Department of Life Science, Kyonggi University, Suwon, Republic of Korea.
Drug Chem Toxicol. 2012 Apr;35(2):225-31. doi: 10.3109/01480545.2011.591401. Epub 2011 Aug 18.
Cadmium, a well-known toxic heavy metal, affects cellular physiology by disturbing cellular signaling pathways. We investigate the effect of cadmium on cellular differentiation using 3T3-L1 preadipocyte cell lines as an in vitro model. Here, it was shown that cadmium (3 μM) significantly decreased both glycerol-3-phosphate dehydrogenase (GPDH) activity and lipid accumulation of differentiating 3T3-L1 cells in a dose-dependent manner. In addition, inhibitory action of cadmium on differentiating 3T3-L1 cells was effective only at the initial stage of 3T3-L1 preadipocyte differentiation. Western blot analysis revealed that cadmium suppressed the expression of CCAAT/enhancer-binding protein alpha (C/EBPα) and peroxisome proliferator-activator receptor gamma (PPARγ) proteins, key transcriptional activators for adipogenesis, in a dose-dependent manner. These results suggest that the inhibitory effects of cadmium on 3T3-L1 preadipocyte differentiation, as indicated by a decrease in GPDH activity and lipid accumulation, a marker of adipogenesis, appeared to be mediated through the downregulated expression of C/EBPα and PPARγ proteins.
镉是一种众所周知的有毒重金属，通过干扰细胞信号通路来影响细胞生理学。我们使用 3T3-L1 前体脂肪细胞系作为体外模型，研究了镉对细胞分化的影响。结果表明，镉（3μM）以剂量依赖的方式显著降低了分化中的 3T3-L1 细胞的甘油-3-磷酸脱氢酶（GPDH）活性和脂质积累。此外，镉对分化中的 3T3-L1 细胞的抑制作用仅在前体脂肪细胞分化的初始阶段有效。Western blot 分析表明，镉以剂量依赖的方式抑制了脂肪生成关键转录激活因子 CCAAT/增强子结合蛋白α（C/EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ）蛋白的表达。这些结果表明，镉对 3T3-L1 前体脂肪细胞分化的抑制作用，表现为 GPDH 活性和脂质积累的降低，这是脂肪生成的标志物，似乎是通过下调 C/EBPα 和 PPARγ 蛋白的表达来介导的。
