Yakimova E T, Kapchina-Toteva V M, Laarhoven L-J, Harren F M, Woltering E J
Regional Research Centre and Extension Service of Floriculture and Agriculture (RCNPO), 1222 Negovan, Sofia, Bulgaria.
Plant Physiol Biochem. 2006 Oct;44(10):581-9. doi: 10.1016/j.plaphy.2006.09.003. Epub 2006 Oct 4.
Cadmium-induced cell death was studied in suspension-cultured tomato (Lycopersicon esculentum Mill.) cells (line MsK8) treated with CdSO(4). Within 24 h, cadmium treatment induced cell death in a concentration-dependent manner. Cell cultures showed recovery after 2-3 days which indicates the existence of an adaptation mechanism. Cadmium-induced cell death was alleviated by the addition of sub muM concentrations of peptide inhibitors specific to human caspases indicating that cell death proceeds through a mechanism with similarities to animal programmed cell death (PCD, apoptosis). Cadmium-induced cell death was accompanied by an increased production of hydrogen peroxide (H(2)O(2)) and simultaneous addition of antioxidants greatly reduced cell death. Inhibitors of phospholipase C (PLC) and phospholipase D (PLD) signalling pathway intermediates reduced cadmium-induced cell death. Treatment with the G-protein activator mastoparan and a cell permeable analogue of the lipid signal second messenger phosphatidic acid (PA) induced cell death. Ethylene, while not inducing cell death when applied alone, stimulated cadmium-induced cell death. Application of the ethylene biosynthesis inhibitor aminoethoxy vinylglycine (AVG) reduced cadmium-induced cell death, and this effect was alleviated by simultaneous treatment with ethylene. Together the results show that cadmium induces PCD exhibiting apoptotic-like features. The cell death process requires increased H(2)O(2) production and activation of PLC, PLD and ethylene signalling pathways.
在硫酸镉处理的悬浮培养番茄（Lycopersicon esculentum Mill.）细胞（MsK8系）中研究了镉诱导的细胞死亡。在24小时内，镉处理以浓度依赖的方式诱导细胞死亡。细胞培养物在2 - 3天后显示出恢复，这表明存在一种适应机制。添加亚微摩尔浓度的人半胱天冬酶特异性肽抑制剂可减轻镉诱导的细胞死亡，这表明细胞死亡通过一种与动物程序性细胞死亡（PCD，凋亡）相似的机制进行。镉诱导的细胞死亡伴随着过氧化氢（H₂O₂）产生的增加，同时添加抗氧化剂可大大减少细胞死亡。磷脂酶C（PLC）和磷脂酶D（PLD）信号通路中间体的抑制剂可减少镉诱导的细胞死亡。用G蛋白激活剂马斯托帕兰和脂质信号第二信使磷脂酸（PA）的细胞可渗透类似物处理可诱导细胞死亡。乙烯单独应用时不诱导细胞死亡，但可刺激镉诱导的细胞死亡。应用乙烯生物合成抑制剂氨基乙氧基乙烯甘氨酸（AVG）可减少镉诱导的细胞死亡，同时用乙烯处理可减轻这种作用。这些结果共同表明，镉诱导表现出凋亡样特征的PCD。细胞死亡过程需要增加H₂O₂的产生以及激活PLC、PLD和乙烯信号通路。
