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Aluminum toxicity and Ca depletion may enhance cell death of tobacco cells via similar syndrome

机译:铝中毒和Ca耗竭可能通过类似的综合征增加烟草细胞的细胞死亡

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The main objective of this work is to find opt whether aluminum (Al) toxicity and Ca depletion cause cell death of tobacco cells via similar sequence of events. Tobacco cell suspension culture exhibited maximum fresh weight in the presence of a wide range of Ca concentrations between 0.1-1.0 mM whereas higher concentrations (> 1.0-5.0 mM) gradually lowered cell fresh weight. However, this decrease in fresh weight does not imply a negative impact on cell viability since cell growth recommenced in fresh MS medium with rates mostly higher than those of low Ca. In addition, high Ca seems to be crucial for survival of Al-treated cells. On the other side, tobacco cells exhibited extreme sensitivity to complete deprivation of Ca. Without Ca, cells could not survive for 18 h and substantially lost their growth capability. Evans blue uptake proved membrane damage of Ca-depleted same as Al-treated cells; relative to maintained membrane intactness of calcium-supplemented (control) ones. Percentage of membranedamage and the growth capability (survival) of tobacco cells exhibited a clear negative correlation. Alterations in growth (fresh weight per aliquot) could not be ascribed neither to cell number nor to decreased dry matter allocation (dry weight/fresh weight percentage) but was mainly due to decreased cellular water content. In this context, Ca-depleted cells lost about half their original water content while 100 mu M Al-treated ones retained most of it (ca 87%). This represented the single differencebetween the two treatments (discussed in the text). Nevertheless, such high water content of the Al-treated cells seems physiologically useless since it did not result in improved viability. Similarities, however, included negligible levels of growth capability, maximum levels of membrane damage, and comparable amounts of NO_3~- efflux. As well, both types of treatments led to a sharp decline in osmotic potential that is, in turn, needed for water influx. The above-mentioned sequence of events, inducedby Al application looks, to a great extent, similar to Ca depletion syndrome leading finally to cell death of tobacco cells.
机译:这项工作的主要目的是通过类似的事件序列,找出铝(Al)毒性和Ca耗竭是否导致烟草细胞死亡。在0.1-1.0 mM之间的宽范围Ca浓度存在的情况下,烟草细胞悬浮培养物显示最大鲜重,而较高浓度(> 1.0-5.0 mM)逐渐降低细胞鲜重。但是,这种新鲜体重的减少并不意味着对细胞活力的负面影响,因为在新鲜的MS培养基中,细胞生长重新开始,其生长速率大多高于低Ca的生长速率。此外,高钙似乎对铝处理细胞的存活至关重要。另一方面,烟草细胞对完全剥夺Ca表现出极大的敏感性。如果没有钙,细胞将无法存活18小时,并且基本丧失了生长能力。伊文思蓝的摄取证明了与铝处理细胞相同的,缺钙的细胞膜损伤。相对于维持钙补充(对照)的完整的膜完整性而言。膜损伤百分比和烟草细胞的生长能力(存活)表现出明显的负相关性。生长的变化(每等份的鲜重)既不能归因于细胞数目,也不能归因于干物质分配的减少(干重/新鲜重量百分比),但这主要是由于细胞含水量降低。在这种情况下,贫钙细胞损失了约一半的原始水分,而100μMAl处理的细胞保留了大部分水分(约87%)。这代表了两种处理之间的唯一差异(在本文中进行了讨论)。然而,铝处理的细胞的如此高的水分含量在生理上似乎是无用的,因为它没有导致提高的生存力。然而,相似之处包括可忽略的生长能力水平,最大的膜损伤水平和相当的NO_3〜-外排量。同样,两种类型的处理均导致渗透势急剧下降,这反过来又是水流入所需要的。由Al施用引起的上述事件序列在很大程度上看起来类似于Ca耗竭综合征,最终导致烟草细胞死亡。

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