极地大气汞亏损研究进展

汞是唯一以气态单质形态随大气循环参与全球迁移的重金属元素,大气汞的长距离传输是汞的生物地球化学循环的重要特性之一,对全球汞循环有着重要的影响.由于汞的全球传输与沉降,汞在极地的污染不容忽视.科学工作者分别于1995年、2000年在北极和南极地区发现了大气汞亏损现象,并提出了对大气汞迁移转化的新认识,促进了对特殊气候、环境下汞在大气中的形态转化及其对陆地生态系统的影响研究.目前对极地大气汞亏损过程及其影响了解仍不够深入.本文从极地大气汞的分布、大气汞亏损的发生机制、沉降汞的归趋以及生物响应等综述了近年来对极地大气汞亏损的研究工作,并对极地大气汞亏损今后的研究方向作了展望,为特殊气候环境下大气汞的迁移转化机理研究提供借鉴.     

贵州省环境中汞污染现状与分布特征

贵州是我国汞矿的主要产地,其储量和产量均居全国首位,因此造成了该区域环境受到广泛的汞污染。从大的区域尺度上研究汞的污染分布特征对于了解该区域汞的污染现状有很好的指导作用。通过对贵州省汞污染源及各环境介质中汞污染情况的调查,首先阐释了万山、务川、滥木厂等几个主要汞矿区及燃煤和有机化工等行业的汞污染现状;并从大气、土壤和水体等环境介质方面综合分析了贵州地区汞的暴露水平与分布特征;采用ArcGIS 10.0描绘了各环境介质中总汞及甲基汞的分布特征。结果表明贵州省东北部与西南部汞矿区汞污染程度较高,大气、土壤和水体中的总汞分布呈明显的区域性,汞矿毗邻区域明显高于其他区域,矿区和城镇水体中甲基汞浓度较高,表明汞矿区和人为活动等因素影响水体中的甲基汞的分布。     

贵阳市大气降水中汞的分布特征

于2008年7-9月对贵阳市中心城区采集的21个大气降水进行了总汞、甲基汞及阴、阳离子浓度的测定,分析了大气降水中总汞与阴阳离子间的相互关系.结果表明:大气降水中总汞的平均含量为18 ng·L-1,变化范围为0.4～57.4 ng·L-1;甲基汞的平均含量为0.07 ng·L-1,变化范围为0.02～0.2 ng·L-1.大气降水中的阴离子以SO2-4和NO-3为主,其浓度平均值分别为151和145 mol·L-1;阳离子主要以Ca2+为主,平均浓度达到了123 mol·L-1,变化范围为3.7～560 mol·L-1,其次是NH4+和Mg2+,其浓度平均值分别为52.2和20.4 mol·L-1.通过分析降水中总汞和阴阳离子之间的相互关系,发现总汞和阴离子SO2-4具有显著的相关性,与F-有一定的相关性,而与NO-3不具有相关性.由此初步判定,大气降水中的总汞主要来源于燃煤等人为释放源.     

陕西旬阳汞矿区大气降水中汞形态分布特征

2012年7月—2013年9月对旬阳汞矿区大气降水中总汞、活性汞和溶解气态汞污染特征以及微量元素浓度进行了调查,分析了汞与微量元素浓度之间的相关性。结果表明:旬阳汞矿区大气降水中总汞、活性汞和溶解气态汞浓度的平均值分别为(48±43)、(13±9.0)和(3.8±3.6)ng·L~(-1),浓度变化范围分别为4.4~253、0.39~43和0.41~17 ng·L~(-1);大气降水中活性汞和溶解气态汞分别占总汞浓度的27%和7.9%,其他无机汞形态是其主要存在形态,占总汞浓度的65%;雨水的pH平均值为5.4,变化范围为4.2~6.7;大气降水中Hg和Sb、Se呈显著的正相关,R~2分别为0.67和0.54,说明Hg和Sb、Se具有相同的来源,其中旬阳汞矿的开采和汞锑冶炼等人为释放源为主要贡献源,其次为燃煤源。     

