辣椒对镉胁迫的生理响应

以福湘5号、兴蔬215和川腾1号这3个辣椒品种为材料,用含有0mg/L、100mg/L、200mg/L、300mg/L重金属镉的1/2霍格兰培养液对具10片真叶的辣椒苗进行处理,7d后测定各项生理指标。结果表明,镉对辣椒的生长有很强的毒害作用,随着镉胁迫浓度的升高,3个辣椒品种的生物量、叶片叶绿素含量、电导率、丙二醛含量和活性氧清除系统酶活性都受到了不同程度的影响。在镉胁迫下,辣椒植株的株高、根长、鲜重受到明显抑制,根系发育畸形,叶片黄化。镉胁迫的毒害作用在3个辣椒品种间有差异。其中川腾1号耐镉胁迫能力较强,福湘5号次之,兴蔬215最差。     

镉胁迫对西瓜幼苗生长及其叶片解剖结构和生理特性的影响

该研究以‘北抗1号’西瓜幼苗为试验材料,采用实验室盆栽方法,考察在不同浓度镉胁迫(0、60、120、180和240 mg/L)处理下西瓜幼苗的生长及其叶片生理特性和解剖结构的变化特征,初步探讨西瓜耐受镉胁迫的生理机制。结果显示：(1)在镉胁迫条件下,西瓜幼苗的生长受到抑制,随着镉胁迫浓度的增加,西瓜幼苗的叶片形态黄化现象逐渐加重,根系形态逐渐纤弱,株高、茎粗、茎节数和叶片数均呈现下降趋势。(2)镉胁迫下,西瓜幼苗叶片主脉中细胞受损,主脉直径显著减小,叶肉组织疏密度显著降低。(3)随着镉胁迫浓度的升高,西瓜幼苗的含水量、净光合速率、SOD活性等显著降低,丙二醛和游离脯氨酸含量显著升高,POD活性和可溶性蛋白含量先升高后降低,生理特性受到显著影响。研究发现,‘北抗1号’西瓜幼苗对镉有一定的适应性,在低浓度(60 mg/L)镉胁迫处理下,西瓜幼苗的形态特征、生理特性变化不显著,但在高浓度(180 mg/L)镉胁迫下,幼苗的生长受到严重抑制,渗透调节系统以及生物膜保护系统严重受损。     

镉胁迫对烟草根抗氧化能力和激素含量的影响

采用水培试验,研究了镉胁迫对烟草(Nicotiana tabacum)根内的超氧阴离子含量、可溶性蛋白质含量、抗氧化系统SOD、POD、CAT、APX、GR活性、膜质过氧化水平及激素IAA、ABA、GA3、ZR含量的影响。结果显示烟草根中的超氧阴离子含量随着镉浓度增大而升高;镉浓度为5mg/L时,可溶性蛋白质含量增加,但随着镉浓度增加,可溶性蛋白质含量急剧下降;SOD、CAT、APX活性在镉浓度为5mg/L时上升,但随着镉浓度升高其活性下降;POD,GR活性在镉浓度为5-25mg/L时上升,在镉浓度为50mg/L时下降,但仍高于对照;MDA含量随着镉浓度增加而升高;IAA氧化酶活性在镉浓度5mg/L时下降,但随着镉浓度的升高而降低;IAA含量在镉浓度为5mg/L时上升,但随着镉浓度增加,IAA氧化酶活性升高,导致IAA含量逐渐下降;镉胁迫对烟草根中ABA合成表现为促进作用;GA3含量在镉浓度为5mg/L时上升,但随着镉浓度的增加其含量逐渐下降;ZR含量在镉胁迫下迅速减少。     

