Microplastics are a novel pollutant that adversely affect freshwater benthic organisms. However, few studies have investigated the mechanism underlying the bioaccumulation and the toxicity of microplastics. In this study, microplastics bioaccumulation of wild Cipangopaludina chinensis in the Songhua River were utilized, and a 28-day aquatic toxicity test was performed to determine the effects of exposure to polyethylene terephthalate (PET), the bioaccumulation of PET, and changes in multiple biomarkers in the muscle, gill, and kidney tissues. The concentration pattern of microplastics was as follows: kidney tissue > muscle tissue > gill tissue. Microplastic ingestion caused AChE inhibition led to significant increases in redox and energy metabolism indicators. Furthermore, the IBR analysis presented a "response-resistance-breakdown" process, indicating that Cipangopaludina chinensis possessed resistance with time (D14 and D21) and concentration (0.10 mg/L and 1.00 mg/L) thresholds. Tissue sensitivity to microplastics was ranked as gill > muscle > kidney, which was the opposite order of microplastic accumulation. These findings implied that less sensitive tissues stored a larger amount of pollutants, suggesting a reduction in tissue sensitivity to microplastics with higher microplastic occurrence rates. This study provides new insights into biological resistance to pollutant stress, warranting further investigation into the underlying mechanisms.

中文翻译：

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聚对苯二甲酸乙二醇酯微塑料在 Cipangopaludina chinensis 中的生物积累和生化影响：组织特异性分析和体内平衡破坏


微塑料是一种新型污染物，对淡水底栖生物产生不利影响。然而，很少有研究调查微塑料的生物积累机制和毒性。本研究利用松花江野生 Cipangopaludina chinensis 的微塑料生物积累，并进行了 28 天的水生毒性测试，以确定暴露于聚对苯二甲酸乙二醇酯 （PET） 的影响、PET 的生物积累以及肌肉、鳃和肾脏组织中多种生物标志物的变化。微塑料的浓度模式如下： 肾组织 > 肌肉组织 > 鳃组织。微塑料摄入导致 AChE 抑制导致氧化还原和能量代谢指标显着增加。此外，IBR 分析呈现“响应-抗性-击穿”过程，表明 Cipangopaludina chinensis 具有对时间 （D14 和 D21） 和浓度 （0.10 mg/L 和 1.00 mg/L） 阈值的抗性。组织对微塑料的敏感性被排在鳃 > 、 > 肾脏 、 与微塑料积累相反的顺序上。这些发现表明，不太敏感的组织储存了更多的污染物，这表明组织对微塑料的敏感性降低，微塑料发生率更高。这项研究为生物对污染胁迫的抵抗力提供了新的见解，值得进一步研究其潜在机制。