贵州汞矿区居民食用大米的甲基汞暴露及健康风险评价

贵州汞矿区居民食用的大米、蔬菜、猪肉和饮水均表现出较高的总汞含量,但仅有大米富集甲基汞.万山汞矿区3个村庄居民食用大米甲基汞的摄入量占总摄入量的平均比例分别为97.5%、94.1%和93.5%,且不同研究对象每日食用大米的甲基汞摄入量与其头发甲基汞含量之间存在显著的相关关系,这证实了食用大米是贵州汞矿区居民甲基汞暴露的主要途径.土法炼汞工人的头发总汞含量显著高于一般居民和对照组,其头发甲基汞占总汞的平均比例仅为12.4%,说明土法炼汞释放的汞蒸气的影响.贵州汞矿区居民头发甲基汞含量相比对照组均有一定程度的升高,部分居民食用大米的日甲基汞摄入量已经超过JECFA 2003年制定的标准(0.23 μg·d-1·kg-1),大部分超过美国环保局的推荐值(0.1 μg·d-1·kg-1),特别是铜仁垢溪和老屋场地区居民存在一定的甲基汞暴露风险,其他汞矿区人群也存在通过食用大米甲基汞暴露的潜在风险.     

贡嘎山原始森林区苔藓植物重金属含量及其对汞的吸附特征

采集了贡嘎山海螺沟原始森林区的7种主要苔藓,分析了其重金属（Hg、Cr、Cd、Ni、Pb、Cu、Mn、Zn和Fe）含量,并选择两种分布较广的赤茎藓和多枝砂藓进行汞吸附试验.结果表明,贡嘎山海螺沟原始森林区7种苔藓的重金属含量均较低,除Cd含量与欧美地区背景值相当外,其他均低于欧美地区的背景含量,表明该地区大气未受重金属污染,大气环境质量良好. 两种苔藓对汞的吸附是一个主动快速的过程,2 h左右即达到吸附平衡,其吸附特征能很好地用Langmuir和Freundlich方程拟合,由Langmuir方程计算的两种苔藓对汞的最大吸附量分别为15.24和8.19 mg·g^-1,表明它们具有较强的汞吸附能力,可用作大气汞污染的指示生物.     

长白山森林地区河流中汞的时空分布特征

采集并测定了枯水期和丰水期长白山北坡几条河流的水样,研究了长白山地区河流中总汞和甲基汞的时空变化规律.长白山北坡地区河流总汞的变化范围为2.0～20 ng·L-1,受北方燃煤等人为活动影响,枯水期总汞含量高于丰水期;甲基汞的变化范围为0.12～0.55 ng·L-1,不同季节的甲基汞变化不大.水体汞含量随海拔的升高而降低,汇入松花江的几条河流对松花江水体的影响较为明显,随着河流的汇入溶解态汞含量下降,颗粒态汞含量升高.与世界上其他一些森林水体对比发现,长白山水体甲基汞含量较低,但总汞含量较高.估计研究地区河流一年将向下游地区输出33 kg的总汞以及200 g甲基汞,这将进一步加剧下游水体汞的负担.     

我国自然源汞排放研究进展

由于特殊的物理化学性质,汞是唯一主要以气态单质形式存在于大气的重金属污染物,可通过大气环流进行全球性的传输。大气汞主要来自于人为活动和自然过程的汞排放。建立和优化全球和区域大气汞排放清单对研究全球大气汞的迁移转化规律及其环境健康效应具有重要意义。由于影响因素较为复杂,目前国内外自然源清单研究与人为源清单研究相比较为滞后。我国约十分之一的国土面积位于环太平洋汞矿化带上,且我国主要自然源汞排放通量与欧洲和北美同类型地区相比偏高。近些年来,国内研究人员在自然源汞排放研究领域开展了大量的研究工作,为建议和优化我国的自然源汞排放清单提供了重要的科学依据。本文总结了近年来我国自然源汞排放的研究进展,分析水体、土壤和植被等自然源汞排放通量分布规律、内在机理和影响因素;同时对我国自然源汞排放存在的不足及未来需要开展的工作进行了展望。     

桂林市汽车尾气汞污染

采集了桂林市郊4条公路剖面大气、土壤和蔬菜各56件样品,分析测定了其汞含量,以了解桂林市郊汽车尾气汞污染状况.结果表明,公路剖面汞含量均呈对称单峰型分布.汽车尾气汞污染扩散的影响范围约200 m.大气汞含量与蔬菜和土壤的汞污染具有明显的相关性.公路系统汽车尾气汞污染强度随公路路龄、车流量增大而增强.公路系统汞污染主要来源于汽车尾气汞污染,根源于燃油富含汞.公路剖面土壤48%样品汞含量超过了国家无公害蔬菜基地土壤汞含量标准.桂阳公路剖面蔬菜汞含量是国家无公害农产品质量标准(0.29+0.03 μg·g-1)的1.1～1.7倍.表明,桂林市公路系统剖面已受到一定程度的汞污染.     

