Suppr超能文献

镉离子诱导的酵母质膜损伤及其锌离子的缓解作用:对粟酒裂殖酵母细胞和重组质膜囊泡的研究

Cd2+-induced damage to yeast plasma membrane and its alleviation by Zn2+: studies on Schizosaccharomyces pombe cells and reconstituted plasma membrane vesicles.

作者信息

Aßmann S, Sigler K, Höfer M

机构信息

Institute of Botany, University of Bonn, D-53115 Bonn, Germany

出版信息

Arch Microbiol. 1996 Apr;165(4):279-84. doi: 10.1007/s002030050327.

Abstract

In Schizosaccharomyces pombe, Cd2+ shares the same uphill uptake system with Zn2+. Both heavy metals inhibited growth, respiration, H+/glucose uptake, and glucose-induced proton extrusion, Cd2+ being a 10-15-fold stronger inhibitor. In contrast, both had a similar effect on the plasma membrane H+-ATPase, enhancing its affinity for ATP and reducing the rate of ATP splitting. Cd2+ caused protracted strong fluidization of the plasma membrane of energized cells, whereas deenergized cells, phosphatidylcholine liposomes, and plasma membrane fragments, either purified or incorporated into the liposomes, exhibited only a short initial fluidization. Zn2+, which caused only a marginal membrane fluidization, suppressed the fluidizing action of Cd2+. The fluidizing effect of both heavy metals on liposomes was reduced by the presence of plasma membrane fragments in the liposome membrane. At 50 &mgr;M, Cd2+ brought about loss K+ (18 K+/1 Cd2+) from energized, but not from deenergized cells since Cd2+ must first accumulate in the cells before causing a detectable effect. A simple membrane disruption by external Cd2+ is, therefore, unlikely to be the main mechanism of cadmium-induced potassium loss in intact cells. Zn2+ had virtually no effect below 1 mM concentration, and it again weakened the K+-releasing effect of Cd2+. Cd2+ caused a strong loss of K+ also from K+-containing liposomes, probably because of a direct interaction with liposome phospholipids. Incorporation of plasma membrane fragments into the liposomes reduced the K+ loss sixfold.

摘要

在粟酒裂殖酵母中,Cd2+与Zn2+共用相同的上坡摄取系统。两种重金属均抑制生长、呼吸、H+/葡萄糖摄取以及葡萄糖诱导的质子外排,Cd2+的抑制作用强10 - 15倍。相比之下,二者对质膜H+-ATP酶的作用相似,均增强其对ATP的亲和力并降低ATP水解速率。Cd2+导致供能细胞的质膜长时间强烈的流动性增加,而失能细胞、磷脂酰胆碱脂质体以及纯化的或掺入脂质体的质膜片段仅表现出短暂的初始流动性增加。仅引起轻微膜流动性增加的Zn2+抑制了Cd2+的流动性增加作用。脂质体膜中质膜片段的存在降低了两种重金属对脂质体的流动性增加作用。在50 μM时,Cd2+导致供能细胞而非失能细胞的K+流失(18个K+/1个Cd2+),因为Cd2+必须先在细胞中积累才能产生可检测到的效应。因此,外部Cd2+引起的简单膜破坏不太可能是完整细胞中镉诱导钾流失的主要机制。在浓度低于1 mM时,Zn2+几乎没有作用,并且它再次削弱了Cd2+的钾释放效应。Cd2+也导致含K+脂质体的大量K+流失,这可能是由于与脂质体磷脂的直接相互作用。将质膜片段掺入脂质体可使K+流失减少六倍。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验