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来源: 编辑: 人气:4941 时间:2017-06-26

  凯茵化工讯 记者从合肥工业大学获悉,该校科研人员发现了双酚A对神经元突触可塑性及单细胞功能的影响,探明了双酚A干扰神经功能的生理机制。研究论文日前相继发表在国际重要学术期刊《先进科学》等刊物上。

  双酚A是一种常见的有机化工原料。作为一种环境类雌激素,会诱导神经系统相关的学习和记忆障碍,但其生理机制尚未探明。

  合肥工业大学食品科学与工程学院胡繁副教授课题组在实验中发现,出生后21天至49天的幼年期大鼠每天按照每千克体重1毫克的剂量,持续暴露在双酚A下后,负责学习和记忆的海马区锥体神经元的树突棘密度降低28.8%,突触前递质释放和突触后受体表达减少16.4%,长时程突触增益降低了33.8%,记忆行为成绩降低了17.4%,从而导致严重的空间记忆能力损伤等行为和生理功能改变。

  据介绍,实验采用的幼年期大鼠相当于巴斯夫树脂人类1至12岁的成长期,而采用的双酚A剂量低于美国食品药品监督局的无全身毒性剂量标准。

  鉴于双酚A的长期大量使用,目前在大气粉尘和水中已有广泛的分布。这一研究成果表明,在双酚A干扰下,大脑在信息输入的源头已经出现损伤。通过揭示双酚A干扰大脑功能的神经生理机制,该成果为临床评测和防治双酚A引起的脑功能损伤提供了重要理论依据和突破口。

Bisphenol A is such a "scourge" of brain function

Kailin Chemical News reporter learned from Hefei University of Technology, the school researchers found that bisphenol A on neuronal synaptic plasticity and single-cell function, to explore the physiological mechanism of bisphenol A disruption of nerve function. Research papers have been published in the important international academic journals "advanced science" and other publications.

Bisphenol A is a common organic chemical raw material. As an environmental estrogen, it induces nervous system-related learning and memory impairment, but its physiological mechanism has not been elucidated yet.

Associate Professor Hu Fan, Department of Food Science and Engineering, Hefei University of Technology Task Force In the experiment, we found that 21 to 49 days after birth, juvenile rats were treated with 1 mg per kilogram of body weight every day, After phenol A, the density of dendritic spines in hippocampal pyramidal neurons responsible for learning and memory decreased by 28.8%, the pre-synaptic transmission and post-synaptic receptor expression decreased by 16.4%, and the long-term synaptic gain decreased 33.8%, memory performance decreased by 17.4%, resulting in serious spatial memory impairment and other behavioral and physiological changes. According to reports, the experimental juvenile rats are equivalent to human growth of 1 to 12 years of age, and the use of bisphenol A dose lower than the US Food and Drug Administration without systemic toxicity dose standard.

Given the long-term extensive use of bisphenol A, there is now widespread distribution in atmospheric dust and water. The results of this study show that under the interference of bisphenol A, the brain has been damaged at the source of information input. By revealing the neurophysiological mechanism that bisphenol A interferes with brain function, the results provide an important theoretical basis and breakthrough for clinical evaluation and prevention and treatment of bisphenol A-induced brain damage.

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