植物叶片吸滞PM_(2.5)等大气颗粒物定量研究方法初探——以毛白杨为例

以毛白杨为例,提出一种利用激光粒度仪和天平定量评估植物叶片吸滞细颗粒物(PM2.5,直径d≤2.5μm)等大气颗粒物能力的方法——洗脱称量粒度分析法(EWPA),实现了对植物叶片吸滞大气颗粒物质量和粒径分布的直接、准确测定,可操作性强.首先,进行预试验对试验方法的稳定性进行检验;其次,通过对叶片进行清洗、离心洗液、烘干等步骤收集其吸滞的颗粒物,然后对颗粒物称量,并采用激光粒度仪测定颗粒物的粒径分布;最后,利用叶面积和林分叶面积指数数据换算得到单位面积叶片和林分的各径级颗粒物吸滞量.在北京市奥林匹克森林公园内一片毛白杨林分(27 d未经历降雨)中应用该法,测得毛白杨叶片吸滞大气颗粒物的粒径均值为17.8μm,吸滞PM2.5、可吸入颗粒物(PM10,d≤10μm)和总悬浮颗粒物(TSP,d≤100μm)的体积百分比分别为13.7%、47.2%和99.9%;叶片的PM2.5、PM10、TSP和总颗粒物吸滞量分别为8.88×10-6、30.6×10-6、64.7×10-6和64.8×10-6g·cm-2;林分的PM2.5、PM10、TSP和总颗粒物吸滞量分别为0.963、3.32、7.01和7.02 kg·hm-2.     

基于超声清洗的树木叶面颗粒物粒径分布与吸滞效率研究——以银杏和油松为例

明确在常规叶片清洗方法(泡洗或泡洗+刷洗)上增加超声清洗对叶面各径级颗粒物滞纳量定量评估的影响,并在此基础上研究叶面颗粒物的粒径分布和吸滞效率,可进一步提高城市树木大气颗粒物吸滞能力的定量评估精度。该文以城市森林建设常用阔叶树种银杏(Ginkgo biloba)和针叶树种油松(Pinus tabuliformis)为研究对象,于雨后(降水量15 mm)4天(短滞尘时长)和14天(长滞尘时长)分别采集叶样,并依次对其进行泡洗(WC)、刷洗(BC)、超声清洗(UC)等洗脱程序,然后对每个清洗步骤下叶片洗脱液中颗粒物的质量和粒径分布进行测试,并依此估算叶片各径级颗粒物的吸滞效率。结果表明,以"泡洗+刷洗+超声清洗"清洗流程的测试结果为参照,若只对叶片进行泡洗,则银杏和油松对大气颗粒物(PM1,粒径d≤1μm)、PM2.5(d≤2.5μm)、PM5(d≤5μm)、PM10(d≤10μm)吸滞量会分别被低估约一半(54%、53%、53%和53%)和40%(42%、42%、42%和42%);若只进行"泡洗+刷洗",则银杏和油松对相应径级颗粒物的吸滞量仍会分别被低估约15%(17%、16%、15%和15%)和20%(21%、20%、20%和20%)。油松叶面颗粒物粒径分布呈双峰曲线,而银杏叶面颗粒物粒径则呈单峰分布,且银杏叶面颗粒物平均粒径在短、长滞尘时长下均大于油松。油松叶片对PM1、PM2.5、PM5、PM10和总悬浮颗粒物的吸滞效率分别为8.96、23.92、23.96、23.96和23.96 mg·m–2·d–1,分别比银杏叶片高112%、73%、34%、37%和42%。     

大气颗粒物对健康的影响

<正>近年来研究发现,大气颗粒物严重影响人体健康,PM2.5每年造成80万人死亡,排在所有致死因素的第13位[1].大气颗粒物是悬浮于空气中颗粒的总称,按照其空气动力学粒径分为总悬浮颗粒物(TSP空气动力学直径小于100μm,下同)、可吸入颗粒物(PM10)、细颗粒物(PM2.5)和超细颗粒物(PM0.1)[2].不     

