Delhaize E, Jackson P J, Lujan L D, Robinson N J
Genetics Group, Mail Stop M886, Life Sciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico 87545.
Plant Physiol. 1989 Feb;89(2):700-6. doi: 10.1104/pp.89.2.700.
The effects of Cd on poly(gamma-glutamylcysteinyl)glycine [(gammaEC)(n)G] biosynthesis and formation of (gammaEC)(n)G:Cd complexes were measured in two cell lines of Datura innoxia with differing Cd tolerance. In addition, RNA synthesis, protein synthesis, and GSH concentrations were measured during a 48 hour exposure to Cd. Exposure to 250 micromolar CdCl(2) was toxic to the sensitive line, whereas the tolerant line survived and grew in its presence. Cd-sensitive cells synthesized the same amount of (gammaEC)(n)G as tolerant cells during an initial 24 hour exposure to 250 micromolar CdCl(2). However, rates of (gammaEC)(n)G:Cd complex formation differed between the two cell lines with the sensitive cells forming complexes later than tolerant cells. In addition, the complexes formed by sensitive cells were of lower molecular weight than those of tolerant cells and did not bind all of the cellular Cd. Pulse-labeling of cells with l-[(35)S]cysteine resulted in equivalent rates of incorporation into the (gammaEC)(n)G of both cell lines during the initial 24 hours after Cd. Rates of protein and RNA synthesis were similar for both cell lines during the initial 8 hours after Cd but thereafter declined rapidly in sensitive cells. This was reflected by a decline in viability of sensitive cells. The GSH content of both cell lines declined rapidly upon exposure to Cd but was higher in sensitive cells throughout the experiment. These results show that the biosynthetic pathway for (gammaEC)(n)G synthesis in sensitive cells is operational and that relative overproduction of (gammaEC)(n)G is not the mechanism of Cd-tolerance in a Cd-tolerant cell line of D. innoxia. Rapid formation of (gammaEC)(n)G:Cd complexes that bind all of the cellular Cd within 24 hours appears to correlate with tolerance in these cells.
在两种对镉耐受性不同的紫花曼陀罗细胞系中,测定了镉对聚(γ-谷氨酰半胱氨酰)甘氨酸[(γEC)nG]生物合成以及(γEC)nG:镉复合物形成的影响。此外,在暴露于镉48小时期间,测定了RNA合成、蛋白质合成和谷胱甘肽(GSH)浓度。暴露于250微摩尔氯化镉对敏感细胞系有毒,而耐受细胞系在其存在下存活并生长。在最初24小时暴露于250微摩尔氯化镉期间,镉敏感细胞合成的(γEC)nG量与耐受细胞相同。然而,两种细胞系中(γEC)nG:镉复合物的形成速率不同,敏感细胞形成复合物的时间比耐受细胞晚。此外,敏感细胞形成的复合物分子量低于耐受细胞,并且没有结合所有细胞内的镉。用l-[(35)S]半胱氨酸对细胞进行脉冲标记,在镉处理后的最初24小时内,两种细胞系中(γEC)nG的掺入速率相当。镉处理后的最初8小时内,两种细胞系的蛋白质和RNA合成速率相似,但此后敏感细胞中的合成速率迅速下降。这反映在敏感细胞活力的下降上。两种细胞系的GSH含量在暴露于镉后迅速下降,但在整个实验过程中,敏感细胞中的GSH含量更高。这些结果表明,敏感细胞中(γEC)nG合成的生物合成途径是有效的,并且(γEC)nG的相对过量产生不是紫花曼陀罗镉耐受细胞系中镉耐受的机制。(γEC)nG:镉复合物在24小时内迅速形成并结合所有细胞内的镉,这似乎与这些细胞的耐受性相关。