镉对一株深色有隔内生真菌生长、矿质营养与草酸分泌的影响

【背景】深色有隔内生真菌(dark septate endophyte,DSE)广泛定殖于镉(Cd)污染生境的植物根系,具有增强植物镉耐性的重要生态功能,但人们关于DSE对镉胁迫的生理响应的了解有限。【目的】研究一株DSE嗜鱼外瓶霉(Exophiala pisciphila)对镉胁迫的矿质营养与低分子量有机酸分泌的响应。【方法】采用液体培养法,研究不同浓度(0、25、50、100、200、400 mg/L)镉胁迫对DSE菌丝生长、矿质元素(氮、磷、钾、硫、镁、铁、钙)与镉含量、草酸分泌的影响。【结果】随着镉胁迫浓度增加,菌丝生物量显著下降,降幅为22.8%−90.6%,菌丝的氮、钾和铁含量分别减少26.0%−52.8%、53.8%−92.9%和12.8%−34.3%,而磷、镁和钙含量分别增加15.4%−111.4%、20.4%−31.4%和35.1%−62.5%,硫含量在100 mg/L镉胁迫时增加25.1%。镉胁迫还导致培养液pH值下降,草酸浓度及单位菌丝草酸分泌量显著增加。相关分析发现,菌丝镉含量与硫呈显著负相关(P<0.05),与菌丝钾含量呈极显著负相关(P<0.01),与草酸分泌量呈极显著正相关(P<0.01)。【结论】镉胁迫显著抑制DSE的生长,改变矿质元素的吸收,促进草酸分泌。     

干旱胁迫下镉处理对互叶醉鱼草幼苗生长、镉积累及光合生理的影响

为探究干旱条件下,互叶醉鱼草(Buddleja alternifolia Maxim.)幼苗对重金属镉胁迫的生长及光合生理响应机制,以两年生互叶醉鱼草幼苗为试验材料,设置对照与干旱两个水分处理组(土壤相对含水率分别为:65%—60%,35%—30%),每个水分处理条件下再分别设置3个镉处理浓度(0.28、(0.6+0.28)、(1.2+0.28)mg/kg),共6个处理。测定不同水分及镉处理对互叶醉鱼草生长、生物量、光合参数及体内重金属含量的影响。结果表明:干旱与镉复合胁迫下植物的存活率为100%。镉胁迫、干旱与镉复合胁迫均不同程度抑制了互叶醉鱼草幼苗生长、生物量积累、植株的光合作用及叶绿素含量,且其光合和叶绿素含量的降幅明显大于单一镉胁迫。镉胁迫下,互叶醉鱼草幼苗单株最高镉富集量为69.33 mg/kg,而复合胁迫下单株最高镉富集量为50.68 mg/kg。以上结果表明:干旱胁迫能够加重镉胁迫对植物的影响,使复合胁迫下互叶醉鱼草生长、光合生理及镉富集能力下降。但单一镉胁迫下,互叶醉鱼草对镉具有更强的耐受性,并有较高的生物富集能力,且干旱与Cd复合胁迫下互叶醉鱼草幼苗仍有一定的镉积累量。因此在干旱半干旱区园林绿化以及Cd污染地区的生态建设中,互叶醉鱼草是一种具有巨大应用潜力和前景的灌木树种。     

镉胁迫对烟草叶激素水平、光合特性、荧光特性的影响

采用不同浓度镉胁迫（0mg/L、5mg/L、25mg/L、50mg/L）的水培试验,分别用感应耦合等离子体、紫外分光光度计、酶联免疫法、光合作用仪、叶绿素荧光分析仪研究了镉胁迫3d对烟草(Nicotiana tabacum L.)叶内镉含量、IAAO活性、激素（IAA、ABA、GA3、Z）水平、光合特性及荧光特性的影响。结果显示烟草叶内镉含量随着胁迫浓度增加而显著增加;IAAO活性在镉为5mg/L时下降,然后随着镉浓度增加而显著上升;IAA含量在镉为5mg/L时上升,但随着镉浓度增加而显著下降;ABA含量随着镉浓度上升而增加;GA3含量在5mg/L时上升,然后随着镉浓度增加而显著下降;Z含量随着镉浓度增加而显著下降;叶绿素a、叶绿素b和类胡萝卜素含量均随镉胁迫浓度增大而显著减少;光合参数（Pn、Gs、Ci、Tr）及荧光参数（ Fv/ Fo、Fv/Fm、ФPSⅡ、qP）均随镉胁迫浓度增大而下降。     

