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微波诱导的32P掺入大鼠脑突触体磷酸肌醇的研究。

Microwave induced stimulation of 32Pi incorporation into phosphoinositides of rat brain synaptosomes.

作者信息

Gandhi C R, Ross D H

机构信息

Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.

出版信息

Radiat Environ Biophys. 1989;28(3):223-34. doi: 10.1007/BF01211259.

Abstract

Exposure of synaptosomes to microwave radiation at a power density of 10 mW/sq cm or more produced stimulation of the 32Pi-incorporation into phosphoinositides. The extent of 32Pi incorporation was found to be much more pronounced in phosphatidylinositol-4-phosphate (PIP), and phosphatidylinositol-4,5-bisphosphate (PIP2) as compared to phosphatidylinositol (PI) and phosphatidic acid (PA). Other lipids were also found to incorporate 32Pi but no significant changes in their labeling were seen after exposure to microwave radiation. Inclusion of 10 mM lithium in the medium reduced the basal labeling of PIP2, PIP and PI and increased PA labeling. Li+ also inhibited the microwave stimulated PIP2, PIP and PI labeling but had no effect on PA labeling. Calcium ionophore, A23187, inhibited the basal and microwave stimulated 32Pi labeling of PIP and PIP2, stimulated basal labeling of PA and PI and had no effect on microwave stimulated PA and PI labeling. Calcium chelator, EGTA, on the other hand, had no effect on basal labeling of PA and PI, stimulated basal PIP and PIP2 labeling but did not alter microwave stimulated labeling of these lipids. Exposure of synaptosomes to microwave radiation did not alter the chemical concentration of phosphoinositides indicating that the turnover of these lipids was altered. These results suggest that low frequency microwave radiation alter the metabolism of inositol phospholipids by enhancing their turnover and thus may affect the transmembrane signalling in the nerve endings.

摘要

将突触体暴露于功率密度为10毫瓦/平方厘米或更高的微波辐射下,会刺激32Pi掺入磷酸肌醇。与磷脂酰肌醇(PI)和磷脂酸(PA)相比,发现32Pi掺入磷脂酰肌醇-4-磷酸(PIP)和磷脂酰肌醇-4,5-二磷酸(PIP2)的程度更为明显。还发现其他脂质也掺入32Pi,但暴露于微波辐射后其标记没有明显变化。培养基中加入10 mM锂会降低PIP2、PIP和PI的基础标记,并增加PA标记。Li+还抑制微波刺激的PIP2、PIP和PI标记,但对PA标记没有影响。钙离子载体A23187抑制PIP和PIP2的基础和微波刺激的32Pi标记,刺激PA和PI的基础标记,对微波刺激的PA和PI标记没有影响。另一方面,钙螯合剂EGTA对PA和PI的基础标记没有影响,刺激基础PIP和PIP2标记,但不改变这些脂质的微波刺激标记。将突触体暴露于微波辐射不会改变磷酸肌醇的化学浓度,表明这些脂质的周转率发生了改变。这些结果表明,低频微波辐射通过增强肌醇磷脂的周转率来改变其代谢,从而可能影响神经末梢的跨膜信号传导。

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