Excessive molybdenum (Mo) and cadmium (Cd) cause toxic effects on animals, but their joint effects on pyroptosis in kidney of ducks remain unclear. 160 healthy 7-day-old ducks were randomly divided into four groups which were fed with basal diet containing different dosages of Mo or/and Cd for 16 weeks. On the 4th, 8th, 12th and 16th weeks, kidney tissue and serum were collected. The results showed that Mo or/and Cd could significantly elevate their contents in kidney, disturb the homeostasis of trace elements, cause renal function impairment and histological abnormality, and oxidative stress as accompanied by increasing hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) concentrations and decreasing glutathione peroxidase (GSH-Px), catalase (CAT) and total-superoxide dismutase (T-SOD) activities. Simultaneously, Mo or/and Cd could markedly increase interleukin-1β (IL-1β), interleukin-18 (IL-18) contents and the expression levels of pyroptosis-related genes (NOD-like receptor protein-3 (NLRP3), Caspase-1, apoptosis-associated speck-like protein (ASC), NIMA-related kinase 7 (NEK7), Gasdermin A (GSDMA), Gasdermin E (GSDME), IL-1β and IL-18) and proteins (NLRP3, Caspase-1 p20, ASC and Gasdermin D (GSDMD)). Moreover, the changes of above these indicators were more obvious in combined group. Taken together, the results illustrate that Mo and Cd might synergistically lead to oxidative stress and induce pyroptosis via NLRP3/Caspase-1 pathway, whose mechanism is somehow related to Mo and Cd accumulation in duck kidneys.

过量的钼（Mo）和镉（Cd）对动物有毒性作用，但它们对鸭肾细胞焦亡的联合作用尚不清楚。160只健康的7日龄鸭子随机分为4组，分别饲喂含不同剂量Mo或/和Cd的基础日粮16周。第4、8、12、16周采集肾组织和血清。结果表明，Mo或/和Cd可显着提高其在肾脏中的含量，扰乱微量元素的稳态，引起肾功能损害和组织学异常，并伴有过氧化氢（H ₂ O ₂) 和丙二醛 (MDA) 浓度并降低谷胱甘肽过氧化物酶 (GSH-Px)、过氧化氢酶 (CAT) 和总超氧化物歧化酶 (T-SOD) 的活性。同时，Mo或/和Cd可显着增加白细胞介素1β（IL-1β）、白细胞介素18（IL-18）含量和细胞焦亡相关基因（NOD样受体蛋白3（NLRP3）、Caspase -1、凋亡相关斑点样蛋白 (ASC)、NIMA 相关激酶 7 (NEK7)、Gasdermin A (GSDMA)、Gasdermin E (GSDME)、IL-1β 和 IL-18) 和蛋白质 (NLRP3、Caspase- 1 p20、ASC 和 Gasdermin D (GSDMD)。而且，上述指标的变化在联合组中更为明显。综上所述，结果表明 Mo 和 Cd 可能通过 NLRP3/Caspase-1 途径协同导致氧化应激并诱导细胞焦亡，