The toxicity of microplastics and their leachates to embryonic development of the sea cucumber Apostichopus japonicus.

Microplastic pollution has been widely detected across the global ocean, posing a major threat to a wide variety of marine biota. To date, the deleterious impacts of microplastics have predominantly been linked to their direct exposure, while the potential risks posed by the leachates emanating from microplastics have received comparatively less attention. Here, the toxicity of virgin plasticized polyvinyl chloride (PVC) microspheres and their leachates were evaluated on the embryo-larval development of sea cucumber Apostichopus japonicus using an in-vitro assay. Results showed that a significant toxic effect of both PVC microspheres and their leachates on the embryo development and larval growth of sea cucumbers follows a dose-dependent and time-dependent pattern. Nonetheless, the toxicity of PVC leachates surpasses that of the microspheres themselves. Abnormal developmental phenotypes, such as aberrant gastrulation, misaligned mesenchymal cells, and delayed arm development, were also observed in embryos and larvae treated with PVC. Further chemical analyses of PVC microspheres and leachates revealed the existence of five distinct phthalate esters (PAEs), with DIBP (diisobutyl phthalate) and DBP (dibutyl phthalate) exhibiting higher concentrations in the PVC leachates. This finding suggests that the elevated toxicity of plastic leachate may be attributed to the leaching of phthalate additives from the plastic particles.

Sulfide causes histological damage, oxidative stress, metabolic disorders and gut microbiota dysbiosis in juvenile sea cucumber Apostichopus japonicus Selenka.

Sulfide is a common harmful substance in sediments, with an especially high risk for deposit feeder organisms. The sea cucumber Apostichopus japonicus is a typical benthic feeder, and its intestine is the first line of defense and serves as a crucial barrier function. In this study, histological, physiological, gut microbiota, and metabolomic analyses were performed to explore the toxic response in the intestine of juvenile A. japonicus exposed to 0, 0.8, and 1.6 mg/L sulfide stress for 96 h. The results revealed sulfide-induced intestinal inflammatory symptoms and oxidative stress. Moreover, gut bacterial composition was observed after sulfide exposure, with an increase in Proteobacteria and a decrease in Cyanobacteria and Planctomycetes. Specifically, sulfide increased a set of sulfide-removing bacteria and opportunistic pathogens while decreasing several putative beneficial substance-producing bacteria. The metabolomic analysis indicated that sulfide also disturbed metabolic homeostasis, especially lipid and energy metabolism, in intestine. Interestingly, several intestinal bacteria were further identified to be significantly correlated with metabolic changes; for example, the decreased abundance levels of Bacillus, Corynebacterium, and Psychromonas were positively correlated with important energy metabolites, including maleic acid, farnesyl pyrophosphate, thiamine, butynoic acid, and deoxycholic acid. Thus, our research provides new insights into the mechanisms associated with the intestinal metabolic and microbiota response involved in sulfide stress adaptation strategies of juvenile A. japonicus.