重金属镉胁迫对白纹伊蚊幼虫海藻糖代谢的影响

【目的】深入了解镉对白纹伊蚊Aedes albopictus的毒害作用机理和白纹伊蚊对极端环境的适应机制,揭示重金属胁迫对白纹伊蚊种群发生、疾病传播等可能存在的影响,为卫生害虫防控等提供参考依据。【方法】分别用200 mL配制好的50, 100, 200, 300和400 mg/L镉溶液对放置于320 mL一次性杯中长势一致的白纹伊蚊3龄末至4龄初幼虫急性染毒12 h,以双蒸水养殖幼虫作为对照。通过生化方法测定处理后12 h白纹伊蚊幼虫体内海藻糖、葡萄糖和总糖原含量以及可溶性海藻糖酶(TRE1)和膜结合型海藻糖酶(TRE2)活力,并采用qRT PCR测定这些幼虫体内海藻糖合成酶基因(TPS), TRE1和TRE2表达量。【结果】在200和300 mg/L重金属镉处理12 h时白纹伊蚊幼虫海藻糖含量显著增加,在高镉浓度(300和400mg/L)处理时葡萄糖含量显著下降,而不同镉浓度急性处理对总糖原含量没有影响。TRE1和TRE2活力在高镉浓度(300和400 mg/L)处理时显著下降。300 mg/L镉处理组TPS相对表达量达到最高值,TRE1和TRE2相对表达量在高镉浓度(300和400 mg/L)处理时显著下降,与酶活力变化趋势表现一致。【结论】当镉浓度低于半致死浓度(217 mg/L)时,镉急性胁迫使白纹伊蚊幼虫TPS基因表达上调,而TRE基因则表达量下降,TRE活力降低,从而促使葡萄糖转化为海藻糖,通过海藻糖的积累来应对镉胁迫压力。这些结果说明海藻糖在白纹伊蚊在重金属应激中起一定作用,白纹伊蚊幼虫可以通过合成海藻糖从而提高应对镉胁迫的抗逆能力。     

外源脱落酸对小麦幼苗抗镉胁迫能力的影响

以小麦(Triticum aestivum L.)为试材,采用水培法研究了100mg/L镉(Cd2+)胁迫条件下施用外源脱落酸(ABA)对小麦幼苗生长及某些生理生化指标的影响。结果表明:(1)100mg/L Cd2+胁迫下,小麦叶片膜脂过氧化产物丙二醛(MDA)含量显著提高,植株生长受到抑制;(2)外源ABA能够明显提高Cd2+胁迫小麦幼苗的根系活力,增加其叶片SOD、CAT和POD活性,促进其脯氨酸积累,降低MDA的含量,并以5.0μmol/L ABA的效果最明显;(3)1.0～5.0μmol/L外源ABA不同程度地缓解Cd2+胁迫对小麦幼苗生长的抑制作用,且5.0μmol/L时效果最明显,其株高、根长、总干重分别比单一Cd2+胁迫处理显著提高6.73%、149%和10.52%,而10.0μmol/LABA反而加重了Cd2+对小麦幼苗生长的伤害。因此,适宜浓度的外源ABA能够通过增加体内保护酶活性和脯氨酸含量来缓解Cd2+胁迫对小麦幼苗生长的抑制作用,增强小麦幼苗的抗Cd2+胁迫能力,并以5.0μmol/L ABA处理效果最好。     

