首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Diisodecyl phthalate aggravates the formaldehyde-exposure-induced learning and memory impairment in mice
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Diisodecyl phthalate aggravates the formaldehyde-exposure-induced learning and memory impairment in mice

机译:邻苯二甲酸二乙二醇酯加剧了小鼠中甲醛暴露诱导的学习和记忆障碍

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摘要

Diisodecyl phthalate (DIDP) is a new type of phthalate used in the coating of pharmaceutical pills and in plastic food wrappers. This research was conducted to investigate whether DIDP could cause learning and memory impairment in mice, using formaldehyde (FA) to construct a positive control. Behavioral analysis showed that oral administration of 15 mg kg(-1)d(-1) DIDP combined with inhalation of 1 mg m(-3) FA led to learning and memory impairment in mice. Histopathological observations of the brain showed that the pathological alterations in the hippocampi. Detection of testosterone (T) and estradiol (E2) levels in the brain and serum showed that E2 levels were associated with learning and memory disorders. Reactive oxygen species (ROS), reduced glutathione (GSH), malondialdehyde (MDA), and 8-hydroxy-2-deoxyguanosine (8-OH-dG) revealed the increased oxidative stress levels. Detection of caspase-3, NF-kappa B, the phosphorylated cAMP response-element binding protein (p-CREB) and the brain derived neurotrophic factor (BDNF) showed that the protective effect mediated by BDNF, is reduced. However, some of these effects were blocked by the administration of Vitmin E (VitE, 100 mg kg(-1)d(-1)) or 17 beta-estradiol (17 beta-E2, 100 mu g kg(-1)). These data suggest that DIDP may aggravate the FA-exposure-induced learning and memory impairment in mice, and that 17 beta-E2 could be utilized to avoid these adverse effects.
机译:邻苯二甲酸二乙二醇酯(DIDP)是一种新型的邻苯二甲酸酯,用于药物丸涂层和塑料食品包装。进行该研究以调查DIDP是否可能导致小鼠的学习和内存损伤,使用甲醛(FA)来构建阳性对照。行为分析表明,15mg kg(-1)d(-1)DIDP的口服给药与吸入1mg m(-3)FA导致小鼠的学习和记忆障碍。大脑的组织病理学观察表明,海马病理改变。脑和血清中睾酮(T)和雌二醇(E2)水平的检测表明,E2水平与学习和记忆障碍有关。反应性氧物质(ROS),降低的谷胱甘肽(GSH),丙二醛(MDA)和8-羟基-2-脱氧核苷酸(8-OH-DG)显示出增加的氧化应激水平。检测Caspase-3,NF-Kappa B,磷酸化阵营响应 - 元素结合蛋白(P-CREB)和脑衍生的神经营养因子(BDNF)表明,由BDNF介导的保护作用降低。然而,通过vitmin E(vite,100mg kg(-1)d(-1))或17β-雌二醇(17β-E2,100μgkg(-1))阻断这些效果中的一些效果。这些数据表明,DIDP可能会加剧小鼠的FA暴露诱导的学习和内存损伤,并且可以利用17个β-E2来避免这些不利影响。

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