Lead affects the proliferation and apoptosis of chicken embryo fibroblasts by disrupting intracellular calcium homeostasis and mitochondrial function

Lead (Pb) is a ubiquitous environmental toxic heavy metal that induces pathological and physiological changes in various cells and organ systems, affecting cell proliferation, apoptosis, and survival. Although the mechanisms of Pb toxicity in mammalian fibroblasts have been extensively studied, its effects on avian fibroblasts, particularly chicken embryo fibroblasts (CEFs), remain unclear. This study investigated the effects of Pb on CEF proliferation and apoptosis, and the underlying molecular mechanisms in vitro. Our results demonstrated that Pb treatment significantly inhibited the proliferation of CEFs and induced cell cycle arrest in the G₀/G₁ phase. The apoptosis rate in Pb-treated cells was increased in a dose- and time-dependent manner, and the mitochondrial membrane potential was significantly reduced, indicating mitochondrial dysfunction. The level of reactive oxygen species was significantly increased, while the intracellular calcium ion concentration was significantly elevated in Pb-treated cells, positively correlating with Pb concentration. Real-time quantitative PCR analysis of apoptotic markers showed that Pb treatment significantly upregulated BAX, TP53, CASP3, CASP8, and FAS expression while downregulating BCL2 expression in a dose-dependent manner, indicating the induction of apoptosis. In summary, we elucidated the molecular mechanisms by which Pb induces apoptosis in CEFs and demonstrated the involvement of multiple pathways, including oxidative stress, mitochondrial dysfunction, calcium ion homeostasis imbalance, and cell cycle arrest. Our study revealed the mechanisms of Pb toxicity in CEFs, providing vital evidence for understanding Pb toxicity in avian cells and scientific support for assessing the effect of Pb pollution on poultry farming.