镉胁迫对小报春幼苗生长及生理特性的影响

该研究采用盆栽控制试验,测定不同浓度(0、5、50、100、150、200 mg/kg)土壤Cd胁迫下小报春幼苗生长及生理生化指标,以探究小报春(Primula forbesii Franch.)对重金属镉(Cd)污染的抗性和敏感性,为新型香花地被植物应用于Cd污染土壤提供理论依据。结果表明:(1)低浓度(5 mg/kg)Cd胁迫能促进小报春株高和根长的伸长,高浓度(≥150 mg/kg)Cd胁迫下株高、根长和生物量明显降低。(2)随Cd胁迫浓度增加,小报春幼苗叶片光合作用、叶绿素含量、SOD和CAT活性先上升后下降,而其超氧阴离子产生速率、过氧化氢、丙二醛含量、叶相对电导率和POD活性持续升高。(3)在Cd胁迫条件下,小报春体内K、Zn含量降低,叶和根中Ca、Mg含量显著增加,体内Cd含量明显升高,且根系Cd含量远远高于叶和叶柄。研究发现,小报春幼苗对Cd胁迫具有一定的耐性,低浓度(5 mg/kg)Cd胁迫对小报春生长影响较小,但高浓度(≥150 mg/kg)Cd胁迫对小报春产生明显的毒害作用,影响其正常生长;小报春可能通过增强体内抗氧化酶系统活性、增加叶和根中Ca、Mg含量和根系截留镉来减轻镉胁迫的伤害,提高自身耐受镉胁迫能力。     

日本引进芸薹属白菜型种质资源耐镉性评价鉴定

为了丰富我国芸薹属资源中低镉资源的多样性,本研究对日本引进的79份白菜型资源在幼苗期进行较高(30 mg/L)和中度(10 mg/L)的镉胁迫处理,从而对其开展耐镉性和镉积累特性研究,相较于传统采用镉污染的土壤进行培养的方法,具有省时、省力、稳定性高等优点。结果显示,79份资源的耐镉性变异丰富,较高(30 mg/L)和中度(10 mg/L)的镉胁迫处理下筛选到稳定耐镉和镉敏感的材料各3份。镉积累特性分析发现,稳定耐镉材料地上部和胚根的Cd含量均显著低于镉敏感材料,并且D069胚根和地上部的镉含量都显著低于其他材料,D125的迁移系数相对较低,具有较高的育种利用价值。本研究筛选得到的D069和D125两份耐镉和低积累资源丰富了国内芸薹属资源中低积累镉的基因库,将极大促进芸薹属污染安全新品种培育进程,可有效推动镉污染农田的安全利用效率。     

Cadmium carcinogenesis

Cadmium is a heavy metal of considerable environmental and occupational concern. Cadmium compounds are classified as human carcinogens by several regulatory agencies. The most convincing data that cadmium is carcinogenic in humans comes from studies indicating occupational cadmium exposure is associated with lung cancer. Cadmium exposure has also been linked to human prostate and renal cancer, although this linkage is weaker than for lung cancer. Other target sites of cadmium carcinogenesis in humans, such as liver, pancreas and stomach, are considered equivocal. In animals, cadmium effectively induces cancers at multiple sites and by various routes. Cadmium inhalation in rats induces pulmonary adenocarcinomas, in accord with its role in human lung cancer. Cadmium can induce tumors and/or preneoplastic lesions within the rat prostate after ingestion or injection. At relatively high doses, cadmium induces benign testicular tumors in rats, but these appear to be due to early toxic lesions and loss of testicular function, rather than from a specific carcinogenic effect of cadmium. Like many other metals, cadmium salts will induce mesenchymal tumors at the site of subcutaneous (s.c.) or intramuscular (i.m.) injections, but the human relevance of these is dubious. Other targets of cadmium in rodents include the liver, adrenal, pancreas, pituitary, and hematopoietic system. With the exception of testicular tumors in rodents, the mechanisms of cadmium carcinogenesis are poorly defined. Cadmium can cause any number of molecular lesions that would be relevant to oncogenesis in various cellular model systems. Most studies indicate cadmium is poorly mutagenic and probably acts through indirect or epigenetic mechanisms, potentially including aberrant activation of oncogenes and suppression of apoptosis.     

