Detection of long chain per- and polyfluoroalkyl substances (PFAS) in the benthic Golden tilefish (Lopholatilus chamaeleonticeps) and their association with microscopic hepatic changes.

Oceans are major sinks for anthropogenic pollutants, including per- and polyfluoroalkyl substances (PFAS). Although PFAS have been detected in surface waters globally, this is the first report of PFAS in a deep (170-400 m) demersal species in the Gulf of Mexico (GoM). Golden Tilefish (Lopholatilus chamaeleonticeps) plasma extracts (n = 185) were investigated for the presence of PFAS using ultra-high performance liquid chromatography-tandem mass spectrometry. A subset of liver tissues (n = 51) were also analyzed for microscopic hepatic changes (MHCs). Overall, nine of the 110 PFAS targeted were detected in Tilefish plasma at relatively high frequencies. Plasma concentrations of total PFAS (Σ9PFAS) ranged from below the detection limit to 27.9 ng g-1 w.w. Significant regional differences were observed with the highest concentrations of PFAS detected in the north central region of the GoM, where substantial industrialization and discharges from the Mississippi River occur. Compared to most wildlife and matrices analyzed globally, the PFAS profiles in Tilefish were unique as they are dominated by PFUnDA. Profile differences are hypothesized to be the result of Tilefish's distinctive lifestyle, habitat, diet, and partitioning characteristics of long-chain PFAS. Several MHCs were identified in this subset of Tilefish that could be detrimental to their health. Significant correlations between PFAS concentrations and biometric indices and MHCs were evident, however, additional research is needed to investigate the role PFAS and PFAS combined with chemical admixtures may play in inducing observed hepatic changes and other physiological effects in Tilefish. These findings give insight into the fate of PFAS at depth in aquatic ecosystems and are cause for concern regarding the health of other deep water benthic biota in GoM and other deepwater sinks for PFAS.

Developmental exposure to valproic acid alters the expression of microRNAs involved in neurodevelopment in zebrafish.

Congenital malformations are a prevalent cause of infant mortality in the United States and their induction has been linked to a variety of factors, including exposure to teratogens. However, the molecular mechanisms of teratogenicity are not fully understood. MicroRNAs are an important group of small, non-coding RNAs that regulate mRNA expression. MicroRNA roles in early embryonic development are well established, and their disruption during development can cause abnormalities. We hypothesized that developmental exposure to teratogens such as valproic acid alters microRNA expression profiles in developing embryos. Valproic acid is an anticonvulsant and mood-stabilizing drug used to treat epilepsy, bipolar disorder and migraines. To examine the effects of valproic acid on microRNA expression during development, we used zebrafish embryos as a model vertebrate developmental system. Zebrafish embryos were continuously exposed to valproic acid (1mM) or vehicle control (ethanol) starting from 4h post-fertilization (hpf) and sampled at 48 and 96hpf to determine the miRNA expression profiles prior to and after the onset of developmental defects. At 96hpf, 95% of the larvae showed skeletal deformities, abnormal swimming behavior, and pericardial effusion. Microarray expression profiling was done using Agilent zebrafish miRNA microarrays. Microarray results revealed changes in miRNA expression at both time points. Thirteen miRNAs were differentially expressed at 48hpf and 22 miRNAs were altered at 96hpf. Among them, six miRNAs (miR-16a, 18c, 122, 132, 457b, and 724) were common to both time points. Bioinformatic target prediction and examination of published literature revealed that these miRNAs target several genes involved in the normal functioning of the central nervous system. These results suggest that the teratogenic effects of valproic acid could involve altered miRNA expression.