夜郎湖水库水体不同形态汞的时空分布

于2006年7月(夏季)、2007年1月(冬季)和3月(春季)采集了贵州省夜郎湖水库水样,研究了不同形态汞(总汞、溶解态汞、颗粒态汞)的时空分布特征及其影响因素.结果表明,夏季水体总汞、溶解态汞、颗粒态汞平均含量分别为4.48±2.59、2.37±1.40、2.11±1.86 ng·L-1,均显著高于冬季和春季(P＜0.001),而冬春2季不同形态汞含量无明显差异.水质参数悬浮颗粒物(SPM)和硝酸盐(NO-3)与不同形态汞之间均存在显著的正相关关系,表明这些参数对于不同形态汞的季节分布起着重要作用.夏季农业耕作活动相对活跃,表层土壤的扰动增加,雨水冲刷农田土壤,带进大量的外源颗粒物,致使夜郎湖水体夏季总汞水平较高.空间分布表明,夜郎湖水库夏季总汞平均浓度从水库入库河流至大坝方向、出库河流呈现总体下降的分布趋势,但水体各采样剖面没有明显的分布规律.     

Mutual adaptation between mouse transglutaminase 4 and its native substrates in the formation of copulatory plug

Formation of copulatory plugs by male animals is a common means of reducing competition with rival males. In mice, copulatory plugs are formed by the coagulation of seminal vesicle secretion (SVS), which is a very viscous and self-clotting fluid containing high concentration of proteins. In its native state, mouse SVS contains a variety of disulfide-linked high-molecular-weight complexes (HMWCs) composed of mouse SVS I-III, which are the major components of mouse SVS. Further, mouse SVS I-III are the substrates for transglutaminase 4 (TGM4), a cross-linking enzyme secreted from the anterior prostate. According to activity assays, mouse TGM4 prefers a mild reducing and alkaline environment. However, under these conditions, the activity of mouse TGM4 toward SVS I-III was much lower than that of a common tissue-type TGM, TGM2. On the other hand, mouse TGM4 exhibited much higher cross-linking activity than TGM2 when native HMWCs containing SVS I-III were used as substrates under non-reducing condition. By the action of TGM4, the clot of SVS became more resistant to proteolysis. This indicates that the activity of TGM4 can further rigidify the copulatory plug and extend its presence in the female reproductive tract. Together with the properties of TGM4 and the nature of its disulfide-linked SVS protein substrates, male mice can easily transform the semen into a rigid and durable copulatory plug, which is an important advantage in sperm competition.     

DNA sequence and physical mapping of the canine transglutaminase 1 gene

The transglutaminase 1 gene (TGM1) encodes an enzyme necessary for cross-linking the structural proteins that form the cornified envelope, an essential component of the outermost layer of the skin, the stratum corneum. Reported here is the complete coding region of canine TGM1, its chromosome localization, and its map position in the integrated canine linkage-radiation hybrid map. Canine TGM1 consists of 2,448 nucleotides distributed over 15 exons. The nucleotide sequence has 90% identity to human TGM1. The deduced canine TGM1 protein is 816 amino acids long and is 92% identical to human TGM1. Using fluorescence in situ hybridization, we localized canine TGM1 to dog (Canis familiaris) chromosome 8 (CFA 8q). Canine TGM1 localized to CFA 8 on the integrated linkage-radiation hybrid map in the interval FH2149-MYH7. Characterizing the coding region of canine TGM1 is a first step in examining the role of this enzyme in normal and defective cornification in the dog.     

Epidermal growth factor receptor-mediated tissue transglutaminase overexpression couples acquired tumor necrosis factor-related apoptosis-inducing ligand resistance and migration through c-FLIP and MMP-9 proteins in lung cancer cells

