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二甲基亚砜处理的Friend红白血病细胞中Na +,K + -泵活性的降低并非由于Na +,K + -ATP酶的部分失活所致。

A reduction in the activity of the Na+, K+-pump in dimethylsulfoxide-treated Friend erythroleukemia cells is not due to partial inactivation of the Na+, K+-ATPase.

作者信息

Schaefer A, Munter K H, Geck P, Koch G

出版信息

J Cell Physiol. 1984 Jun;119(3):335-40. doi: 10.1002/jcp.1041190312.

Abstract

Treatment of Friend-erythroleukemia cells with 1.5% dimethylsulfoxide (DMSO) caused a decrease in ouabain sensitive 86Rb+-uptake beginning six to seven hours after DMSO addition indicating a reduced function of the Na+, K+-pump. However, analysis of the ouabain sensitive 86Rb+-uptake after Na+-preloading of the cells as well as measurements on the Na+, K+-ATPase activity in isolated membrane fragments revealed that no inhibition of the Na+, K+-ATPase occurred during the first 12 hours. On the contrary the Na+, K+-ATPase activity was initially enhanced and then returned to control levels during the early phase of induction by DMSO. On the other hand, 22Na+-transport into DMSO-treated cells was reduced similar to the ouabain sensitive 86Rb+ uptake in cells without Na+ preloading. The piretanide sensitive 86Rb+-uptake, due to the Na+, K+, 2Cl - cotransport system was inhibited after seven hours exposure to DMSO. Some three hours after DMSO addition the incorporation of 35S-methionine into proteins began to decrease, which was accompanied with or followed by a reduction in the methionine uptake of DMSO treated cells. Membrane-potential-dependent tetraphenylphosphonium cation uptake was not altered relative to the controls in the first 12 hours following DMSO addition. These results suggest that the reduced activity of the Na+, K+-pump in Friend cells after DMSO exposure is not due to inhibition of the Na+, K+-ATPase, but most probably due to a smaller Na+-influx, which results from inhibition of Na+-cotransport processes (amino acid uptake, Na+, K+, 2Cl - cotransport system).

摘要

用1.5%二甲基亚砜(DMSO)处理弗瑞德红白血病细胞,在加入DMSO后6至7小时,哇巴因敏感的86Rb+摄取量开始下降,表明Na+,K+-泵功能降低。然而,对细胞进行Na+预加载后对哇巴因敏感的86Rb+摄取的分析以及对分离膜片段中Na+,K+-ATP酶活性的测量显示,在最初12小时内未发生对Na+,K+-ATP酶的抑制。相反,在DMSO诱导的早期阶段,Na+,K+-ATP酶活性最初增强,然后恢复到对照水平。另一方面,22Na+转运到经DMSO处理的细胞中减少,类似于未进行Na+预加载的细胞中对哇巴因敏感的86Rb+摄取。由于Na+,K+,2Cl-共转运系统,在暴露于DMSO 7小时后,吡咯他尼敏感的86Rb+摄取受到抑制。加入DMSO约3小时后,35S-甲硫氨酸掺入蛋白质的过程开始减少,同时或随后伴随着经DMSO处理的细胞中甲硫氨酸摄取的减少。在加入DMSO后的最初12小时内,膜电位依赖性四苯基鏻阳离子摄取相对于对照没有改变。这些结果表明,DMSO暴露后弗瑞德细胞中Na+,K+-泵活性降低不是由于对Na+,K+-ATP酶的抑制,而很可能是由于较小的Na+内流所致,这是由Na+共转运过程(氨基酸摄取、Na+,K+,2Cl-共转运系统)的抑制引起的。

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