Deng Haochu, Taishi Yezi, Wang Guoxia, Kong Yuebing, Zhang Ruoting, Zheng Xin
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China.
Department of Geriatrics, The First Hospital of Jilin University, Changchun 130021, China.
Ecotoxicol Environ Saf. 2025 Jan 15;290:117566. doi: 10.1016/j.ecoenv.2024.117566. Epub 2024 Dec 20.
Long-chain chlorinated paraffins (LCCPs) are industrial raw materials extensively utilized worldwide. Recently, their environmental impact has escalated, exacerbating challenges in animal husbandry and contributing to pollution from the food industry, which poses certain risks to animal growth and development. However, the toxicological effects of LCCPs exposure on poultry remain inadequately understood. The liver is a critical organ in poultry, serving not only as the largest digestive gland but also as the center of metabolism. Consequently, this study employed primary chicken embryo hepatocyte as a model to investigate the toxicological effects of LCCPs exposure and its potential mechanisms of action. Our findings indicate that the proliferation capacity of primary chicken embryo hepatocytes exposed to LCCPs at concentrations of 1, 10, and 100 μg/L was significantly diminished, with an observed arrest in the G0/G1 phase and a notable reduction in the proportion of cells in the G2/M phase. Additionally, we observed that LCCPs exposure markedly decreased the autophagy levels in primary chicken embryo hepatocytes while significantly increase the levels of apoptosis. To elucidate the molecular mechanisms underlying LCCP-induced apoptosis in these cells, we assessed oxidative stress levels (ROS) and mitochondrial membrane potential, and found that the level of ROS was significantly increased, and the level of mitochondrial membrane potential was significantly decreased in primary chicken embryo hepatocytes after exposure to LCCPs. To further clarify whether LCCPs induced apoptosis in primary chicken embryo hepatocytes through oxidative stress, oxidative stress inhibitors (NAC) were used, and it was found that apoptosis caused by LCCPs exposure was significantly alleviated. These data suggest that LCCPs exposure could induce apoptosis in primary chicken embryo hepatocytes through oxidative stress. In conclusion, the current work shows that LCCPs have multiple toxic effects on primary chicken embryo hepatocytes, and lays a theoretical foundation for future research on the harmful effects of LCCPs in the poultry industry.
长链氯化石蜡（LCCPs）是在全球广泛使用的工业原料。最近，它们对环境的影响不断升级，加剧了畜牧业面临的挑战，并导致食品工业产生污染，这对动物的生长发育构成了一定风险。然而，LCCPs暴露对家禽的毒理学影响仍未得到充分了解。肝脏是家禽体内的关键器官，不仅是最大的消化腺，也是新陈代谢的中心。因此，本研究以原代鸡胚肝细胞为模型，研究LCCPs暴露的毒理学影响及其潜在作用机制。我们的研究结果表明，暴露于浓度为1、10和100μg/L的LCCPs的原代鸡胚肝细胞的增殖能力显著降低，观察到细胞停滞在G0/G1期，且G2/M期细胞比例显著降低。此外，我们观察到LCCPs暴露显著降低了原代鸡胚肝细胞的自噬水平，同时显著增加了细胞凋亡水平。为了阐明LCCP诱导这些细胞凋亡的分子机制，我们评估了氧化应激水平（ROS）和线粒体膜电位，发现暴露于LCCPs后，原代鸡胚肝细胞中的ROS水平显著升高，线粒体膜电位水平显著降低。为了进一步阐明LCCPs是否通过氧化应激诱导原代鸡胚肝细胞凋亡，我们使用了氧化应激抑制剂（NAC），发现LCCPs暴露引起的细胞凋亡得到了显著缓解。这些数据表明，LCCPs暴露可通过氧化应激诱导原代鸡胚肝细胞凋亡。总之，目前的工作表明LCCPs对原代鸡胚肝细胞有多种毒性作用，为未来研究LCCPs在家禽业中的有害影响奠定了理论基础。
