锰对植物毒害及植物耐锰机理研究进展

含锰矿渣的排放造成了严重的土壤锰污染。揭示锰毒害和植物的耐锰机制对于污染土壤治理具有重要意义。研究表明,高浓度的Mn2＋能够抑制根系Ca2＋、Fe2＋和Mg2＋等元素的吸收及活性,引起氧化性胁迫导致氧化损伤,使叶绿素和Rubisco含量下降、叶绿体超微结构破坏和光合速率降低。而锰超累积植物则具有多种解毒或耐性机制,如区域化、有机酸螯合、外排作用、抗氧化作用和离子交互作用等。根系主要通过有机酸的螯合作用促进植物对Mn^2＋的转运解毒,同时能够将过量的Mn^2＋区域化在根细胞壁中;叶片可通过酚类物质或有机酸螯合Mn^2＋,并将其区域化在叶片表皮细胞和叶肉细胞的液泡中（或通过表皮毛将Mn^2＋排出体外）。其中,金属转运蛋白在植物对Mn^2＋的吸收、转运、累积和解毒过程中发挥着重要作用。     

植物对重金属镉的耐受机制

镉离子（Cd^2＋）具有强植物毒性,抑制植物生长,甚至使植物死亡。由于长期的环境选择和适应进化,植物发展出耐受机制,可减轻或避免Cd^2＋的毒害。硫转运蛋白、硫还原相关酶类以及半胱氨酸、谷胱甘肽和植物螯合肽合成基因的表达受Cd^2＋调控。同时这些基因的过表达也能提高植物对Cd^2＋的耐性。植物抗氧化系统对Cd^2＋胁迫诱发的活性氧的清除作用,具转运Cd^2＋活性的质膜转运蛋白促进Cd^2＋经共质体途径向木质部运输、装载,而后随蒸腾流向地上部迁移,具转运Cd^2＋活性的液泡膜转运蛋白促进Cd^2＋进入液泡的隔离作用,都在植物对Cd^2＋的耐性中起作用。     

铝减轻过量锰对大豆生长的不利影响

以大豆为材料,研究了铝（Al）对过量锰（Mn）胁迫下大豆生理生化状况的影响。结果表明：Al抑制了植物对Mn的吸收运输,降低了Mn在地上部的积累,减轻了高Mn对大豆地上部生长的抑制程度、改善了叶片叶绿素含量降低的现象并降低了高Mn诱导产生的氧化胁迫伤害程度;此外,Al主要降低了叶片细胞壁和细胞器中Mn的含量,而对细胞可溶性组分中Mn含量没有影响。     

植物ABC和MATE转运蛋白与次生代谢物跨膜转运

植物产生大量的次生代谢物,不但对植物自身适应性具有极其重要的作用,而且有着巨大的实用价值。次生代谢物的跨膜转运是植物次生代谢工程研究的一个新兴领域。ABC（ATP-binding cassette）和MATE（multidrug and toxin extrusion）转运蛋白与生物体内多种物质的跨膜转运有关,在植物次生代谢物的运输过程中均发挥着重要作用。文章主要综述了ABC和MATE转运蛋白在植物次生代谢物跨膜转运中的研究进展。     

金属离子胁迫产生植物膜脂过氧化的能力与离子的极化能力正相关

金属离子胁迫导致植物产生多种生理损伤,其中包括膜脂的过氧化。不同的金属离子诱导植物产生膜脂过氧化差异很大,迄今对这些差异与金属离子性质之间的具体关系所知甚少。金属离子对阴离子和其他分子的作用主要取决于其电荷数量、半径大小和电子层结构,亦即取决于其极化作用。作者以水培拟南芥与油菜为材料,以不同极化作用的金属离子（Li^＋、Na^＋、K^＋、ca^2＋、Fe^2＋与Fe^3＋）为研究对象,检测了极化作用不同的金属离子胁迫拟南芥与油菜1、3、5 d后膜脂过氧化产物丙二醛（Malondialdehyde,MDA）的含量变化。结果发现,相同浓度的一价离子Li^＋、Na^＋与K^＋’胁迫5 d后,离子半径较小的Li^＋诱导拟南芥与油菜产生的丙二醛比Na^＋与K^＋高2倍以上;相同浓度下电子层结构相同的Fe^3＋与Fe^2＋胁迫5 d后,电荷高的Fe^3＋诱导拟南芥产生的丙二醛比Fe^2＋高2倍以上,而Fe^3＋诱导油菜产生的丙二醛比Fe^2＋高5倍以上;相同浓度的二离子Fe^2＋与ca^2＋胁迫,电子层结构复杂的Fe^2＋比ca^2＋诱导更多的丙二醛产生。运用离子势综合表征离子极化能力,则丙二醛的含量与离子势大小显著正相关。上述结果说明,金属离子诱导膜脂过氧化的胁迫能力与金属极化作用正相关,即电荷越高、离子半径越小及电子层越复杂,产生氧化胁迫程度越强。     

