三丁基氯化锡对离体大鼠胸腺细胞能量代谢、大分子合成、前体摄取及环磷酸腺苷生成的影响。

Effects of tri-n-butyltin chloride on energy metabolism, macromolecular synthesis, precursor uptake and cyclic AMP production in isolated rat thymocytes.

作者信息

Snoeij N J, Punt P M, Penninks A H, Seinen W

出版信息

Biochim Biophys Acta. 1986 Dec 3;852(2-3):234-43. doi: 10.1016/0005-2728(86)90228-8.

Abstract

The inhibitor of oxidative phosphorylation tri-n-butyltin chloride (TBTC) causes membrane damage and disintegration of isolated rat thymocytes at concentrations higher than 1 microM. From a concentration of 0.1 microM, TBTC disturbs energy metabolism as indicated by an increase in methylglucose uptake, glucose consumption and lactate production and by a decrease in cellular ATP levels. Over the same TBTC concentration range, the incorporation of DNA, RNA and protein precursors are markedly reduced. Moreover the production of cyclic AMP upon stimulation of the cells with prostaglandin E1 is effectively inhibited. These effects cannot be explained by an inhibition of nucleoside kinase activity, amino acid uptake or adenylate cyclase activity. The effects of TBTC on macromolecular synthesis and cyclic AMP production are possibly due to a disturbance of the cellular energy state.

摘要

氧化磷酸化抑制剂三丁基氯化锡（TBTC）在浓度高于1微摩尔时会导致分离的大鼠胸腺细胞的膜损伤和崩解。从0.1微摩尔的浓度开始，TBTC会干扰能量代谢，表现为甲基葡萄糖摄取、葡萄糖消耗和乳酸生成增加以及细胞ATP水平降低。在相同的TBTC浓度范围内，DNA、RNA和蛋白质前体的掺入明显减少。此外，用前列腺素E1刺激细胞后，环磷酸腺苷的生成受到有效抑制。这些作用不能通过抑制核苷激酶活性、氨基酸摄取或腺苷酸环化酶活性来解释。TBTC对大分子合成和环磷酸腺苷生成的作用可能是由于细胞能量状态的紊乱。