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Genetic differences in ethanol consumption: effects on iron, copper, and zinc regulation in mouse hippocampus
Biometals ( IF 4.1 ) Pub Date : 2021-06-27 , DOI: 10.1007/s10534-021-00327-8
Byron C Jones 1 , Keith M Erikson 2 , Megan K Mulligan 1 , Carolina Torres-Rojas 1 , Wenyuan Zhao 1 , Daming Zhuang 1 , Lu Lu 1 , Robert W Williams 1
Affiliation  

One common characteristic of neurodegenerative diseases is dysregulation of iron, usually with observed increases in its concentration in various regions. Heavy alcohol consumption is believed to contribute to such iron dysregulation in the brain with accompanying dementia. To examine this effect and related genetic-based individual differences in an animal model, we subjected female mice from 12 BXD recombinant inbred strains to 16 weeks of alcohol consumption using the drinking in the dark (DID) method. Daily consumption was recorded and at the end of 16 weeks hippocampus tissues harvested. Concentrations of iron, copper and zinc were measured using X-ray fluorescence technology. The results showed that, DID increased iron overall across all strains, ranging from 3 to 68%. Copper and Zinc both decreased, ranging from 0.4–42 and 5–35% respectively. Analysis of variance revealed significant strain by treatment interactions for all three metals. Additionally, in the DID group, we observed strain differences in reduction of hippocampus mass. These findings are particularly interesting to us because high alcohol consumption in humans has been associated with neurodegeneration and dementia related to disruption of iron regulation. The findings of alcohol consumption associated decreases in copper and zinc are novel. The role of copper regulation and neurological function related to alcohol consumption is as yet largely unexplored. The role of zinc is better known as a neuromodulator in the hippocampus and appears to be protective against neurological damage. It would seem then, that the alcohol-related decrease in zinc in the hippocampus would be of concern and warrants further study.



中文翻译:

乙醇消耗的遗传差异:对小鼠海马体铁、铜和锌调节的影响

神经退行性疾病的一个共同特征是铁失调,通常在不同区域观察到其浓度增加。据信,大量饮酒会导致大脑中的这种铁失调,并伴有痴呆症。为了检查动物模型中的这种效应和相关的基于遗传的个体差异,我们使用黑暗中饮酒 (DID) 方法对来自 12 个 BXD 重组近交系的雌性小鼠进行了 16 周的饮酒。记录每日消耗,并在 16 周结束时收集海马组织。使用 X 射线荧光技术测量铁、铜和锌的浓度。结果表明,DID 增加了所有菌株的整体铁含量,范围从 3% 到 68%。铜和锌均下降,幅度为 0。分别为 4-42 和 5-35%。方差分析显示,所有三种金属的处理相互作用都产生了显着的应变。此外,在 DID 组中,我们观察到海马体质量减少的应变差异。这些发现对我们来说特别有趣,因为人类大量饮酒与铁调节中断相关的神经变性和痴呆有关。饮酒与铜和锌减少相关的发现是新颖的。与饮酒相关的铜调节和神经功能的作用在很大程度上尚未得到探索。锌的作用在海马体中作为神经调节剂而广为人知,似乎可以防止神经损伤。那样的话,

更新日期:2021-06-28
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