Transcriptome analysis reveals benzotriazole ultraviolet stabilizers regulate networks related to inflammation in juvenile zebrafish (Danio rerio) brain.

Abstract

Benzotriazole ultraviolet stabilizers (BUVSs) are widely applied ultraviolet absorbing compounds in industrial materials and personal care products. Due to their ubiquitous use and reports of bio-accumulation in aquatic organisms, these compounds are significant environmental pollutants; however, data are limited for BUVSs toxicity. In this study, juvenile zebrafish (Danio rerio) were exposed to 4 commonly used BUVSs (UV-234, UV-326, UV-329, and UV-P) at one dose of 10 or 100 μg/L for 28 days. To characterize the underlying mechanisms of different BUVSs-induced toxicities, we performed global transcriptome sequencing (RNA-Seq) in the brain (100 μg/L). There were 390, 575, 483, and 470 differentially expressed genes (DEGs) detected following UV-234, UV-326, UV-329, and UV-P exposure at 100 μg/L, respectively. Only 59 genes were identified as DEGs following exposure to each of the BUVSs, suggesting that these chemicals can induce unique responses in fish. Noteworthy was that there were 81 common gene networks (~10%) identified following exposure to BUVSs, many of which were related to inflammation and immune function. Uniquely regulated pathways affected by different BUVSs included those related to mitochondrial respiration, interleukin 1/brain-damaging signaling, dopaminergic signaling, and adrenergic receptor cascades. Furthermore, quantitative PCR (qPCR) results revealed that mgst1 levels were increased in fish from the 100 μg/L UV-329 treatment, while the expression of pck2 was significantly down-regulated in fish from both the 10 and 100 μg/L UV-P treatment. Transcriptomic data suggest that BUVSs can alter mitochondrial bioenergetics, alter expression of a broad range of genes in the oxidative stress response, and can induce pathways related to the immune system in zebrafish brain.