镉诱导龙葵程序性死亡过程中线粒体的生理响应OA

Plant tolerance to cadmium is closely related to its cell death regulation. The response mechanism of mitochondria as energy and death signaling hubs is a key gap in understanding plant adversity adaptation. In this study,we investigated the physiological response mechanism of mitochondria during cadmium stress-induced programmed cell death(PCD)in the cadmium hyperaccumulator plant Solanum nigrum L.. The study simulated different concentrations of cadmium stress by nutrient solution culture,and the physiological changes of S. nigrum mitochondria were analyzed and ultrastructural observations were made. The results showed that the reactive oxygen species(ROS)content in S. nigrum mitochondria increased after cadmium treatment,the concentration of mitochondrial MDA increased,and the integrity of the mitochondrial membrane was disrupted. In particular,under 200 μmol/L Cd stress,the mitochondrial membrane potential decreased by 51.90％,the opening of the mitochondrial membrane permeability transition pore was enlarged by 47.61％,and the Cyt c/a ratio decreased by 30.66％. In addition,with increasing cadmium concentration,the mitochondrial Ca2+content gradually increased and Ca2+-ATPase activity gradually decreased,leading to cytoplasmic Ca2+destabilization. Studies have shown that Cd stress causes severe damage to the structure and function of the mitochondrial membrane of S. nigrum,induces the accumulation of large amounts of ROS in the mitochondria,and the release of mitochondrial cytochrome c and the increase in Ca2+will further activate the signaling pathway of PCD in S. nigrum cells,which will have a serious negative impact on the growth and development of S. nigrum .