北京常见阔叶绿化植物滞留PM2.5能力与叶面微结构的关系

叶片是植物滞留大气颗粒物的主要载体,对城市环境质量的改善发挥着巨大作用。该文用洗脱法测定了北京市20种常见阔叶绿化植物单位叶面积滞留总悬浮颗粒物(TSP)及PM2.5(颗粒直径≤2.5μm)的质量,并利用扫描电子显微镜观察了叶表面的微结构,分析比较了20种道路绿化植物叶片去除TSP与PM2.5的能力,以探讨典型植物叶表面微结构特征对大气颗粒物拦截效果的影响机理。结果显示:(1)不同植物单位叶面积滞留TSP和PM2.5的量均存在显著差异,变化范围分别为0.40~3.44g/m2和0.04~0.39g/m2。(2)叶表面沟槽宽度的不同可能是不同植物滞留TSP和PM2.5差异的主要原因,沟槽宽度过宽和过窄均不利于叶片捕集颗粒物,且颗粒物滞留量随沟槽深度增加而增大。(3)气孔密度较大的叶片表面颗粒物滞留量较大。研究表明,灌木与藤本植物单位叶面积对TSP和PM2.5的平均滞留量均大于乔木;叶表面沟槽宽度为5μm左右时对PM2.5滞留量较大;悬铃木(Platanus acerifolia)、木槿(Hibiscus syriacus)和大叶黄杨(Buxus sinica)单位叶面积滞留TSP与PM2.5量与其他供试植物相比均较大。     

PM_(2.5)致炎症作用及其机制研究进展

大气细颗粒物(PM2.5)能够深入下呼吸道,直达肺泡,并且能透过肺呼吸道屏障,进入循环系统,随血流而到达全身各靶器官,对其组织细胞造成伤害。除诱发呼吸系统疾病外,PM2.5还能致心血管疾病、糖尿病、恶性肿瘤等多种疾病的发生和发展。PM2.5致局部组织或系统的急性或慢性炎症、炎症细胞的浸润、炎症因子的异常表达与释放等,被认为是致人体健康损伤的重要机制。在综述PM2.5与炎症细胞的相互作用、炎症因子的表达与释放等致炎症效应新成果的基础上,概述了近年来人们对于PM2.5致炎症作用机制的新认识。     

大气细颗粒污染物 PM2.5 浓度及对肺上皮细胞炎性因子的影响

目的:研究大气细颗粒污染物(PM2.5)浓度及对肺上皮细胞(A549细胞)炎性因子的影响。方法:测定2013年1月至2013年12月北京市某城区PM2.5浓度,比较不同PM2.5浓度对A549细胞炎性因子IL-6、TNF-α表达水平的影响。结果:北京市细颗粒污染物PM2.5日均值春季、夏季、秋季、冬季分别为174.3μg/m3、143.5μg/m3、166.7μg/m3、189.6μg/m3,四季超标率差异无统计学意义(P>0.05);大气细颗粒污染物PM2.5对肺上皮细胞IL-6、TNF-α的影响,春季、夏季、秋季、冬季四季之间差异无统计学意义(P>0.05);随着PM2.5浓度升高IL-6、TNF-α表达水平升高,差异有统计学意义(P<0.05);随着染毒时间延长IL-6、TNF-α表达水平升高,差异有统计学意义(P<0.05)。结论:大气细颗粒污染物浓度升高会使肺上皮细胞炎性因子表达增强。     

春季典型天气下城市街头绿地内大气颗粒物浓度变化特征

以无锡市河埒口休闲广场街头绿地为对象,研究了典型天气条件(晴天、多云、雨后阴天)下绿地内4种粒径颗粒物(TSP、PM10、PM2.5和PM1)的质量浓度变化规律及其影响因素。结果表明:(1)绿地内TSP、PM10、PM2.5和PM1质量浓度日均值均为:晴天多云雨后阴天。雨后阴天的PM10、PM2.5和PM1浓度均极显著高于晴天和多云,多云天气的PM2.5和PM1浓度极显著高于晴天。多云和阴天天气下PM2.5和PM1质量浓度的增幅远高于TSP和PM10。(2)在观测时段内,晴天和多云4种粒径颗粒物的日变化曲线基本一致,上午浓度高于下午,7:00和13:00—15:00分别出现峰值和低谷;雨后阴天时,随时间推进颗粒物浓度呈递增趋势。晴天时小粒径颗粒物所占比例日变化与其浓度协同变化,多云和雨后阴天时则基本呈相悖状态。(3)3种天气条件下,街头绿地内仅晴天时PM2.5浓度达到国家二类功能区质量要求,其他均超出二级浓度限值。(4)晴天街头绿地内主要为粒径2.5~10μm的PM10污染,污染较轻;而多云和雨后阴天时TSP、PM10和PM2.5污染均较严重,TSP污染以粒径10μm的颗粒物为主,PM10以粒径2.5μm的为主,PM2.5主要为1~2.5μm范围内的颗粒物污染。(5)空气相对湿度是无锡高湿环境下影响颗粒物浓度的最主要因子。晴天,颗粒物浓度与风速、气温、光照强度呈显著负相关,与相对湿度、车流量呈显著正相关;多云天气大气颗粒物浓度与湿度呈显著正相关,与其他因素相关性均未达显著水平;雨后阴天时大气颗粒物浓度与湿度呈负相关,与其他指标相关性不显著。     

