Microplastics (MPs) have attracted growing attention worldwide as an increasingly prevalent environmental pollutant. In addition, chicken meat is currently the most widely consumed kind of poultry in the global market. Consumer demand for chicken is on the rise both at home and abroad. As a result, the safety of chicken raising has also received significant attention. The lungs play an essential role in the physiological activities of chickens, and they are also the most vulnerable organs. Lung injury is difficult to repair after the accumulation of contaminants, and the mortality rate is high, which brings huge economic losses to farmers. The research on the toxicity of MPs has mainly focused on the marine ecosystem, while the mechanisms of toxicity and lung damage in chickens have been poorly studied. Thus, this study explored the effects of exposure to polystyrene microplastics (PS-MPs) at various concentrations for 42 d on chicken lungs. PS-MPs could cause lung pathologies and ultrastructural abnormalities, such as endoplasmic reticulum (ER) swelling, inflammatory cell infiltration, chromatin agglutination, and plasma membrane rupture. Simultaneously, PS-MPs increased the expression of genes related to the heat shock protein family (Hsp60, Hsp70, and Hsp90), ER stress signaling (activating transcription factor 6 (ATF6), ATF4, protein kinase RNA-like ER kinase (PERK), and eukaryotic translation initiation factor 2 subunit α (eIF2α)), pyroptosis-related genes (NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), interleukin-1β (IL-1β), cysteinyl aspartate-specific proteinase 1 (Caspase1), and gasdermin-D (GSDMD)), and the inflammatory signaling pathway (nuclear factor-κB (NF-κB), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2)). The above results showed that PS-MP exposure could result in lung stress, ER stress, pyroptosis, and inflammation in broilers. Our findings provide new scientific clues for further research on the mechanisms of physical health and toxicology regarding MPs.
作为一种普遍的环境污染物，微塑料（MPs）已引起全球关注。鸡作为目前全球消费最广泛的家禽，随着消费者的需求不断上升，其饲养的安全性受到极大关注。肺是鸡生理活动中的重要器官，也是最脆弱的器官。因污染物积累导致的鸡的肺损伤难以修复，死亡率较高，给饲养者带来巨大经济损失。目前，对MPs毒性研究主要集中在海洋生态系统，而对鸡的毒性和肺损伤机制的研究相对较少。本研究主要探讨了不同浓度的聚苯乙烯微塑料（PS-MPs）暴露42天对鸡肺的影响。结果显示，PS-MPs可引起鸡肺病理和超微结构的异常，具体包括内质网肿胀、炎症细胞浸润、染色质凝集和质膜破裂。同时，PS-MPs可增加以下相关基因的表达：热休克蛋白（Hsp60、Hsp70、Hsp90）、内质网应激信号通路（ATF6、ATF4、PERK、eIF2α）、焦亡相关基因（NLRP3、ASC、IL-1β、Caspase1、GSDMD）和炎症通路（NF-κB、iNOS、COX-2）。综上所述，PS-MPs暴露可导致肉鸡肺应激、内质网应激、焦亡和炎症反应，为进一步研究MPs的生理健康和毒理学机制提供了新的科学线索。.
作为一种普遍的环境污染物，微塑料（MPs）已引起全球关注。鸡作为目前全球消费最广泛的家禽，随着消费者的需求不断上升，其饲养的安全性受到极大关注。肺是鸡生理活动中的重要器官，也是最脆弱的器官。因污染物积累导致的鸡的肺损伤难以修复，死亡率较高，给饲养者带来巨大经济损失。目前，对MPs毒性研究主要集中在海洋生态系统，而对鸡的毒性和肺损伤机制的研究相对较少。本研究主要探讨了不同浓度的聚苯乙烯微塑料（PS-MPs）暴露42天对鸡肺的影响。结果显示，PS-MPs可引起鸡肺病理和超微结构的异常，具体包括内质网肿胀、炎症细胞浸润、染色质凝集和质膜破裂。同时，PS-MPs可增加以下相关基因的表达：热休克蛋白（Hsp60、Hsp70、Hsp90）、内质网应激信号通路（ATF6、ATF4、PERK、eIF2α）、焦亡相关基因（NLRP3、ASC、IL-1β、Caspase1、GSDMD）和炎症通路（NF-κB、iNOS、COX-2）。综上所述，PS-MPs暴露可导致肉鸡肺应激、内质网应激、焦亡和炎症反应，为进一步研究MPs的生理健康和毒理学机制提供了新的科学线索。
Keywords: Endoplasmic reticulum stress; Inflammation; Lung; NLRP3 inflammasome; Polystyrene microplastics.