汞在微生物中的跨膜运输机制研究进展

甲基汞是一种强亲脂性、高神经毒性的有机汞化合物,可以通过生物富集或生物放大造成人类甲基汞暴露。环境中甲基汞的产生主要是厌氧微生物所调控的无机汞的甲基化。主流观点认为厌氧微生物对汞的甲基化是一种细胞内反应,因此,甲基汞的产生速率不仅与环境中具有汞甲基化能力的厌氧微生物的存在与活性相关,同时也与无机汞在微生物细胞中的跨膜运输过程有着重要联系。要明确无机汞经微生物甲基化的机制,就必须了解无机汞被微生物细胞生物吸收的过程,即无机汞在微生物中的跨膜运输路径。目前研究认为该过程主要有Mer抗汞操纵子转运体系、被动扩散、促进扩散和主动运输4种路径。本综述主要围绕无机汞被微生物细胞生物吸收的这4种路径展开,将系统介绍科学界对这4种路径的最新研究进展,并对相关研究进行展望,指出无机汞经促进扩散或主动运输进入到微生物细胞内将是未来研究的重点。     

蓟运河汉沽地区河泥中汞的微生物甲基化作用

汞的生物转化作用的研究开始于60年代末,Wood等(1968)研究了生物甲基化的机制,认为汞甲基化有酶和非酶两种作用,甲基化作用是通过甲基钴氨素中的甲基转移来完成的。瑞典生物学家Jensen和Jernel(?)v(1969)提出在湖泊底泥里微生物有形成甲基汞的功能,汞甲基化的速度与底泥里的微生物活动有密切的相关性。由此,微生物汞甲基化作用得到人们的注视,Yamada等(1972)在厌氧条件下研究了匙形梭菌(Clostridium cochlearium)的汞甲基化作用。Vonk等(1973)发现在通气条件下一些细菌和真菌可使氯化汞甲基化形成少量的甲基汞。Fagerstr(?)m和Jernel(?)v(1972)曾报道,通气条件下汞转化过程中甲基化的主要产物是一甲基汞,厌氧条件下汞甲基化的产物大部是二甲基汞。但是,人们总是认为甲基化的主要产物为一甲基汞,而二甲基汞形成的数量则很少(Iverson等,1978)。这些汞化合物在水体中引起危害。     

硫酸盐还原菌对汞的甲基化作用及其影响因子

从受氯碱化工废水严重污染的湖北鸭儿湖 1号氧化塘底泥中分离获得了硫酸盐还原菌 ,研究了其生理特性和环境因子对其生长的影响。并在实验室条件下建立了模拟厌氧水环境 ,通过正交实验获得汞甲基化的最佳条件 ,研究了该条件下硫酸盐还原菌在好氧和厌氧状况下对汞的甲基化作用 ,以及非生物甲基化作用。同时又分别作了单因素实验 ,并用高效液相色谱法测定了水样中不同形态的汞。结果显示 ,该硫酸盐还原菌营厌氧生活 ,在35℃、pH7 0、0 7%的盐度、0 5g/LFe2 和不含硫化物等条件下 ,可达到最佳生长状态。水环境中汞的甲基化作用主要发生在有微生物为媒介的厌氧环境下 ,汞的非生物甲基化作用和好氧环境下的甲基化作用均可忽略不计。厌氧环境下 ,水体温度、pH值、硫化物和盐度等诸多环境因素对汞的微生物甲基化作用的影响也进行了研究与讨论。     

汞甲基化细菌研究进展

汞甲基化细菌在厌氧条件下将无机汞(Hg)转化成最高毒性的甲基汞(MeHg),通过生物富集以及在食物链中的生物放大造成人类甲基汞暴露.本文综述了水环境中汞甲基化细菌的种类、系统发生、甲基化机理、甲基汞生成的空间位置和影响因素.水环境中汞甲基化主要发生在海洋、海湾、河流和湖泊的厌氧沉积物中.硫酸盐还原菌和铁还原菌是主要的汞甲基化细菌,它们的种类、群落结构和分布制约了甲基汞的生成,从而影响人体健康.汞甲基化的生化机理的研究表明,甲基汞可能产生于不同的代谢途径,但是对于汞甲基化机理仍没有一致的认识.沉积物中汞甲基化细菌的分布影响甲基汞生成的空间位置和甲基化率.因此,水环境中的地球化学因素影响甲基化细菌的分布、甲基化率和甲基汞的生成.     