丹皮酚对PM2.5诱导的支气管上皮细胞IL-8表达的影响

目的:观察丹皮酚对PM2.5诱导支气管上皮细胞(BEAS-2B)分泌IL-8的影响。方法:BEAS-2B细胞传代培养,分别加入丹皮酚(15μmol/L、30μmol/L)预处理1 h,ELISA法检测不同浓度的PM2.5悬液(25μg/m L、50μg/m L、100μg/m L)对BEAS-2B细胞分泌IL-8蛋白的影响。结果:随着PM2.5悬液浓度的升高,BEAS-2B细胞上清液中IL-8水平逐渐增高;丹皮酚干预后能够显著降低BEAS-2B细胞上清液中IL-8水平(P0.05),并呈浓度依赖性。结论:丹皮酚具有抑制PM2.5诱导的BEAS-2B细胞分泌IL-8蛋白表达的作用,并呈浓度依赖性。     

可吸入颗粒物和细颗粒物基本特征、监测方法及森林调控功能

可吸入颗粒物(PM10)和细颗粒物(PM2.5)既是造成空气污染的主要原因之一,也是大部分城市的首要污染物.本文在分析PM10和PM2.5对环境和人类健康影响的基础上,重点综述了PM10和PM2.5组成、来源、质量浓度变化规律及影响因素;介绍了PM10和PM2.5监测网络布局、分析方法的原理和特点;归纳了个体和区域尺度上森林去除PM10和PM25的研究方法、速率和影响机制.探讨了目前该领域研究中存在的问题:由于缺乏不同梯度和背景地区大气PM10和PM2.5比较观测研究,未能揭示各类因素对PM10和PM2.5的复合影响;合理布局PM10和PM2.5监测网络、正确选择监测方法,并以手工方法所获数据作为比对和校验,是保证监测数据有效性的基础;有关森林去除PM2.5研究较少,未能在细胞、组织、器官和个体水平上阐明其去除PM10和PM2.5的生理过程和生态学机理.     

妊娠期PM2.5,暴露影响子代鼠主要脏器发育

目的探讨妊娠期大气细颗粒物PM2.5(颗粒直径≤2.5μm)暴露对子代鼠主要脏器发育的影响。方法孕鼠随机分为空白组、对照组、PM2.5低剂量组、PM2.5中剂量组、PM2.5高剂量组。利用气管滴注方法,建立小鼠妊娠期PM2.5暴露模型。通过HE染色和PAS反应,观察妊娠期暴露于PM2.5后新生子代鼠主要脏器的病理形态学改变,通过电子显微镜观察细胞超微结构变化。结果与空白组和对照组相比,PM2.5模型组新生子代鼠心、肝、脾、肺和肾组织结构均受损,可见炎症等病理改变。子代鼠主要脏器超微结构出现不同程度的细胞核周隙局部增宽、自噬体增多、线粒体嵴模糊和断裂等变化。结论妊娠期暴露于PM2.5可导致新生子代鼠心、肝、脾、肺、肾等主要脏器出现组织形态异常。这可能是PM2.5致生后远期慢性疾病发生的解剖学基础和发育源性病因。     