质膜转运蛋白及其与植物耐盐性关系研究进展

植物细胞质膜有两种主要功能：⑴溶质运输（进出细胞）,溶质运输主要由转运蛋白完成;⑵信号传导,即接收信号并引发细胞生理生化响应。盐分过多对植物的伤害主要是离子毒害。质膜转运蛋白活性环境变化能做现迅速响应。本文简要叙述了植物细胞质膜转运蛋白类型、分子特性、生理功能及其活性调节。介绍了植物细胞质膜Ｈ＾＋－ＡＴＰａｓｅ、质膜氧化还原系统、质膜离子载体和离子通道对盐胁迫的响应及其这些响应与植物耐盐性之间的关     

液泡膜转运蛋白在植物细胞代谢中的作用

液泡是植物细胞的一个多功能细胞器,其主要通过膜运输系统执行功能。液泡膜转运蛋白可以控制细胞内物质的储存和运输,参与细胞内的应答胁迫反应,隔离毒性离子,防止细胞质受害,调节Ca^2＋浓度和pH,维持细胞内环境的稳定。本文主要对液泡膜转运蛋白在营养储存、逆境胁迫、细胞内环境稳态中发挥的作用进行综述,以期为进一步阐释液泡复杂生理功能提供一些借鉴。     

植物抗旱和耐重金属基因工程研究进展

干旱和重金属污染严重影响植物的生长发育.植物耐逆相关基因的克隆和功能鉴定研究,为通过基因工程途径提高植物的抗逆性奠定了理论基础.水分亏缺、高盐、低温和重金属胁迫都能诱导LEA(late embryogenesis abundant protein)基因的表达.转基因研究表明,LEA蛋白具有抗旱保护作用、离子结合特性以及抗氧化活性;水孔蛋白存在于细胞膜和液泡膜上,在细胞乃至整个植物体水分吸收和运输过程中发挥重要作用.干旱和盐胁迫促进水孔蛋白基因转录物的积累.过量表达水孔蛋白可增强水分吸收和运输,提高植物的抗旱能力.金属转运蛋白参与重金属离子的吸收、运输和累积等过程.这些蛋白基因在改良草坪草植物的抗旱节水和耐重金属能力等方面具有潜在的应用价值.     

锰对植物毒害及植物耐锰机理研究进展

含锰矿渣的排放造成了严重的土壤锰污染。揭示锰毒害和植物的耐锰机制对于污染土壤治理具有重要意义。研究表明, 高浓度的Mn²⁺能够抑制根系Ca²⁺、Fe²⁺和Mg²⁺等元素的吸收及活性, 引起氧化性胁迫导致氧化损伤, 使叶绿素和Rubisco含量下降、叶绿体超微结构破坏和光合速率降低。而锰超累积植物则具有多种解毒或耐性机制, 如区域化、有机酸螯合、外排作用、抗氧化作用和离子交互作用等。根系主要通过有机酸的螯合作用促进植物对Mn²⁺的转运解毒, 同时能够将过量的Mn²⁺区域化在根细胞壁中; 叶片可通过酚类物质或有机酸螯合Mn²⁺, 并将其区域化在叶片表皮细胞和叶肉细胞的液泡中(或通过表皮毛将Mn²⁺排出体外)。其中, 金属转运蛋白在植物对Mn²⁺的吸收、转运、累积和解毒过程中发挥着重要作用。     