中亚热带常绿阔叶林凋落物分解过程中汞的动态变化及迁移机理

森林凋落物对于汞在林地土壤的生物地球化学循环中起到重要作用,为研究森林凋落物分解过程中汞的迁移转化特征,以重庆四面山风景名胜区典型林分(常绿阔叶林)作为研究对象。于2014年3月—2015年3月连续监测典型林分凋落物中各形态汞浓度和有机质变化量,同时监测周围土壤中汞浓度变化。结果表明:四面山典型林分凋落物分解过程中汞浓度整体上升,总汞浓度(初始浓度:78 ng/g)的增幅最高达53%,甲基汞浓度(初始浓度:0.32 ng/g)最高增幅达138%;在春季和夏季,水溶态和酸溶态两种活性态汞含量分别增加了851%和96%,在分解前期和末期,凋落物汞的中惰性汞比例最高,占比达75%。土壤腐殖质层中总汞和甲基汞浓度比较稳定。凋落物中活性态汞通过雨水淋洗进入土壤与有机质络合并发生甲基化/去甲基化过程,通过地表径流、地下径流进入水体。凋落物中C含量减少了22%,N含量增加了15%,总汞浓度与C/N比呈负相关,与N含量呈正相关。凋落物中微生物C、N含量整体增加,与汞浓度峰值同步,且夏季含量显著高于冬季含量(P0.05),说明微生物与凋落物固定汞和汞的甲基化过程密切相关。     

DNA甲基化与多发性骨髓瘤

DNA甲基化是目前肿瘤领域研究中研究最多的表观遗传学机制之一.主要发生在DNA的CpG岛.DNA的甲基化通过甲基转移酶(DNA methyltransfeases,DNMTs)完成.DNA甲基化在多种肿瘤的发生、发展中都起到了重要的作用.大量研究发现,甲基化与多发性骨髓瘤的发生、发展及诊断治疗等有密切关系.深入探讨多发性骨髓瘤(MM)相关的甲基化可为MM发病机制的研究及治疗提供新的思路.     

DNA甲基化与病毒感染的研究进展

DNA甲基化是基因表达的表观遗传调控机制之一,在细胞分化和疾病发生过程中发挥着重要的作用。病毒感染可导致DNA甲基化水平变化,从而影响疾病的发生与发展。随着全基因组甲基化测序等生物学新技术的飞速发展,对DNA甲基化也有了更深的认识。现就DNA甲基化和去甲基化的主要影响因素以及病毒感染过程中导致甲基化水平改变的机制做一概述,为从表观遗传角度研究病毒致病机制提供一定的理论依据。     

植物离体培养过程中DNA甲基化变异研究进展

表现遗传变异对于植物的生长发育起着重要作用,主要包括DNA甲基化、组蛋白修饰、染色体重塑和RNA干涉等.DNA甲基化是一种最重要的表现遗传机制,在植物离体培养过程中广泛存在,本文对植物离体培养过程的DNA甲基化变异现象、影响因素及机理等情况进行综述.     

土壤汞污染生物修复技术研究进展

汞作为常温下唯一的一种液态金属,在环境中分布十分广泛,极易造成土壤污染。生物修复是一种用于土壤汞污染治理的重要修复技术,该技术因具有修复成本低、绿色环保等优点而受到重视。对现有的土壤汞污染生物修复技术进行了评述,主要涉及植物修复技术、微生物修复技术和动物修复技术的研究和应用情况:植物修复技术主要研究汞在植物体内代谢机理和规律,微生物修复技术研究侧重于利用外源微生物降解土壤中汞,动物修复技术研究较少,目前仅见有关蚯蚓富集汞的报道。现代生物修复技术已经发展成为一门包括土壤化学、植物生物学、生态学、土壤微生物学、分析化学及分子生物学等多学科融合性技术,借助这些学科力量可以对植物提取汞根际微界面过程和植物体内微界面过程、微生物和动物汞富集机制有更深刻的认识。综述最后对目前土壤汞污染生物修复技术主要研究方向进行总结和归纳,明确了汞污染生物修复领域存在的几大问题以及研究方向。     

