Abstract

Fluoride has been found to cause detrimental effects on fish gills. Despite essential roles in various metabolism activities, whether and how miRNAs participate in the course of toxicity caused by fluoride in gills is still unclear. In this study, male zebrafish were exposed to 0, 20, 40 mg/L fluoride for 60 days to study the underlying osmotic regulatory mechanism by determining the influences of fluoride on the miRNAs and regulated genes in gills. mRNAs were isolated from the gills and the expression profiles were analyzed by using Illumina Hiseq 2500 platforms. Expressions of 7 differentially miRNAs and some related-genes in gills were validated by qRT-PCR. The results showed that miRNAs expressions were notably altered by fluoride. A total of 584 and 327 miRNAs were remarkably changed after 20 and 40 mg/L fluoride exposure, of which 322 were increased and 262 were decreased in 20 mg/L fluoride group, whereas 219 were elevated and 108 were reduced in 40 mg/L fluoride group. The differentially expressive miRNAs confirmed by qRT-PCR were consistent with micro-assay data. Cluster of Orthologous Groups of proteins (COG) function classification showed that the target genes of differentially expressive miRNAs are mainly related to signal transduction mechanisms, replication, transcription, inorganic ion transport and metabolism, repair and recombination, and energy formation and transformation. In addition, fluoride disturbed the expressions of target genes involved in the osmoregulation of the gill in the fluoride-exposed zebrafish, such as the increased expressions of OSTF1 and the decreased expressions of Na⁺-K⁺-ATPase, CFTR, and AQP-3, which provides a possibility that miRNAs regulation induced by fluoride has an effects on osmotic regulation, providing new hints to the osmotic regulatory mechanism of the toxicity caused by fluoride in zebrafish, and distinguishes new biomarkers of miRNAs for fluoride toxicity.

*Original abstract online at https://www.sciencedirect.com/science/article/abs/pii/S0166445X21000485

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