Cadmium (Cd) is a type of toxic metal, in most cases, coming from fuel burning and aquatic plants. The cells of organisms can be caused serious damage, including pyroptosis, exposure to low concentrations of Cd in long-term. Pyroptosis is a recently discovered Caspase-1-mediated cell death. In this study, lymphocytes were extracted from the pronephros and spleens in carps, respectively. After treating cells with low concentration of Cd, the mRNA and protein expression levels of pyroptosis-related genes, NLRP3, Caspase-1, and pro-inflammatory cytokines, increased obviously. And the content of reactive oxygen species (ROS) and mitochondria reactive oxygen species (mtROS) increased significantly, we also found the activities of CAT, GSH-px and T-SOD reduce significantly, and the content of MDA have a clear upward trend. We then added NLRP3 inhibitor, Glyburide, to the Cd-treated group, further confirming that NLRP3 is a key gene in pyroptosis pathways by detecting the mRNA and protein expression levels. Besides, the rupture of the cell membrane was also confirmed by Hoechst/PI double staining, red fluorescence increased obviously in the Cd treatment group. The experiment revealed that Cd exposure induces pyroptosis of lymphocytes in carp pronephros and spleens by activating NLRP3. Inhibition of NLRP3 activity can slow down the degree of lymphocytes pyroptosis. Thus, the above information provides a new avenue toward understanding the partial mechanism of Cd exposure-induced pyroptosis.

镉（Cd）是一种有毒金属，在大多数情况下，其来自燃料燃烧和水生植物。长期以来，可能会导致生物体细胞严重受损，包括热解，暴露于低浓度的Cd中。细胞凋亡是最近发现的Caspase-1介导的细胞死亡。在这项研究中，分别从鲤鱼的前肾和脾中提取淋巴细胞。用低浓度的镉处理细胞后，与凋亡相关基因，NLRP3，Caspase-1和促炎细胞因子的mRNA和蛋白表达水平明显增加。活性氧（ROS）和线粒体活性氧（mtROS）的含量明显增加，CAT，GSH-px和T-SOD的活性明显降低，MDA的含量有明显的上升趋势。然后，我们添加了NLRP3抑制剂，通过检测Cd处理组的格列本脲，通过检测mRNA和蛋白质表达水平，进一步证实了NLRP3是促凋亡途径中的关键基因。此外，Hoechst / PI双重染色也证实了细胞膜的破裂，Cd处理组红色荧光明显增加。实验表明，Cd暴露通过激活NLRP3诱导鲤鱼前脾和脾中淋巴细胞的热解。抑制NLRP3活性可以减慢淋巴细胞焦磷酸化的程度。因此，以上信息为了解Cd暴露引起的细胞凋亡的部分机制提供了新途径。Hoechst / PI双重染色也证实了细胞膜的破裂，Cd处理组红色荧光明显增加。实验表明，Cd暴露通过激活NLRP3诱导鲤鱼前脾和脾中淋巴细胞的热解。抑制NLRP3活性可以减慢淋巴细胞焦磷酸化的程度。因此，以上信息为了解Cd暴露引起的细胞凋亡的部分机制提供了一条新途径。Hoechst / PI双重染色也证实了细胞膜的破裂，Cd处理组红色荧光明显增加。实验表明，Cd暴露通过激活NLRP3诱导鲤鱼前脾和脾中淋巴细胞的热解。抑制NLRP3活性可以减慢淋巴细胞焦磷酸化的程度。因此，以上信息为了解Cd暴露引起的细胞凋亡的部分机制提供了一条新途径。