汞在新建水库食物网中生物累积与风险评价研究进展

汞是唯一参与全球循环的液态重金属。1974年,自美国学者Smith首次报道水库中鱼类总汞含量高于邻近自然湖泊以来,水库中鱼类汞升高的风险成为新建水库环境影响评价中的重要内容之一。汞在水库生态系统生物组分和非生物组分中含量升高的现象先后在世界各国报道,包括加拿大、美国、芬兰、泰国和巴西等。通过对系列的野外研究进行回顾,表明了水库形成后生态系统中汞的甲基化过程发生了变化。水库形成对汞在食物网中的鱼类、底栖生物、浮游生物的累积产生影响。水库中汞的生物累积、迁移转化主要与被淹没土壤和植物腐解过程有着直接或间接的关系。水库形成后,总汞、甲基汞和甲基汞比例在生态系统食物网各组分中的变化并不一致。蓄水后,水体中总汞变化较小,甲基汞和甲基汞比例上升明显;浮游生物尤其是浮游动物中总汞升高,但甲基汞和甲基汞比例升高更为明显;与浮游动物类似,底栖水生昆虫中总汞升高,甲基汞和甲基汞比例升高也更为明显;鱼类作为食物网顶级消费者,甲基汞比例一般在80%以上,在水库形成后鱼类总汞和甲基汞均明显升高,但甲基汞比例变化已经不大。这些变化揭示了水库形成后甲基汞在食物网传递的两个主要可能途径,一是微型生物食物网。通过悬浮颗粒物、浮游植物、浮游动物这一环节,甲基汞和甲基汞比例有明显的增加。第二个途径是底层生物食物网。通过悬浮颗粒物、细菌、碎屑食性底栖水生昆虫、肉食型底栖水生昆虫环节,甲基汞和甲基汞比例明显增加。这两种途径均能导致以水生昆虫、小鱼、甲壳类等为食的肉食性鱼类汞含量增加。水库形成后,生态系统中汞的甲基化发生了明显的"加速"过程。这种"加速"过程最直接的因素是成库后大量土壤淹没使得汞的甲基化平衡被打破。这个过程主要有两方面的影响。一方面是直接影响,被淹没土壤和植被在腐解过程中主动或被动地将甲基汞释放到水库生态系统中;另一方面是间接影响,被淹没土壤和植被的腐解使水库底部形成厌氧环境,有利于无机汞从被淹没土壤和植被中溶出,为甲基化反应提供充裕的、可供甲基化的无机汞,同时腐解产生的大量营养物质为微生物提供丰富食物来源,使硫酸盐还原菌大量繁殖,促进无机汞的甲基化。在我国,有关汞在新建水库食物网中生物累积和风险评价的研究有待进一步加强。     

Mercury methylation from unexpected sources: molybdate-inhibited freshwater sediments and an iron-reducing bacterium

Methylmercury has been thought to be produced predominantly by sulfate-reducing bacteria in anoxic sediments. Here we show that in circumneutral pH sediments (Clear Lake, CA) application of a specific inhibitor of sulfate-reducing bacteria at appropriate concentrations typically inhibited less than one-half of all anaerobic methylation of added divalent mercury. This suggests that one or more additional groups of microbes are active methylators in these sediments impacted by a nearby abandoned mercury mine. From Clear Lake sediments, we isolated the iron-reducing bacterium Geobacter sp. strain CLFeRB, which can methylate mercury at a rate comparable to Desulfobulbus propionicus strain 1pr3, a sulfate-reducing bacterium known to be an active methylator. This is the first time that an iron-reducing bacterium has been shown to methylate mercury at environmentally significant rates. We suggest that mercury methylation by iron-reducing bacteria represents a previously unidentified and potentially significant source of this environmental toxin in iron-rich freshwater sediments.     

