Selenium deficiency and brain functions
Selenium deficiency and brain functions
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缺硒与脑功能
DOI：
--
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
C. Watanabe
中科院分区：
文献类型：
--
作者：
C. Watanabe
硒是人体必需的微量元素之一。虽然在过去的十年中，许多硒蛋白已被确定，硒和硒蛋白的生理作用仍有待阐明。由于碘甲状腺原氨酸脱碘酶（DI），调节甲状腺激素的组织水平，（可能）硒蛋白，硒可能有特定的作用，发育的大脑。事实上，当啮齿动物在围产期缺硒时，胎儿的甲状腺激素经济受到干扰，这可能导致在缺硒动物中观察到的大脑发育异常和出生后行为异常。当动物断奶后硒耗尽，甲状腺激素对大脑发育的作用是最小的，神经化学和神经生理学的改变被发现在多巴胺能系统。这些出生后耗尽的啮齿动物也表现出异常的旷场行为，这与围产期耗尽的动物观察到的不同。将硒缺乏状态转换为这些神经化学，神经生理和行为功能的分子事件在很大程度上是未知的，需要进一步研究。硒与汞化合物之间的相互作用也一直是众多研究的焦点，但关于硒的生理（营养）水平与产前甲基汞（MeHg）毒性之间的相互作用的报道却不多。实验结果表明，缺硒的啮齿动物更容易受到甲基汞的产前毒性。值得注意的是，甲基汞专门改变硒在胎儿/新生儿脑中的代谢。硒酶的活动，如谷胱甘肽过氧化物酶和DI在动物产前甲基汞暴露的改变的意义进行了讨论，在有关甲基汞的神经行为毒性。
Selenium has been long recognized as one of the essential trace elements. Although many selenoproteins have been identified in the last decade, the physiological roles of Se and selenoproteins remain to be elucidated. Since iodothyronine deiodinases (DIs), which regulate the tissue levels of thyroid hormone, are (likely to be) selenoproteins, Se might have specific roles for developing brain. In fact, when rodents are depleted of Se perinatally, the thyroid hormone economy of the fetus is disturbed, which may lead to the abnormal development of the brain and to the abnormal postnatal behavior observed in Se-deficient animals. When the animals were depleted of Se after weaning, when the role of thyroid hormone on brain development is minimal, neurochemical and neurophysiological alterations were found in the dopaminergic system. These postnatally-depleted rodents also showed abnormal open-field behavior, which was distinct from that observed with perinatally-depleted animals. The molecular events that convert Se-deficient status to these neurochemical, neurophysiological, and behavioral functions are largely unknown, and need to be further examined. The interaction between Se and mercury compounds has also been the focus of many research, but there have been few reports on the interaction between the physiological (nutritional) level of Se and the toxicity of prenatal methylmercury (MeHg). Experimental findings showed that Se-deficient rodents are more susceptible to the prenatal toxicity of MeHg. It is noteworthy that MeHg specifically altered the metabolism of Se in fetal/neonatal brain. Significance of the alteration of the activities of selenoenzymes such as glutathione peroxidase and DIs in animals by prenatal MeHg exposure are discussed in relation to the neurobehavioral toxicity of MeHg.
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影响因子：
15.9
作者：
Croteau, W;Davey, JC;StGermain, DL
通讯作者：
StGermain, DL
DOI：
10.1172/jci118299
发表时间：
1995-11
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
D. Salvatore;S. Low;M. Berry;A. Maia;John W. Hamey;W. Croteau;Donald;L. Germain;P. Larsen
通讯作者：
D. Salvatore;S. Low;M. Berry;A. Maia;John W. Hamey;W. Croteau;Donald;L. Germain;P. Larsen
影响因子：
5.1
作者：
Steuerwald, U;Weihe, P;Grandjean, P
通讯作者：
Grandjean, P
培养的大鼠星形胶质细胞硒蛋白 P 的合成和分泌。
DOI：
10.1016/s0304-4165(00)00035-0
发表时间：
2000
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Yang,X;Hill,KE;Maguire,MJ;Burk,RF
通讯作者：
Burk,RF
影响因子：
--
作者：
BURK, RF;HILL, KE;BELLEW, T
通讯作者：
BELLEW, T