Wuhan University Journal of Natural Sciences TOTAL CONTENTS

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Environmental chemical stressors as epigenome modifiers: a new horizon in assessment of toxicological effects

In eukaryotic cells, chromatin transformation from euchromatin into heterochromatin as a means of controlling gene expression and replication has been known as the ‘‘accessibility hypothesis' '. The interplay of epigenetic changes including histone modifications, DNA methylation, RNA interference(RNAi) and other func- tional epigenetic components are intricate. It is believed that these changes are well-programmed, inherited and can be modified by environmental contaminant stressors. Environmentally-driven epigenetic alterations during development, e.g. embryonic, foetal or neonatal stage, may influence disease susceptibility in adulthood. Therefore, understanding how epigenome modifications develop in response to environmental chemicals and, how epigenetic-xenobiotic interactions influence human health will shed new insights into gene-environment interactions in the epidemiology of several diseases including cancer. In this review, we consider studies of chemical modifiers including nutritional and xenobiotic effects on epigenetic components in vitro or in vivo. By examining the most-studied epigenome modifications and how their respective roles are interlinked, we highlight the central role of xenbiotic- modified epigenetic mechanisms. A major requirement will be to study and understand effects following environmentally-relevant exposures. We suggest that the study of epigenetic toxicology will open up new opportunities to devise strategies for the prevention or treatment of at-risk populations.     

低氧与表观遗传学互作的研究进展

表观遗传学是指基因组DNA序列不发生改变的情况下,基因表达水平发生变化从而导致的可遗传表型变化的现象.表观遗传可通过与低氧诱导因子(HIF)家族协同作用,以促使细胞适应低氧环境,从而参与到低氧应答的调控过程中.现就表观遗传学通过以下四个方面与低氧应答进行综述:1)VHL与PDH3调控HIF稳定性;2)通过影响HIF-1α共激活复合物的活性、HRE位点的修饰、HIF结合位点或附近区域的染色质活性,阻止HIF与HRE位点结合;3)组蛋白脱甲基酶对低氧应答相关基因的转录调控;4)低氧环境引起细胞内整体的组蛋白修饰程度和DNA甲基化水平改变.     

组蛋白促进[Ru(bpy)2(dppz)]2+和MWCNTs在ITO电极上的阳极共沉积

应用计时库仑法、循环伏安法、微分脉冲伏安法、荧光光谱和扫描电镜等方法研究了组蛋白(His)、[Ru(bpy)2(dppz)]2+(bpy = 2,2-联吡啶,dppz = 邻联二吡啶[3,2-a:2,3-c]吩嗪)和多壁碳纳米管(MWCNTs)在铟锡氧化物(ITO)电极上的电化学共沉积。结果表明,His能促进[Ru(bpy)2(dppz)]2+和MWCNTs在ITO电极上的阳极共沉积(1.2 V vs. Ag/AgCl),所获得的复合膜呈现两对由表面电化学过程控制的氧化还原峰;通过研究His浓度和pH值对复合膜中Ru(III)/Ru(II)氧化还原反应的影响,阐明了His作为媒介体调控[Ru(bpy)2(dppz)]2+和MWCNTs在ITO电极上共沉积的机理。在最优化条件下,复合物中[Ru(bpy)2(dppz)]2+发生氧化的电量在0.01~0.2 mgL-1和0.2~5.0 mgL-1区间内与His浓度呈线性关系,其线性回归方程分别为Q/C = 3.24(0.27) 10-6 + 2.95 (0.09) 10-4 CHis/mgL-1 (R = 0.993)和Q/C = 5.92(0.25) 10-5 + 6.26 (0.62) 10-6 CHis/mgL-1 (R = 0.998)。该研究提供的新方法可以应用于具有良好氧化还原性能的无机生物纳米复合材料的制备及蛋白质的固定与检测。     

Histone deacetylases: Focus on the nervous system

Neurodegenerative disease strikes millions worldwide and there is mounting evidence suggesting that underlying the onset and progression of these debilitating diseases is inappropriate neuronal apoptosis. Recent reports have implicated a family of proteins known as histone deacetylases (HDACs) in various neuronal processes including the neuronal death program. Initial headway in this field has been made largely through the use of broad-spectrum HDAC inhibitors. In fact, pharmacological inhibition of HDAC activity has been shown to protect neurons in several models of neurodegeneration. The observation that HDAC inhibitors can have opposing effects in different paradigms of neurodegeneration suggests that individual members of the HDAC protein family may play distinct roles that could depend on the specific cell type under study. The purpose of this review is to detail work involving the use of HDAC inhibitors within the context of neurodegeneration and examine the roles of individual HDAC members in the nervous system with specific focus on neuronal cell death. Received 25 January 2007; received after revision 3 April 2007; accepted 26 April 2007