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在小鼠新生脑发育的关键阶段,γ 射线与甲基汞的相互作用加剧了发育神经行为效应。

Interaction of gamma-radiation and methyl mercury during a critical phase of neonatal brain development in mice exacerbates developmental neurobehavioural effects.

机构信息

Department of Environmental Toxicology, Evolutionary Biology Centre, Uppsala University, Norbyvägen 18A, Uppsala, Sweden.

出版信息

Neurotoxicology. 2010 Mar;31(2):223-9. doi: 10.1016/j.neuro.2010.01.002. Epub 2010 Jan 7.

Abstract

In our environment, mammals (including humans) are exposed to various types of ionizing radiation and both persistent and non-persistent toxic chemicals. It is known that ionizing radiation, as well as methyl mercury, can induce neurotoxicological and neurobehavioural effects in mammals. These developmental neurotoxic effects can be seen following exposure during gestation. There is a lack of knowledge concerning the effects and consequences of low-dose exposure during critical phases of perinatal and/or neonatal brain development, and of the combination of ionizing radiation and environmental chemicals. A recent study has indicated that low doses of ionizing radiation to the human brain during infancy influence cognitive ability in adulthood. In the present study, 10-day old neonatal male NMRI mice were exposed to a single oral dose of MeHg (0.40 or 4.0 mg/kg bw). Four hours after the MeHg exposure the mice were subjected to (60)Co gamma-radiation on one occasion at doses of 0.2 and 0.5 Gy. The animals were then subjected to a spontaneous behaviour test at 2 and 4 months, and a water maze test at the age of 5 months. Neither the single dose of MeHg (0.4 mg/kg bw) nor the radiation dose of 0.2 Gy affected their spontaneous behaviour, whereas the co-exposure to external gamma-radiation and MeHg caused developmental neurotoxic effects. The study shows that gamma-radiation and MeHg can interact and significantly exacerbate developmental neurotoxic effects, as manifested by disrupted spontaneous behaviour, lack of habituation, and impaired learning and memory functions.

摘要

在我们的环境中,哺乳动物(包括人类)会接触到各种类型的电离辐射和持久性及非持久性有毒化学物质。已知电离辐射和甲基汞均可诱发哺乳动物的神经毒性和神经行为效应。这些发育神经毒性效应可在妊娠期暴露后显现。对于围产期和/或新生儿大脑发育的关键阶段的低剂量暴露以及电离辐射与环境化学物质的联合作用的影响和后果,我们知之甚少。最近的一项研究表明,婴儿期大脑接受的低剂量电离辐射会影响成年后的认知能力。在本研究中,10 日龄新生雄性 NMRI 小鼠接受了单次口服甲基汞(0.40 或 4.0mg/kg bw)处理。在接受甲基汞处理 4 小时后,将这些小鼠单次接受(60)Coγ射线照射,剂量分别为 0.2 和 0.5Gy。然后,在 2 个月和 4 个月时对动物进行自发行为测试,在 5 个月龄时进行水迷宫测试。单一剂量的甲基汞(0.4mg/kg bw)或 0.2Gy 的辐射剂量均未影响它们的自发行为,而外照射γ射线与甲基汞共同暴露则导致了发育神经毒性效应。该研究表明,γ射线和甲基汞可相互作用并显著加重发育神经毒性效应,表现为自发行为中断、缺乏习惯化以及学习和记忆功能受损。

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