The hepatopancreas is one of the largest organs playing crucial roles in metabolism and detoxification in crustacean invertebrates. Although toxicities have been increasingly documented for the two ubiquitous pollutants, hexabromocyclododecane (HBCD) and microplastics (MPs), in model animals, little is known about their impacts on the hepatopancreas of crustaceans. To fill this knowledge gap, the effects of MPs and HBCD, alone or in combination, on the hepatopancreas were evaluated in a commercially important crustacean species (the whiteleg shrimp) by histological observation as well as quantification of hepatic lesion-, metabolism-, and detoxification-related parameters. In addition, to reveal potential mechanisms underlying the hepatoxicity observed, the accumulation of HBCD in the shrimp and the status of oxidative stress were also investigated. Our results demonstrated that exposure of the whiteleg shrimp to MPs and HBCD for 4 weeks resulted in evident histological injury in the hepatopancreas and marked elevation in hepatic lesion markers (alanine aminotransferase and aspartate aminotransferase) in the hemolymph. Moreover, both metabolism (activity of phosphofructokinase, contents of lactic acid and adenosine triphosphate, and expression of metabolism-related genes) and detoxification (contents of cytochrome P450, UDP-glucuronosyltransferase, and glutathione, activity of glutathione S-transferase, and expression of detoxification-related genes) were found to be disrupted by the pollutants tested. In addition, exposure to MPs and HBCD also led to alterations in the contents and/or activities of antioxidant enzymes and resulted in oxidative damage to the hepatopancreas (indicated by marked elevation in malondialdehyde content). Furthermore, a significant amount of HBCD accumulated in shrimp treated with HBCD-containing seawater. The data also illustrated that HBCD-MP coexposure was more toxic than single exposure to these pollutants. These findings suggest that MPs and HBCD may exert hepatotoxic impacts on whiteleg shrimp by accumulating in vivo and inducing oxidative stress, which could pose a severe threat to the health of this important crustacean species.

肝胰腺是最大的器官之一，在甲壳类无脊椎动物的新陈代谢和解毒过程中起着至关重要的作用。尽管越来越多地记录了两种普遍存在的污染物六溴环十二烷 (HBCD) 和微塑料 (MP) 在模型动物中的毒性，但人们对它们对甲壳类动物肝胰腺的影响知之甚少。为填补这一知识空白，通过组织学观察以及肝损伤、代谢和代谢的量化，评估了 MPs 和六溴环十二烷单独或组合对具有重要商业价值的甲壳类动物（白对虾）肝胰腺的影响。解毒相关参数。此外，为了揭示观察到的肝毒性、六溴环十二烷在虾体内的积累和氧化应激状态的潜在机制也被调查了。我们的结果表明，白对虾暴露于 MPs 和六溴环十二烷 4 周会导致肝胰腺发生明显的组织学损伤，并且血淋巴中的肝损伤标志物（谷丙转氨酶和天冬氨酸转氨酶）显着升高。此外，代谢（磷酸果糖激酶的活性、乳酸和三磷酸腺苷的含量以及代谢相关基因的表达）和解毒（细胞色素P450、UDP-葡萄糖醛酸转移酶和谷胱甘肽、谷胱甘肽 S-转移酶的活性和解毒相关基因的表达）被发现被测试的污染物破坏。此外，接触 MPs 和 HBCD 还会导致抗氧化酶的含量和/或活性发生变化，并导致肝胰腺氧化损伤（表现为丙二醛含量显着升高）。此外，用含六溴环十二烷的海水处理过的虾体内积累了大量六溴环十二烷。数据还表明，与单次接触这些污染物相比，HBCD-MP 共同接触的毒性更大。这些发现表明 MPs 和 HBCD 可能通过体内蓄积对白对虾产生肝毒性影响并诱发氧化应激，这可能对这种重要的甲壳类动物的健康构成严重威胁。