Reproductive Biology and Toxicology Laboratory, UNESCO Satellite center of Trace Element Research & School of Studies in Zoology, Jiwaji University, Gwalior, M.P., India.
Reproductive Biology and Toxicology Laboratory, UNESCO Satellite center of Trace Element Research & School of Studies in Zoology, Jiwaji University, Gwalior, M.P., India.
J Chem Neuroanat. 2020 Jul;106:101784. doi: 10.1016/j.jchemneu.2020.101784. Epub 2020 Mar 20.
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.
行为损伤是长期使用移动设备最实际的后果,但潜在原因仍知之甚少。因此,本研究旨在通过观察大鼠海马体中的氧化还原状态、胆碱酯酶活性、细胞、遗传毒性损伤和认知改变,确定移动诱导行为改变的可能机制。这项研究是在 24 只雄性 Wistar 大鼠上进行的,随机分为四组(每组 6 只):第 I 组为假暴露(对照)大鼠,第 II-IV 组分别为每天暴露于微波辐射(900 MHz)1、2 和 4 小时,共 90 天。暴露 90 天后,大鼠通过 T 迷宫评估学习能力。丙二醛(MDA)水平显著升高,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,表明移动设备发射的电磁辐射(EMR)导致细胞氧化应激,细胞内氧化还原状态降低。乙酰胆碱酯酶(AChE)水平的降低表明脑细胞内神经递质传递发生改变。在辐射暴露的海马体中也观察到细胞退化。总之,本研究表明,微波辐射会引起氧化应激,降低氧化还原状态,并导致 DNA 损伤,随后工作记忆能力会随时间呈下降趋势。这项研究揭示了氧化还原状态、细胞退化和胆碱能活性降低之间的关联,这可能导致行为改变。
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