In this study, we evaluated accumulation and adverse effects of ingestion of microplastics in the monogonont rotifer (Brachionus koreanus). The dependence of microplastic toxicity on particle size was investigated by measuring several in vivo end points and studying the ingestion and egestion using 0.05-, 0.5-, and 6-μm nonfunctionalized polystyrene microbeads. To identify the defense mechanisms activated in response to microplastic exposure, the activities of several antioxidant-related enzymes and the phosphorylation status of mitogen-activated protein kinases (MAPKs) were determined. Exposure to polystyrene microbeads of all sizes led to significant sizedependent effects, including reduced growth rate, reduced fecundity, decreased lifespan and longer reproduction time. Rotifers exposed to 6-μm fluorescently labeled microbeads exhibited almost no fluorescence after 24 h, while rotifers exposed to 0.05-and 0.5-μm fluorescently labeled microbeads displayed fluorescence until 48 h, suggesting that 6-μm microbeads are more effectively egested from B. koreanus than 0.05-or 0.5-μm microbeads. This observation provides a potential explanation for our findings that microbead toxicity was sizedependent and smaller microbeads were more toxic. In vitro tests revealed that antioxidant-related enzymes and MAPK signaling pathways were significantly activated in response to microplastic exposure in a size-dependent manner.

Microplastic pollution causes a major concern in the marine environment due to their worldwide distribution, persistence, and adverse effects of these pollutants in the marine ecosystem. Despite its global presence, there is still a lack of information on the effect of microplastics on marine organisms at the molecular level. Herein we demonstrated ingestion and egestion of nano- (0.05 μm) and micro-sized (0.5 and 6 μm) polystyrene microbeads in the marine copepod Paracyclopina nana, and examined molecular responses to exposure to microbeads with in vivo endpoints such as growth rate and fecundity. Also, we proposed an adverse outcome pathway for microplastic exposure that covers molecular and individual levels. This study provides the first insight into the mode of action in terms of microplastic-induced oxidative stress and related signaling pathways in P. nana.

Cytochrome P450 (CYP) proteins are involved in the first line of detoxification mechanism against diverse polycyclic aromatic hydrocarbons (PAHs) including benzo[a]pyrene (B[a]P). In aquatic invertebrates, there is still a lack of knowledge on the CYP genes involved in the molecular response to B[a]P exposure due to limited gene information. In this study, we cloned the entire 25 CYP genes in the monogonont rotifer Brachionus koreanus with the aid of next generation sequencing (NGS) technologies and analyzed their transcript profiles with a real-time RT-PCR array to better understand B[a]P-triggered molecular response over different time courses. As a result, B[a]P exposure induced CYP2/3-involved detoxification mechanisms and defensome, including phase II detoxification and antioxidant systems with a modulation of the chaperone heat shock protein (hsp) expression but did not change expression of other CYP clans in B. koreanus . Therefore, we found that B[a]P induced a strong detoxification mechanism to overcome detrimental effects of B[a]P associated with B[a]P-induced growth retardation as a trade-off in fitness costs. Also, this approach revealed that the entire CYP profiling can be a way of providing a better understanding on the mode of action of B[a]P in B. koreanus with respect to molecular defense metabolism.

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