Mercury Methylation from Unexpected Sources: Molybdate-Inhibited Freshwater Sediments and an Iron-Reducing Bacterium

Methylmercury has been thought to be produced predominantly by sulfate-reducing bacteria in anoxic sediments. Here we show that in circumneutral pH sediments (Clear Lake, CA) application of a specific inhibitor of sulfate-reducing bacteria at appropriate concentrations typically inhibited less than one-half of all anaerobic methylation of added divalent mercury. This suggests that one or more additional groups of microbes are active methylators in these sediments impacted by a nearby abandoned mercury mine. From Clear Lake sediments, we isolated the iron-reducing bacterium Geobacter sp. strain CLFeRB, which can methylate mercury at a rate comparable to Desulfobulbus propionicus strain 1pr3, a sulfate-reducing bacterium known to be an active methylator. This is the first time that an iron-reducing bacterium has been shown to methylate mercury at environmentally significant rates. We suggest that mercury methylation by iron-reducing bacteria represents a previously unidentified and potentially significant source of this environmental toxin in iron-rich freshwater sediments.     

Methods for Measuring Specific Rates of Mercury Methylation and Degradation and Their Use in Determining Factors Controlling Net Rates of Mercury Methylation

A method was developed to estimate specific rates of demethylation of methyl mercury in aquatic samples by measuring the volatile ¹⁴C end products of ¹⁴CH₃HgI demethylation. This method was used in conjunction with a ²⁰³Hg²⁺ radiochemical method which determines specific rates of mercury methylation. Together, these methods enabled us to examine some factors controlling the net rate of mercury methylation. The methodologies were field tested, using lake sediment samples from a recently flooded reservoir in the Southern Indian Lake system which had developed a mercury contamination problem in fish. Ratios of the specific rates of methylation/demethylation were calculated. The highest ratios of methylation/demethylation were calculated. The highest ratios of methylation/demethylation occurred in the flooded shorelines of Southern Indian Lake. These results provide an explanation for the observed increases in the methyl mercury concentrations in fish after flooding.     

DNA甲基化的分子机制及其研究进展

DNA甲基化作为一种重要的非永久性但相对长期可遗传的基因修饰,在维持细胞正常的转录活性、DNA损伤修复能力以及在遗传印记、胚胎发育和肿瘤的发生发展中都有不可替代的作用,是分子生物学及医学领域的研究热点。近年来随着高通量测序、表观遗传编辑以及结构分析等技术的飞速发展,对DNA甲基化分子机制层面的研究进一步深入。本研究总结了近年来对DNA甲基化分子机制的相关研究,归纳了全球范围内对DNA甲基化的位点、序列背景与范围近年来的研究进展,也归纳了近年来对影响DNA甲基化的因素的研究,以期对DNA甲基化这一表观遗传学热点进行深入的学习探讨。     

The interplay between diet,gut microbes,and host epigenetics in health and disease

The mechanisms linking the function of microbes to host health are becoming better defined but are not yet fully understood. One recently explored mechanism involves microbe-mediated alterations in the host epigenome. Consumption of specific dietary components such as fiber, glucosinolates, polyphenols, and dietary fat has a significant impact on gut microbiota composition and function. Microbial metabolism of these dietary components regulates important epigenetic functions that ultimately influences host health. Diet-mediated alterations in the gut microbiome regulate the substrates available for epigenetic modifications like DNA methylation or histone methylation and/or acetylation. In addition, generation of microbial metabolites such as butyrate inhibits the activity of core epigenetic enzymes like histone deacetylases (HDACs). Reciprocally, the host epigenome also influences gut microbial composition. Thus, complex interactions exist between these three factors. This review comprehensively examines the interplay between diet, gut microbes, and host epigenetics in modulating host health. Specifically, the dietary impact on gut microbiota structure and function that in-turn regulates host epigenetics is evaluated in terms of promoting protection from disease development.     

Methylmercury and methane production potentials in North Carolina Piedmont stream sediments