Acquired chemoresistance not only blunts anticancer therapy but may also promote cancer cell migration and metastasis. Our previous studies have revealed that acquired tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance in lung cancer cells is associated with Akt-mediated stabilization of cellular caspase 8 and Fas-associated death domain (FADD)-like apoptosis regulator-like inhibitory protein (c-FLIP) and myeloid cell leukemia 1 (Mcl-1). In this report, we show that cells with acquired TRAIL resistance have significantly increased capacities in migration and invasion. By gene expression screening, tissue transglutaminase (TGM2) was identified as one of the genes with the highest expression increase in TRAIL-resistant cells. Suppressing TGM2 dramatically alleviated TRAIL resistance and cell migration, suggesting that TGM2 contributes to these two phenotypes in TRAIL-resistant cells. TGM2-mediated TRAIL resistance is likely through c-FLIP because TGM2 suppression significantly reduced c-FLIP but not Mcl-1 expression. The expression of matrix metalloproteinase 9 (MMP-9) was suppressed when TGM2 was inhibited, suggesting that TGM2 potentiates cell migration through up-regulating MMP-9 expression. We found that EGF receptor (EGFR) was highly active in the TRAIL-resistant cells, and suppression of EGFR dramatically reduced TGM2 expression. We further determined JNK and ERK, but not Akt and NF-κB, are responsible for EGFR-mediated TGM2 expression. These results identify a novel pathway that involves EGFR, MAPK (JNK and ERK), and TGM2 for acquired TRAIL resistance and cell migration in lung cancer cells. Because TGM2 couples TRAIL resistance and cell migration, it could be a molecular target for circumventing acquired chemoresistance and metastasis in lung cancer.     

Phenotypical features of long Q-T syndrome in transgenic mice expressing human Na-K-ATPase alpha(3)-isoform in hearts

To understand why the adult human heart expresses three isoforms of the sodium pump, we generated transgenic mice (TGM) with 2.3- to 5. 5-fold overexpression of the human alpha(3)-isoform of Na-K-ATPase in the heart. Hearts from the TGM had increased maximal Na-K-ATPase activity and ouabain affinity compared with control hearts, even though the density of Na-K-ATPase pump sites (of all isoforms) was similar to that of control mice. In perfused hearts, contractility both at baseline and in the presence of ouabain tended to be greater in TGM than in controls. Surface electrocardiograms in anesthetized TGM had a steeper dependence of Q-T on sinus cycle length, and Q-T intervals measured during atrial pacing were significantly longer in TGM. Q-T dispersion during sinus rhythm also tended to be longer in TGM. Thus TGM overexpressing human alpha(3)-isoform have several of the phenotypical features of human long Q-T syndrome, despite the absence of previously described mutations in Na(+) or K(+) channels.     

Human tissue transglutaminase is inhibited by pharmacologic and chemical acetylation

Human tissue transglutaminase (TGM2) is implicated in the pathogenesis of several neurodegenerative disorders including Alzheimer's, Parkinson's and expanded polyglutamine (polyQ) diseases. TGM2 promotes formation of soluble and insoluble high molecular weight aggregates by catalyzing a covalent linkage between peptide‐bound Q residues in polyQ proteins and a peptide‐bound Lys residue. Therapeutic approaches to modulate the activity of TGM2 are needed to proceed with studies to test the efficacy of TGM2 inhibition in disease processes. We investigated whether acetylation of Lys‐residues by sulfosuccinimidyl acetate (SNA) or aspirin (ASA) would alter the crosslinking activity of TGM2. Acetylation by either SNA and/or ASA resulted in a loss of >90% of crosslinking activity. The Lys residues that were critical for inhibition were identified by mass spectrometry as Lys⁴⁴⁴, Lys⁴⁶⁸, and Lys⁶⁶³. Hence, acetylation of Lys‐residues may modulate the enzymatic function of TGM2 in vivo and offer a novel approach to treatment of TGM2 mediated disorders.     

Hyperosmolarity‐mediated mitochondrial dysfunction requires Transglutaminase‐2 in human Corneal epithelial cells

Hyperosmolar‐induced ocular surface cell death is a key mitochondria‐mediated event in inflammatory eye diseases. Transglutaminase (TGM)‐2, a cross‐linking enzyme, is purported to mediate cell death, but its link to mitochondria is unclear. In the cornea, the integrity of the epithelial cells is important for maintaining transparency of the cornea and therefore functional vision. We evaluated the role of TGM‐2 and its involvement in hyperosmolarity‐stimulated mitochondrial cell death in human corneal epithelial (HCE‐T) cells. HCE‐T cell lines stably expressing either shRNA targeting TGM‐2 (shTG) or scrambled shRNA (shRNA) were constructed. Hyperosmolar conditions reduced viability and increased mitochondrial depolarization in shRNA cells. However, hyperosmolarity failed to induce mitochondrial depolarization to the same extent in shTG cells. Transient overexpression of TGM‐2 resulted in very high levels of TGM‐2 expression in shTG and shRNA cells. In the case of shTG cells after overexpression of TGM‐2, hyperosmolarity induced the same extent of mitochondrial depolarization as similarly treated shRNA cells. Overexpression of TGM‐2 also elevated transamidase activity and reduced viability. It also induced mitochondrial depolarization, increased caspase‐3/7 and ‐9 activity, and these increases were partially suppressed by pan‐caspase inhibitor Z‐VAD‐FMK. Corneal epithelial apoptosis via mitochondrial dysfunction after hyperosmolar stimulation is partially dependent on TGM‐2. This TGM‐2‐dependent mechanism occurs in part via caspase‐3/7 and ‐9. Protection against mitochondrial stress in the ocular surface targeting TGM‐2 may have important implications in the survival of cells in hyperosmolar stress. J. Cell. Physiol. 226: 693–699, 2011. © 2010 Wiley‐Liss, Inc.     

