非热微波辐射引起的脑组织脱水是脑功能损伤的潜在因素

A. Nikoghosyan, Armenuhi Heqimyan, S. Ayrapetyan
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引用次数: 3

摘要

基于我们之前的发现,代谢控制的细胞水化对细胞水介质的物理化学性质的变化很敏感,这些变化是在弱物理信号的作用下发生的,包括非热强度的微波(NT MW),我们假设细胞水介质是NT MW对脑组织作用的主要靶点。为了阐明NT MW诱导的细胞水介质理化性质改变调节细胞水化作用的代谢途径的本质,我们研究了NT MW处理的PS腹腔注射对脑组织水化、45 ca2 +摄取、[3 H]-瓦巴因与细胞膜结合以及细胞内环核苷酸的影响。结果表明,NT MW通过激活膜内高亲和力的瓦巴因受体,刺激camp依赖性的Na + / ca2 +反向交换(R),导致健康(年轻)大鼠脑组织水化,而非健康(老年)大鼠脑组织脱水。由于NT MW辐射诱导的R Na + / ca2 +交换激活导致细胞内ca2 + ([ca2 +] i)增加,因此被认为是导致脑功能损伤的潜在因素,特别是当脑代谢活性下降时(如衰老)。
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Non-thermal microwave radiation-induced brain tissue dehydration as a potential factor for brain functional impairment
Based on our previous finding that metabolically controlled cell hydration is sensitive to the changes of physicochemical properties of cell aqua medium, which take place upon the effect of weak physical signals, including microwaves with non-thermal intensity (NT MW), it has been hypothesized that cell aqua medium serves as a primary target for NT MW effect on brain tissue. To elucidate the nature of the metabolic pathway through which the effect of NT MW-induced changes of physicochemical properties of cell aqua medium modulate cell hydration, the effects of intraperitoneal (IP) injection of PS treated by NT MW on brain tissue hydration, 45 Ca 2+ uptake, [ 3 H]-ouabain binding with cell membrane and intracellular cyclic nucleotides have been studied. The obtained data indicate that PS treated by NT MW through the activation of high affinity ouabain receptors in membrane stimulates cAMP-dependent Na + /Ca 2+ exchange in reverse mode (R), which leads to brain tissue hydration in healthy (young) and dehydration in non-healthy (old) rats. As NT MW radiation-induced activation of R Na + /Ca 2+ exchange leads to the increase of intracellular Ca 2+ ([Ca 2+ ] i), it is considered as a potential factor leading to the brain functional impairment, especially when brain metabolic activity is depressed (e.g. during aging).
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