脱落酸与植物细胞的抗氧化防护

水分胁迫是一种影响植物生长发育、限制植物产量的重要胁迫因子。植物能够通过感知刺激、产生和传导信号、启动各种防护机制来响应与适应水分胁迫。植物激素脱落酸(ABA)作为一种胁迫信号,在调节植物对水分胁迫的反应中起着重要的作用。ABA不仅能诱导气孔关闭,而且能诱导编码耐脱水蛋白的基因表达。正在增加的证据显示,ABA增强水分胁迫的耐性与其诱导抗氧化防护系统有关。本文综述了ABA在诱导活性氧(ROS)产生、调节抗氧化酶基因表达以及增强抗氧化防护系统方面的作用,着重讨论了在ABA诱导的抗氧化防护过程中Ca2 、NADPH氧化酶与ROS之间的交谈机制。     

Manganese as an ecological factor in salt marshes

The plant available manganese concentration (Mn²⁺) of salt-marsh sediments was compared to that of acidic and neutral soils. The mean soil-manganese concentration was higher in the top 1 cm of salt-marsh soil than in the neutral soil and comparable to that of the acidic soil (0–5 cm). A peak in the soil-manganese concentration in the upper marsh was observed one week after the spring tide but this effect was not evident in the lower marsh. Despite these differences, there was no correlation between mean manganese concentration and position on the marsh.The response to manganese of salt-marsh halophytes was studied by measuring growth and root elongation in a range of Mn²⁺ concentrations with and without sodium chloride. Although there was a differential response to manganese between salt-marsh species, manganese resistance was not related to position on the marsh. Most of the species investigated were tolerant of Mn²⁺ at concentrations higher than normally recommended for plant growth. Moreover a salt-marsh ecotype of Festuca rubra was found to have a higher manganese resistance than an inland ecotype of the same species.When sodium chloride was included in the growth medium, salt-marsh plants had a greatly increased resistance to manganese associated with a reduced uptake. This effect is reflected in the tissue-manganese concentration which was lower than in Deschampsia flexuosa although both groups of plants were exposed to a similar range of Mn²⁺ concentrations. It is concluded that sodium chloride markedly reduces the phytotoxicity of manganese in salt marshes.Nomenclature following Clapham, Tutin & Warburg (1968). Flora of the British Isles.The work was carried out while one of us (C. E. Singer) was in receipt of an SERC studentship, which is gratefully acknowledged.     

Manganese oxide reduction as a form of anaerobic respiration

Some instances of bacterial manganese oxide reduction observed in nature and under laboratory conditions are a form of respiration. Anaerobiosis is not a necessary condition for its occurrence, although anaerobic reduction of manganese oxide which is inhibited by air has been reported. It is the kind of manganese reducing microorganism involved which determines whether anaerobic conditions are required. In at least some instances, complexed Mn(III) may be an extracellularly detectable intermediate in bacterial reduction of Mn(IV). A pyrophosphate complex of Mn(III) has been shown to be reduced by a bacterial culture. Only limited information is available to date concerning electron transport pathways in manganese reduction or organic carbon mineralization coupled to manganese respiration.     

Manganese ion as a goitrogen in the female mouse

Effect of excessive ingestion of manganese (Mn) on the mouse thyroid was assessed under the conditions of normal intake of iodide. Female mouse thyroids were enlarged after 7 weeks of administration of 200 mg/l MnCl2 X 4H2O in drinking water; 2.74 +/- 0.25 mg for control (N = 56), and 3.31 +/- 0.28 mg for Mn-treated group (N = 85) (p less than 0.001). In contrast, male mouse thyroids never became goitrous following this treatment. Manganese was goitrogenic to the castrated male mouse, but it had no effect on the testosterone-treated castrated male mouse, indicating the involvement of androgen in goiter formation. Oral administration of Mn did not severely affect blocked T/S of 125I or iodine metabolism in the thyroid. A morphological study, however, revealed that the epithelial cell in the Mn-treated mouse thyroid became flatter than that of the control. The lumens were filed with colloid in Mn-treated female mouse thyroid. The serum levels of thyroxine (T4), but not triiodothyronine (T3), were slightly reduced by Mn. These informations suggest that Mn can be a mild goitrogen for the female mouse and that the etiology of goiter formation can be interpreted by retention of colloid in the lumen.     

Pallidal Index as Biomarker of Manganese Brain Accumulation and Associated with Manganese Levels in Blood: A Meta-Analysis

Objective

The current study was designed to evaluate the sensitivity, feasibility, and effectiveness of the pallidal index (PI) serving as a biomarker of brain manganese (Mn) accumulation, which would be used as an early diagnosis criteria for Mn neurotoxicity.