TGM2 interference regulates the angiogenesis and apoptosis of colorectal cancer via Wnt/β-catenin pathway

Angiogenesis and apoptosis are critical for the growth of colorectal cancer (CRC). The study aimed to investigate the effects of TGM2 in CRC. Forty-two patients were recruited and their TGM2 levels were detected by performing Realtime-qPCR (RT-qPCR), Western blot and immunohistochemistry , respectively. Levels of TGM2, MMP-2 and MMP-9 in four CRC cell lines and in normal cells were determined using RT-qPCR and Western blot. TGM2-siRNA was transfected into LoVo and HCT116 cells, respectively. TGM2 levels, cell viability, cell apoptosis, angiogenesis and related factors were determined. the tumorigenesis rates of mice were detected after TGM2-siRNA transfection. TGM2 were upregulated in patients with CRC. High TGM2 level of CRC patients had a lower survival rate. The levels of TGM2, MMP-2 and MMP-9 were upregulated in all detected CRC cell lines. Silencing TGM2 could inhibit cell viabilities, angiogenesis and suppress the expressions of MMP-2, MMP-9, Wnt3a, β-catenin and Cyclin D1 , whereas cell apoptosis and the expressions of Caspase-3 and TIMP-1 were promoted. Tumor weights and volumes were reduced by TGM2-siRNA interference. The effects of TGM2-siRNA interference might be related to Wnt/β-catenin Pathway. This might prove that TGM2 could be used as a molecular target in the treatment of CRC.     

A dietary supplement abolishes age-related cognitive decline in transgenic mice expressing elevated free radical processes

We previously found that transgenic mice overexpressing growth hormone (TGM) have elevated and progressively increasing free radical processes in brain that strongly correlates with reduced survivorship. Young mature TGM, however, displayed vastly enhanced learning of an eight-choice cued maze and qualitatively different learning curves than normal controls. Here we document the age-related patterns in learning ability of TGM and normal mice. Learning appeared inferior in both genotypes of very young mice but TGM were confirmed to be superior to normal mice upon maturity. Older TGM, however, showed rapid age-related loss of their exceptional learning, whereas normal mice at 1 year of age showed little change. The cognitive decline of TGM was abolished by a complex "anti-aging" dietary supplement formulated to promote membrane and mitochondrial integrity, increase insulin sensitivity, reduce reactive oxygen and nitrogen species, and ameliorate inflammation. Results are discussed in the context of reactive oxygen and nitrogen species, long-term potentiation, learning, aging and neuropathology, based on known impacts of the growth hormone axis on the brain, and characteristics of TGM.     

Transglutaminase 3 expression in C57BL／6J mouse embryo epidermis and the correlation with its differentiation

Epidermal-type transglutaminase 3 (TGM3) is involved in the cross-linking of structural proteins to form the cornified envelope in the epidermis. In the present study, we detected the expression of TGM3 in the mouse embryo using RT-PCR.TGM3 mRNA is weakly presented from E11.5 to E14.5 and increases significantly from E15.5 to birth. Then we determined the spatial and temporal expression pattern of TGM3 in the skin and other organs by in situ hybridization. We found a deprivation of TGM3 in skin at E11.5, while a rich supply in periderm cells and a weak expression in basal cells from E12.5 to E14.5. From the period of E15.5 to E16.5, after keratinization in the epidermis, TGM3 was expressed in the granular and cornified layers. The electron microscopic observation of the C57BL/6J mouse limb bud skin development provided several morphological evidences for the epidermal differentiation. The above findings suggest that the expression of TGM3 plays a important role in the epidermis differentiation in embryogenesis.