Methylated mercury (MeHg) can be produced by all microbes possessing the genes hgcA and hgcB, which can include sulfate-reducing bacteria (SRB), iron-reducing bacteria (FeRB), methane-producing archaea (MPA), and other anaerobic microbes. These microbial groups compete for substrates, including hydrogen and acetate. When sulfate is in excess, SRB can outcompete other anaerobic microbes. However, low concentrations of sulfate, which often occur in stream sediments, are thought to reduce the relative importance of SRB. Although SRB are regarded as the primary contributors of MeHg in many aquatic environments, their significance may not be universal, and stream sediments are poorly studied with respect to microbial Hg methylation. We evaluated suppression of methanogenesis by SRB and the potential contributions from SRB, MPA and other MeHg producing microbes (including FeRB) to the production of MeHg in stream sediments from the North Carolina Piedmont region. Lower methanogenesis rates were observed when SRB were not inhibited, however, application of a sulfate-reduction inhibitor stimulated methanogenesis. Greater MeHg production occurred when SRB were active. Other MeHg producing microbes (i.e., FeRB) contributed significantly less MeHg production than SRB. MPA produced MeHg in negligible amounts. Our results suggest that SRB are responsible for the majority of MeHg production and suppress methanogenesis in mid-order stream sediments, similar to other freshwater sediments. Further investigation is needed to evaluate the generality of these findings to streams in other regions, and to determine the mechanisms regulating sulfate and electron acceptor availability and other potential factors governing Hg methylation and methane production in stream sediments.     

Genome sequence of the mercury-methylating and pleomorphic Desulfovibrio africanus Strain Walvis Bay

Desulfovibrio africanus strain Walvis Bay is an anaerobic sulfate-reducing bacterium capable of producing methylmercury (MeHg), a potent human neurotoxin. The mechanism of methylation by this and other organisms is unknown. We present the 4.2-Mb genome sequence to provide further insight into microbial mercury methylation and sulfate-reducing bacteria.     

Genome sequence of the mercury-methylating strain Desulfovibrio desulfuricans ND132

Desulfovibrio desulfuricans strain ND132 is an anaerobic sulfate-reducing bacterium (SRB) capable of producing methylmercury (MeHg), a potent human neurotoxin. The mechanism of methylation by this and other organisms is unknown. We present the 3.8-Mb genome sequence to provide further insight into microbial mercury methylation.     

Pilot plant for bioremediation of mercury-containing industrial wastewater

Mercury is an extremely toxic pollutant that is currently being emitted mainly by low level industrial sources. It is distributed globally through the atmosphere, from where it precipitates onto the surface of the Earth, enters aquatic organisms, accumulates in fish and finally affects the health of human populations. Microbes have evolved a mechanism for mercury detoxification [mercury resistance operon ( mer)] based on intracellular reduction of Hg(2+) to non-toxic Hg(0) by the mercuric reductase enzyme and subsequent diffusional loss of Hg(0) from the cell. It was shown that Hg(0) produced by microbial detoxification can be retained quantitatively in packed bed bioreactors, in which biofilms of mercury-resistant bacteria are grown on porous carrier material. This review describes operation of this system on a technical, fully automated, scale, and its operation at a chloralkali electrolysis factory. It was shown to work with high efficiency under fluctuating mercury concentrations and to be robust against transiently toxic conditions. The gradient of mercury concentration in the technical scale system exerted a strong selective pressure on the microbial community, which resulted in a succession of mercury-resistant strains at high mercury concentrations and an increase in phylogenetic and functional diversity at low mercury concentrations. Clean-up of mercury-containing wastewater by mercury-resistant microbes is a simple, environmentally friendly and cost-effective alternative to current treatment technologies.     

Mercury Methylation and Demethylation in Anoxic Lake Sediments and by Strictly Anaerobic Bacteria

After spiking anoxic sediment slurries of three acidic oligotrophic lakes with either HgCl₂ at 1.0 μg/ml or CH₃HgI at 0.1 μg/ml, both mercury methylation and demethylation rates were measured. High mercury methylation potentials were accompanied by high demethylation potentials in the same sediment. These high potentials correlated positively with the concentrations of organic matter and dissolved sulfate in the sediment and with mercury levels in fish. Adjustment of the acidic sediment pH to neutrality failed to influence either the methylation or the demethylation rate of mercury. The opposing methylation and demethylation processes converged to establish similar Hg²⁺-CH₃Hg⁺ equilibria in all three sediments. Because of their metabolic dominance in anoxic sediments, mercury methylation and demethylation in pure cultures of sulfidogenic, methanogenic, and acetogenic bacteria were also measured. Sulfidogens both methylated and demethylated mercury, but the methanogen tested only catalyzed demethylation and the acetogen neither methylated nor demethylated mercury.