Methods

The weighted mean difference (WMD) of the PI between control and Mn-exposed groups was estimated by using a random-effects or fixed-effects meta-analysis with 95% confidence interval (CI) performed by STATA software version 12.1. Moreover, the R package “metacor” was used to estimate correlation coefficients between PI and blood Mn (MnB).

Results

A total of eight studies with 281 occupationally Mn-exposed workers met the inclusion criteria. Results were pooled and performed with the Meta-analysis. Our data indicated that the PI of the exposed group was significantly higher than that of the control (WMD: 7.76; 95% CI: 4.86, 10.65; I² = 85.7%, p<0.0001). A random effects model was used to perform meta-analysis. These findings were remarkably robust in the sensitivity analysis, and publication bias was shown in the included studies. Seven out of the eight studies reported the Pearson correlation (r) values. Significantly positive correlation between PI and MnB was observed (r = 0.42; 95% CI, 0.31, 0.52).

Conclusions

PI can be considered as a sensitive, feasible, effective and semi-quantitative index in evaluating brain Mn accumulation. MnB can also augment the evaluation of brain Mn accumulation levels in the near future. However, the results should be interpreted with caution.     

Manganese as a mutagenic agent during in vitro DNA synthesis.

The effect of Mn²⁺, a known mutagen, on the fidelity of DNA synthesis $\text{in vitro}$ by avian myeloblastosis DNA polymerase has been determined. Substitution of Mn²⁺ for Mg²⁺ leads to an enhanced incorporation of noncomplementary deoxynucleotides as well as complementary ribonucleotides with either poly (A) or poly (C) as templates. Since this polymerase lacks any detectable deoxyribonuclease activity, the $\text{in vitro}$ mutagenic effect of Mn²⁺ in promoting errors in base-pairing does not result from any diminished proof-reading function.     

Manganese uptake and transportation as well as antioxidant response to excess manganese in plants]

Manganese (Mn) is an essential micronutrient throughout all stages of plant development. Mn plays an important role in many metabolic processes in plants. It is of particular importance to photosynthetic organisms in the chloroplast of which a cluster of Mn atoms at the catalytic centre function in the light-induced water oxidation by photosystem II, and also function as a cofactor for a variety of enzymes, such as Mn-SOD. But excessive Mn is toxic to plants which is one of the most toxic metals in acid soils. The knowledge of Mn(2+) uptake and transport mechanisms, especially the genes responsible for transition metal transport, could facilitate the understanding of both Mn tolerance and toxicity in plants. Recently, several plant genes were identified to encode transporters with Mn(2+) transport activity, such as zinc-regulated transporter/iron-regulated transporter (ZRT/IRT1)-related protein (ZIP) transporters, natural resistance-associated macrophage protein (Nramp) transporters, cation/H(+) antiporters, the cation diffusion facilitator (CDF) transporter family, and P-type ATPase. In addition, excessive Mn frequently induces oxidative stress, then several defense enzymes and antioxidants are stimulated to scavenge the superoxide and hydrogen peroxide formed under stress. Mn-induced oxidative stress and anti-oxidative reaction are very important mechanisms of Mn toxicity and Mn tolerance respectively in plants. This article reviewed the transporters identified as or proposed to be functioning in Mn(2+) transport, Mn toxicity-induced oxidative stress, and the response of antioxidants and antioxidant enzymes in plants to excessive Mn to facilitate further study. Meanwhile, basing on our research results, new problems and views are brought forward.     

Manganese Intoxication

We have reported two cases of chronic manganese poisoning. Case 1 followed exposure to manganese fumes in cutting and burning manganese steel. Case 2 resulted from exposure to dusts of manganese dioxide, an ingredient used in glazing of ceramics. There were initial difficulties in establishing the correct diagnosis. Prominent clinical features were severe and persistent chronic depressive psychosis (Case 1), transient acute brain syndrome (Case 2) and the presence of various extrapyramidal symptoms in both cases.Manganese intoxication has not previously been reported as occurring in California. With increasing use of the metal, the disease should be considered in the differential diagnosis of neurologic and psychiatric disease.Our observations were made in the period 1964 through 1968. Recently the prognosis of victims of manganese poisoning has been improved dramatically by the introduction of levodopa as a therapeutic agent.