Behavioral impairments are the most pragmatic outcome of long-term mobile uses but the underlying causes are still poorly understood. Therefore, the Aim of the present study to determine the possible mechanism of mobile induced behavioral alterations by observing redox status, cholinesterase activity, cellular, genotoxic damage and cognitive alterations in rat hippocampus. This study was carried out on 24 male Wistar rats, randomly divided into four groups (n = 6 in each group): group I consisted of sham-exposed (control) rats, group II-IV consisted of rats exposed to microwave radiation (900 MHz) at different time duration 1 h, 2 h, and 4 h respectively for 90 days. After 90 days of exposure, rats were assessing learning ability by using T-Maze. A significantly increased level of malondialdehyde (MDA) with concomitantly depleted levels of superoxide dismutase (SOD), catalase (CAT) and redox enzymes (GSH, GPX, GR, GST, G-6PDH) indicated an exposure of mobile emitted EMR induced oxidative stress by the depleted redox status of brain cells. The depletion in the acetylcholinesterase (AChE) level reveals altered neurotransmission in brain cells. Resultant cellular degeneration was also observed in the radiation-exposed hippocampus. Conclusively, the present study revealed that microwave radiation induces oxidative stress, depleted redox status, and causes DNA damage with the subsequent reduction in working memory in a time-dependent manner. This study provides insight over the associative reciprocity between redox status, cellular degeneration and reduced cholinergic activity, which presumably leads to the behavioral alterations following mobile emitted electromagnetic radiation.

中文翻译：

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电磁辐射对氧化还原状态、乙酰胆碱酯酶活性和导致大鼠大脑工作记忆减少的细胞损伤的影响

行为障碍是长期使用移动设备最实用的结果，但其根本原因仍知之甚少。因此，本研究的目的是通过观察大鼠海马的氧化还原状态、胆碱酯酶活性、细胞、基因毒性损伤和认知改变来确定移动诱导行为改变的可能机制。本研究对 24 只雄性 Wistar 大鼠进行，随机分为四组（每组 n = 6）：I 组由假暴露（对照）大鼠组成，II-IV 组由暴露于微波辐射的大鼠组成（900 MHz) 在不同的持续时间分别为 1 小时、2 小时和 4 小时，持续 90 天。暴露 90 天后，大鼠通过使用 T 迷宫评估学习能力。丙二醛 (MDA) 水平显着增加，同时超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 和氧化还原酶（GSH、GPX、GR、GST、G-6PDH）水平降低，表明暴露于移动发射的 EMR 诱导的氧化应激由于脑细胞的氧化还原状态耗尽。乙酰胆碱酯酶 (AChE) 水平的消耗揭示了脑细胞中神经传递的改变。在辐射暴露的海马中也观察到由​​此产生的细胞变性。最后，本研究表明，微波辐射会诱导氧化应激、耗尽氧化还原状态，并导致 DNA 损伤，随后工作记忆以时间依赖性方式减少。这项研究提供了对氧化还原状态、细胞退化和胆碱能活性降低之间关联互惠的见解，