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Mercury (Hg), a heavy metal pollutant worldwide, can be transformed into methylmercury (MeHg) by various aquatic microorganisms in water, thus accumulating along the aquatic food chain and posing a particular challenge to human health. Zooplankton plays a crucial role in aquatic ecosystems and serves as a major component of the food chain. To evaluate the effects of MeHg on the rotifer Brachionus plicatilis and reveal the underlying mechanism of these effects, we exposed B. plicatilis to MeHg by either direct immersion or by feeding with MeHg-poisoned Chlorella pyrenoidesa, respectively, and conducted a transcriptomic analysis. The results showed that B. plicatilis directly exposed to MeHg by immersion showed significant enrichment of the glutathione metabolism pathway for detoxification of MeHg. In addition, the exposure to MeHg by feeding induced a significant enrichment of lysosome and notch signaling pathways of rotifers, supporting the hypothesis that MeHg can induce autophagy dysfunction in cells and disturb the nervous system of rotifers. In two different routes of MeHg exposure, the pathway of cytochrome P450 in rotifers showed significant enrichment for resisting MeHg toxicity. Our results suggest further studies on the potential mechanism and biological responses of MeHg toxicity in other links of the aquatic food chain., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Methylmercury (MeHg) readily accumulates in aquatic organisms while transferring and amplifying in the aquatic food chains. This study firstly explores the in vivo accumulation sites and metabolic regulation of MeHg in the rotifer Brachionus plicatilis by aggregation-induced emission fluorogen (AIEgen) and metabolomics. Fluorescent image analysis by AIEgen showed that MeHg in B. plicatilis mainly occured in the ciliary corona, esophagus, mastax, stomach and intestine in the direct absorption group. In the other group, where B. plicatilis were indirectly supplied with MeHg via food intake, the accumulation of MeHg in the rotifer occurred in the ciliary corona, various digestive organs, and the pedal gland. However, the MeHg accumulated in the rotifer is difficult to metabolize outside the body. Metabolomics analysis showed that the significant enrichment of ABC transporters was induced by the direct exposure of rotifers to dissolved MeHg. In contrast, exposure of rotifers to MeHg via food intake appeared to influence carbon, galactose, alanine, aspartate and glutamate metabolisms. Besides, the disturbed biological pathways such as histidine metabolism, beta-alanine metabolism and pantothenate and CoA biosynthesis in rotifers may be associated with L-aspartic acid upregulation in the feeding group. The significant enrichment of ABC transporters and carbon metabolism in rotifers may be related to the accumulation of MeHg in the intestine of rotifers. In both pathways of MeHg exposure, the arginine biosynthesis and metabolism of rotifers were disturbed, which may support the hypothesis that rotifers produce more energy to resist MeHg toxicity. This study provides new insight into the accumulation and toxicity mechanisms of MeHg on marine invertebrates from the macro and micro perspectives., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)