Shanghai Environmental Protection Key Laboratory for Environmental Standard and Risk Management of Chemical Pollutants, School of Resources & Environmental Engineering, East China University of Science and Technology, Shanghai, 200237, China.
State Environmental Protection Key Lab of Environmental Risk Assessment and Control on Chemical Processes. School of Resources & Environmental Engineering, East China University of Science and Technology, Shanghai, 200237, China.
Environ Sci Pollut Res Int. 2021 Nov;28(43):60704-60716. doi: 10.1007/s11356-021-14908-0. Epub 2021 Jun 23.
It is well accepted that diesel exhaust particles (DEPs) are highly associated with improper function of organ systems. In this study, DEP toxicity was performed by using in vitro human BEAS-2B cell line and in vivo animal model, namely, Caenorhabditis elegans (C. elegans). The potential toxicity of DEP was assessed by the apical endpoints of BEAS-2B cell line and reflections of C. elegans under exposure scenarios of 0~50 μg mL DEP. With the increase of DEP exposure concentration, microscopic accumulations in the cytoplasm of cell line and intestine of C. elegans were observed. Such invasion of DEP impaired the behaviors of C. elegans as well as its un-exposed offspring and caused significant impeded locomotion. Moreover, the disorders of dopaminergic function were observed simultaneously under DEP exposure, specifically manifested by the decreased transcriptional expression of dat-1. The stress responses instructed by the expression of hsp-16.2 were also increased sharply in TJ375 strain of C. elegans at DEP concentrations of 1 and 10 μg mL. In the case of cellular reactions to DEP exposure, the injuries of membrane integrity and the decreased viability of cell line were simultaneously identified, and reactive oxygen species (ROS), damaged DNA fragment, and upregulated apoptosis were monotonically elevated in cell lines with the increase of DEP concentrations. This study provided a systematic insight into toxicity of DEP both in vivo and vitro, demonstrating that DEP exposure could disturb the stability of cell system and further threat the stability of organism.
人们普遍认为，柴油尾气颗粒（DEP）与器官系统功能异常高度相关。在本研究中，通过体外人 BEAS-2B 细胞系和体内动物模型，即秀丽隐杆线虫（C. elegans），研究了 DEP 的毒性。通过 BEAS-2B 细胞系的顶端终点和暴露场景下 C. elegans 的反射来评估 DEP 的潜在毒性，暴露浓度为 0~50 μg mL 的 DEP。随着 DEP 暴露浓度的增加，细胞系和 C. elegans 肠道的细胞质中观察到微观聚集。这种 DEP 的入侵损害了 C. elegans 的行为及其未暴露的后代的行为，并导致其运动显著受阻。此外，在 DEP 暴露下，还观察到多巴胺能功能紊乱，具体表现为 dat-1 的转录表达降低。在 TJ375 品系的 C. elegans 中，在 DEP 浓度为 1 和 10 μg mL 时，由 hsp-16.2 表达指示的应激反应也急剧增加。在细胞对 DEP 暴露的反应方面，同时鉴定出膜完整性损伤和细胞系活力降低，并且随着 DEP 浓度的增加，活性氧（ROS）、受损的 DNA 片段和上调的凋亡呈单调增加。本研究系统地研究了 DEP 在体内和体外的毒性，表明 DEP 暴露会干扰细胞系统的稳定性，并进一步威胁生物体的稳定性。