Reactive oxygen species in pulmonary inflammation by ambient particulates

Exposure to ambient air pollution particles (PM) has been associated with increased cardiopulmonary morbidity and mortality, particularly in individuals with pre-existing disease. Exacerbation of pulmonary inflammation in susceptible people (e.g., asthmatics, COPD patients) appears to be a central mechanism by which PM exert their toxicity. Health effects are seen most consistently with PM with aerodynamic diameter < 2.5 micrometers (PM(2.5)), although 10 micrometers < PM < 2.5 micrometers can also be toxic. Through its metal, semi-quinone, lipopolysaccaride, hydrocarbon, and ultrafine constituents, PM may exert oxidative stress on cells in the lung by presenting or by stimulating the cells to produce reactive oxygen (ROS). In vivo, PM increase cytokine and chemokine release, lung injury, and neutrophil influx. In vitro analysis of PM effects on the critical cellular targets, alveolar macrophages, epithelial cells, and neutrophils, demonstrates PM- and oxidant-dependent responses consistent with in vivo data. These effects have been observed with PM samples collected over years as well as concentrated PM(2.5) (CAPs) collected in real time. Oxidative stress mediated by ROS is an important mechanism of PM-induced lung inflammation.     

Involvement of nitro-compounds in the mutagenicity of urban Pm2.5 and Pm10 in Turin

Fine particles can be active carriers of toxic compounds into the alveoli of the lungs. Among these compounds are numerous mutagens and carcinogens. The direct mutagenicity per unit mass of fine particulate matter (PM) is significantly higher than that of coarse particles, especially in urban areas. In this study, the mutagenic properties of urban PM2.5 and PM10 were evaluated, and the role of nitro-compounds was estimated. PM2.5 and PM10 samplings, and measurements of NOx and some PAHs were performed daily in 2007 in Turin, following a consolidated in vitro test - the Salmonella mutagenicity assay - conducted with organic extracts of PM2.5 and PM10. The mutagenic properties were assessed for each month of sampling with Salmonella typhimurium strain TA98 and TA98-derived strains: a nitroreductase-deficient mutant strain (TA98NR) and an additional nitroreductase-producing plasmid strain (YG1021). The annual measured mean levels of PM2.5 and PM10 were 34±20 and 48±18μg/m(3). The PM2.5/PM10 ratio ranged from 0.36 to 0.89. The Salmonella assay showed higher mutagenicity in autumn/winter (20±15 TA98NR; 54±39 TA98; 173±161 YG1021 net revertants/m(3)) compared with spring/summer (2±2 TA98NR; 7±8 TA98; 24±27 YG1021 net revertants/m(3)) (p<0.01). There are also statistically significant seasonal differences in the gravimetric analysis data. The number of TA98 net revertants per μg of PM2.5 is 6.5 times greater than per μg PM10. Moreover, the bioassay results showed an amplified response in the YG1021 strain and a reduced response in the TA98NR strain. The net revertant ratio TA98NR/YG1021 is 11±4 for organic extracts of PM2.5 and 13±6 for extracts of PM10 (p<0.01). There is a significant correlation between the NOx and PAH concentrations. These findings illustrate the relevant role of nitro compounds, and they underline the priority in improving preventive measures to reduce air pollution by nitrated molecules.     

杭州市中心城区大气PM2.5暴露致大鼠肺部损伤作用研究

目的：探讨杭州市中心城区大气细颗粒物（PM2.5）对大鼠肺部的损伤及其对内质网应激通路的激活作用。方法：在杭州中心城区采用大容积空气颗粒物采样器将PM2.5颗粒采集于石英纤维滤膜上,将收集的PM2.5洗脱于超纯水中,再经真空冰冻干燥处理。将24只雄性SD大鼠随机分为3组：空白对照组,PM2.5低剂量组（5 mg/kg BW）和高剂量组（25 mg/kg BW）。采用气管滴注法进行染毒,每周1次,连续染毒4周。末次染毒24 h后麻醉动物,取左肺行HE染色,观察肺组织病理学改变。以化学比色法检测右肺肺泡灌洗液（BALF）中总抗氧化能力（T-AOC）含量、超氧化物歧化酶（SOD）活性和乳酸脱氢酶（LDH）活性,ELISA法测定BALF中肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）和白介素-6（interleukin-6,IL-6）水平。Western blot法检测肺组织中内质网应激标志物葡萄糖调节蛋白78（GRP78）表达、磷酸化蛋白激酶受体样内质网激酶（PERK）,磷酸化真核细胞翻译起始因子2α（eIF2α）,C/EBP同源蛋白（CHOP）,肌醇依赖酶1α（IRE1α）,X盒结合蛋白1（XBP1）蛋白的水平。结果：与空白对照组相比,低剂量和高剂量PM2.5染毒均能导致大鼠肺部出现明显的肺泡壁增厚、肺泡腔缩小、间质增生和炎细胞浸润,且随着染毒剂量增加组织损伤加重。PM2.5染毒组大鼠BALF中T-AOC含量和SOD活性呈剂量依赖性下降（P<0.05）;而BALF中的LDH活性则呈剂量依赖性上升（P<0.05）。PM2.5染毒导致大鼠肺部促炎因子TNF-α、IL-1β和IL-6的释放呈剂量依赖性增加（P<0.05）。高剂量PM2.5染毒组大鼠肺组织中GRP78、磷酸化PERK（p-PERK）、磷酸化eIF2α（p-eIF2α）、CHOP、IRE1α和剪切型X盒结合蛋白1（XBP1-S）表达显著升高,而未剪切型XBP1（XBP1-U）表达明显下降。结论：杭州市中心城区PM2.5染毒可引起大鼠肺部的炎性损伤,上述损伤可能与肺部氧化应激和内质网应激通路的激活相关。     

Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells

Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm² PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.     

亚热带常绿树种对不同粒径颗粒物的滞留能力

可吸入颗粒物和细颗粒物是大部分城市的首要污染物,对人体健康和环境都有重要影响;而城市植物能吸附大气颗粒物,进而有效降低大气颗粒物浓度。为了深入探究不同树种叶表面特征与自身滞尘效益之间的关系,该研究以浙江省三种常见城市绿化树种(青冈、冬青、红花檵木)为对象,采用重量法提取各样本在3个粒径上(8~100,2.5~8,0.45~2.5μm)的单位叶面积滞尘量(μg·cm~(-2)),并结合叶面积指数估测全株滞尘量。结果表明:三种供试植物叶片对颗粒物平均单位叶面积滞留量在30.4~63.7μg·cm~(-2)之间,而平均单木滞尘量每株在1.36-9.36 g之间。红花檵木因其叶表粗糙、具有绒毛等特征,对颗粒物(0.45~100μm)有最大的吸附能力(63.74±12.0μg·cm~(-2));对于大颗粒物(8~100μm)和细颗粒物(0.45~2.5μm),三种植物叶片均对其分别具有最大(40.9%~57.5%)、最小(15.6%~20.6%)的吸附能力;对于单木滞尘量,青冈因其具有较大叶面积指数等特征,对颗粒物总吸附效果更佳(每株9.36g)。该研究结果表明城市绿化树种对减缓大气颗粒物污染起到重要作用。     

Particulate matter,PM 10 & PM 2.5 levels,and airborne mutagenicity in Chiang Mai,Thailand

Daily levels of particulate matter (PM) in the ambient air (PM 2.5 and PM 10) were measured in a northern city of Thailand (Chiang Mai) from March 1998 to October 1999. Twenty-four-hour air particulate matter samples were collected each day with Airmetric Minivol portable air samplers. Monthly averages of PM 2.5 from four stations in Chiang Mai varied from 15.39 to 138.31microg/m(3) and 27.29 to 173.40 microg/m(3) for PM 10. The PM 2.5 annual average was 58.48 mg/m(3) and PM 10, 86.38 microg/m(3). Daily PM 2.5 (24h values) during the winter months in Chiang Mai frequently exceeded 200-300 microg/m(3). The maximum concentrations of PM 2.5 (24h average) in Chiang Mai air from December 1998 to April 1999 were 2.8-, 3.5-, 4.2-, 6.5- and 3.2-fold higher than the US Environmental Protection Agency (US EPA), PM 2.5, 24h standard of 65 microg/m(3). From May to October, the mean 24h levels of PM 2.5 and PM 10 were at acceptable levels. The data shows that during the winter season (December to March), levels of PM 2.5 and PM 10 in the Chiang Mai atmosphere are very high, and there may be significant health implications associated with these high concentrations. During the summer season, the fine particles were generally within the acceptable levels. To our knowledge, these are the first measurements of PM 2.5 to be reported for the city of Chiang Mai and they indicate considerable ambient fine particle exposures to the Chiang Mai population. In addition, dichloromethane extracts of airborne particulate matter PM 2.5 or PM 10 collected in the months of winter in the city of Chiang Mai were mutagenic to Salmonella typhimurium strain TA100 without metabolic activation. The mutagenicity appeared to track particle concentrations and increased in the presence of S9 mix.     

