活性氧和钙信号参与铅对酵母细胞的毒性作用

以模式生物酵母菌为材料,研究铅对细胞的毒性效应,探讨胞内活性氧(ROS)和Ca~(2+)在铅诱导细胞死亡中的作用。结果显示,浓度为5~100 mg·L~(-1)的硝酸铅可降低酵母细胞活性,诱导酵母细胞死亡,随着铅浓度的提高和作用时间的延长,细胞死亡率增高。在铅处理组酵母细胞中,ROS和Ca~(2+)水平显著升高,线粒体膜电位明显下降;用1 mmol·L~(-1)的外源抗坏血酸(AsA)能降低铅引发的酵母细胞死亡,0.5 mmol·L~(-1)的钙离子螯合剂乙二醇双四乙酸(EGTA)或0.1 mmol·L~(-1)的质膜Ca~(2+)通道特异性抑制剂氯化镧(LaCl_3)亦可明显抑制铅引起的酵母细胞死亡。研究结果表明,铅诱发的酵母细胞死亡与处理组胞内ROS和Ca~(2+)升高有关,高浓度的Ca~(2+)可能通过诱导线粒体膜通透性转变孔道开放,或者高水平ROS可能损伤线粒体膜,致线粒体膜电位下降,继而激活相关下游信号导致细胞死亡。

ROS and Calcium Signal is Involved in Lead Toxicity in Yeast Cells

This paper was conducted to research the cellular toxicity of lead based on the model yeasts to explore the role that intracellular reactive oxygen species (ROS) and Ca²⁺ play in the mechanism of the cell death induced by lead. The results revealed that the cellular bioactivity of yeasts was inhibited by lead nitrate at the concentration from 5 to 100 mg?L^-1and the cell death induced by lead was found. Yeast cellmortality increases with the increase of lead concentration and the extension of time. The levels of ROS and Ca²⁺ elevated significantly and the mitochondrial membrane potential decreased dramaticallyin yeast cells under lead stress. Cell death induced by lead was decreased by ascorbic acid (AsA) at the concentration of 1 mmol?L^-1 and was inhibited by the calcium chelator (EGTA) at the concentration of 0.5 mmol?L^-1 or the specific inhibitor of plasma membrane Ca²⁺ channel (LaCl₃) at the concentration of 0.1 mmol?L^-1. The results showed that cell death induced by lead was related to the levels of intracellular ROS and Ca²⁺. The opening of mitochondrial membrane permeability transition pore channels may be induced by high levels of Ca²⁺, or mitochondrial membranes were broken by high levels of ROS, which lead to decreasing membrane potential and cause cell death by activating down-stream relevant signal pathways.