没有作用。由于亚氨基二苯没有治疗作用,可能需要两亲性来抑制三环类药物的抗抑郁特性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tricyclic antidepressants induce sphingomyelinase deficiency in fibroblast and neuroblastoma cell cultures.

Tricyclic antidepressants (imipramine and desipramine) gave rise to an important decrease of sphingomyelinase activity in murine neuroblastoma and human fibroblast cell cultures. It occurred within 1 to 2 hours at a final concentration of 1 or 2 X 10(-5) M in cell culture medium. Other lysosomal enzymes such as acid lipase, arylsulfatases A and B and hexosaminidases were not modified. Low level of sphingomyelinase activity may be related to the amphiphilic characteristics of the drugs: iminodibenzyle which has the same tricyclic core but is devoid of the side chain necessary for amphiphilic properties had no effect. As iminodibenzyle has no therapeutic action, amphiphilic may be requisite to antidepressant properties of tricyclic drugs.

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