Cadmium bioavailability

Cadmium slowly accumulates in the liver and kidney and has a long biological half-life, estimated to be 2-3 decades in the kidney. If the kidney cadmium concentration reaches a critically high level, proximal tubular damage results, which can be followed by severe bone mineral loss. There are only a few measurements of cadmium bioavailability in foods; however, the data are indicative of lower utilization from foods than from inorganic salts. In animal tissues cadmium is bound primarily to a heat-resistant small protein with a high cysteine content (metallothionein), whereas little is known about the form in which cadmium occurs in the edible parts of plants. Low intakes of many nutrients exacerbate the effects of cadmium and supplemental intakes are protective. Newborn and young animals absorb much higher quantities of cadmium than adults. There is some evidence in animals that females may be more adversely affected than males. Itai-itai disease, a painful disease with kidney damage and bone demineralization, occurred in elderly Japanese women who had borne several children and who were exposed to cadmium via food and drinking water. Inasmuch as cadmium in the U.S. food supply affords an estimated safety factor of only 4- to 15-fold, it is important to establish factors that affect the bioavailability of cadmium from foods.     

Cadmium and mitochondria

The heavy metal cadmium (Cd) a pollutant associated with several modern industrial processes, is absorbed in significant quantities from cigarette smoke, water, food and air contaminations.It is known to have numerous undesirable effects on health in both experimental animals and humans, targeting kidney, liver and vascular system.The molecular mechanism accounting for most of the biological effects of Cd are not well-understood and the toxicity targets are largely unidentified.The present review focuses on important recent advances about the effects of cadmium on mitochondria of mammalian cells.Mitochondria are the proverbial powerhouses of the cell, running the fundamental biochemical processes that produce energy from nutrients using oxygen. They are among the key intracellular targets for different stressors including Cd.This review provides new additional informations on the cellular and molecular aspects of the interaction between Cd and cells, emphasizing alterations of mitochondria as important events in Cd cytotoxicity, thus representing an important basis for understanding the mechanisms of cadmium effect on the cells.     

木槿品种对镉胁迫的生理响应及耐镉能力评价

研究镉胁迫对木槿的生理影响,比较木槿品种的镉耐受能力,为镉污染地区的植物材料选择提供依据.以3个木槿品种为材料,采取盆栽控制试验,测定其生长、生理指标,通过隶属函数分析综合比较品种耐镉能力.木槿的株高与地径增长量、叶绿素A+B与可溶性蛋白含量随胁迫浓度增加呈先上升后降低或逐渐降低趋势,而且随时间延长,降低程度不断加强;...     

南瓜对镉的吸收积累特性研究

对南瓜进行盆栽试验,通过加入不同含量的镉、CaCO₃和草炭土,研究南瓜对镉的吸收积累特性,利用火焰原子吸收法测定。结果表明,南瓜植株对镉的富集量主要集中在茎、根中;当土壤镉含量小于5mg·kg^-1时,对南瓜根的生长有促进作用,当土壤镉含量大于5mg·kg^-1时,开始对根的生长产生抑制作用,抑制作用随镉含量的增大而加强;在土壤中施CaCO₃,能降低南瓜对镉的吸收;在土壤中加入草炭土,在一定范围内,它能促进南瓜对镉的吸收。     

Cadmium carcinogenesis in review

Cadmium is an inorganic toxicant of great environmental and occupational concern which was classified as a human carcinogen in 1993. Occupational cadmium exposure is associated with lung cancer in humans. Cadmium exposure has also, on occasion, been linked to human prostate cancer. The epidemiological data linking cadmium and pulmonary cancer are much stronger than for prostatic cancer. Other target sites for cadmium carcinogenesis in humans (liver, kidney, stomach) are considered equivocal. In rodents, cadmium causes tumors at several sites and by various routes. Cadmium inhalation in rats results in pulmonary adenocarcinomas, supporting a role in human lung cancer. Prostate tumors and preneoplastic proliferative lesions can be induced in rats after cadmium ingestion or injection. Prostatic carcinogenesis in rats occurs only at cadmium doses below those that induce chronic degeneration and dysfunction of the testes, a well-known effect of cadmium, confirming the androgen dependency of prostate tumors. Other targets of cadmium in rodents include the testes, adrenals, injection sites, and hematopoietic system. Various treatments can modify cadmium carcinogenesis including supplemental zinc, which prevents cadmium-induced injection site and testicular tumors while facilitating prostatic tumors. Cadmium is poorly mutagenic and probably acts through indirect mechanisms, although the precise mechanisms remain unknown.