Triclocarban (TCC) is the principal component in personal and health care products because it is a highly effective, broad-spectrum, and safe antibacterial agent. TCC has recently been discovered in aquatic creatures and has been shown to constitute a health danger to aquatic animals. Although several studies have looked into the toxicological effects of TCC on a variety of aquatic animals from algae to fish, the possible gut-toxicity molecular pathway in zebrafish has never been thoroughly explored. We investigated the gut-toxic effects of TCC on zebrafish by exposing them to different TCC concentrations (100 and 1000 μg/L) for 21 days. We discovered for the first time that the MAPK and TLR signaling pathways related to gut diseases were significantly altered, and inflammation (up-regulation of TNF-α, IL-6, and IL-1β) caused by TCC was confirmed to be largely mediated by the aryl hydrocarbon receptor (AHR) and its related cytokines. This was found using the results of qPCR, a transcriptome analysis, and molecular docking (AHR, AHRR, CYP1A1 and CYP1B1). Furthermore, high-throughput 16S rDNA sequencing demonstrated that TCC exposure reduced the bacterial diversity and changed the gut microbial composition, with the primary phyla Fusobacteria and Proteobacteria, as well as the genera Cetobacterium and Rhodobacteraceae, being the most affected. TCC exposure also caused damage to the gut tissue, including an increase in the number of goblet cells and a reduction in the height of the columnar epithelium and the thickness of the muscular layer, as shown by hematoxylin and eosin staining. Our findings will aid in understanding of the mechanism TCC-induced aquatic toxicity in aquatic species.
Keywords: Gut; Inflammation; Microbiota dysbiosis; Triclocarban; Zebrafish.
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