Peimine inhibits the growth and motility of prostate cancer cells and induces apoptosis by disruption of intracellular calcium homeostasis through Ca2+/CaMKII/JNK pathway

Prostate cancer (PC) is one of the most common malignant tumors in man. Peimine (PM) is a bioactive substance isolated from Fritillaria. Previous studies have shown that PM could inhibit the occurrence of a variety of cancers. However, the roles of PM in PC and its related mechanism have not been elucidated. Calcium (Ca²⁺) is an important intracellular messenger involved in a variety of cell processes. In this study, we found that the appropriate doses of PM (2.5, 5, and 10 μM) significantly inhibited the growth of PC cells (DU-145, LNCap, and PC-3), but has no significant effect on normal prostate cells (RWPE-1). In addition, PM treatment inhibited the invasion and migration of PC-3 cells and blocked the epithelial-mesenchymal transition process. These effects were exhibited a dose-dependent manner. Furthermore, the current results also showed that PM treatment significantly increased the Ca²⁺ concentration, the increased Ca²⁺ promoted the phosphorylation of Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK), further inhibited the growth and invasion of PC-3 cells, and induced its apoptosis. Ca²⁺ chelator BAPTA-AM (1 μM) could counteract the increase of intracellular Ca²⁺ concentration. Similarly, JNK pathway inhibitor SP600125 (10 μM) also inhibited cell growth and invasion and induced apoptosis. In addition, experiments in nude mice showed that PM inhibited tumor formation through Ca²⁺/CaMKII/JNK signaling pathway. In conclusion, our results show that PM inhibits the growth and motility of prostate cancer cells and induces apoptosis by disruption of intracellular calcium homeostasis through Ca²⁺/CaMKII/JNK pathway.     

Flavone protects HBE cells from DNA double-strand breaks caused by PM2.5

Ambient air particulate matter 2.5 (PM2.5) contains many harmful components that can enter the circulatory system and produce reactive oxygen species (ROS) in body. Oxidative stress and DNA damage induced by ROS may affect any cellular macromolecule and lead to DNA double-strand breaks (DSBs). Flavonoids, widely distributed in some herbs and berries, have been proved having anti-oxidative or anti-cancer efficacy. In this study, we investigated whether Flavone, a kind of flavonoids, can protect human bronchial epithelial cells (HBE) from DSBs caused by PM2.5 and how this function is probably implemented. We found that cells exposed to PM2.5 obviously induced viability inhibition, DNA damage and part of apoptosis. However, Flavone treatment prior to PM2.5 apparently improved cell viability, and mitigated the formation of 8-hydroxy-2-deoxyguanosine, the expression of DNA damage-relative protein and cell apoptosis. Our studies demonstrated that PM2.5 induced oxidative DSBs while Flavone ameliorated the DNA damage and increased cell viability probably through influencing DNA repair mechanism of cells.     

外源绿原酸缓解黑大豆SB铝毒害的机理研究

该文研究了外源绿原酸(CGA)对Al胁迫下铝敏感型黑大豆SB根生理生化指标以及根中胁迫相关基因表达的变化,探讨外源CGA缓解SB根铝毒害的效果及分子机理。以不同浓度Al和CGA处理SB,筛选出CGA缓解Al毒害的最佳浓度,测定Al含量、抗氧化系统酶活性、14-3-3蛋白与H~+-ATP酶的表达、H~+泵活性。结果表明:低浓度CGA能缓解Al胁迫下黑大豆SB根伸长抑制,并促进侧根数目增加,而高浓度CGA的缓解效果下降;0.01 g·L~(-1) CGA使Al胁迫下SB根尖Al含量与MDA含量下降,促进根系柠檬酸的分泌。RTPCR和Western Bloting分析表明0.01 g·L~(-1) CGA促进Al胁迫下SB根中14-3-3b、14-3-3m、14-3-3k和GHA2基因(质膜H~+-ATP酶)的表达,抑制MATE基因的表达。同时,0.01 g·L~(-1) CGA能促进Al胁迫下质膜H~+-ATP酶蛋白磷酸化水平以及其与14-3-3蛋白结合,且能提高质膜H~+-ATP酶和H~+泵活性。因此推测外源CGA可能通过增加侧根数,增强14-3-3蛋白和质膜H~+-ATP酶基因蛋白表达水平和互作,弥补Al胁迫下MATE表达的抑制,增加柠檬酸的分泌,增强SB对铝毒害的耐受性。