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ABSTRACT The mummichog,Fundulus heteroclitus, an abundant estuarine fish broadly distributed along the eastern coast of North America, has repeatedly evolved tolerance to otherwise lethal levels of aromatic hydrocarbon exposure. This tolerance is linked to reduced activation of the aryl hydrocarbon receptor (AHR) signaling pathway. In other animals, the AHR has been shown to influence the gastrointestinal-associated microbial community, particularly when activated by the model toxic pollutant 3,3′,4,4′,5-pentachlorobiphenyl (PCB-126) and other dioxin-like compounds. To understand host population and PCB-126 exposure effects on mummichog gut microbiota, we sampled two populations of wild fish, one from a PCB-contaminated environment (New Bedford Harbor, MA, USA) and the other from a much less polluted location (Scorton Creek, MA, USA), as well as laboratory-reared F2 generation fish originating from each of these populations. We examined the microbes associated with the gut of these fish using amplicon sequencing of bacterial and archaeal small subunit ribosomal RNA genes. Fish living in the PCB-polluted site had high microbial alpha and beta diversity compared to fish from the low PCB site. These differences between wild fish were not present in laboratory-reared F2 fish that originated from the same populations. Microbial compositional differences existed between wild and lab-reared fish, with the wild fish dominated by Vibrionaceae and the lab-reared fish by Enterococceae. These results suggest that mummichog habitat and/or environmental conditions have a stronger influence on the mummichog gut microbiome compared to population or hereditary-based influences. Mummichog are important eco-evolutionary model organisms; this work reveals their importance for exploring host-environmental-microbiome dynamics. IMPORTANCEThe mummichog fish, a common resident of North America's east coast estuaries, has evolved the ability to survive in waters contaminated with toxic chemicals that would typically be deadly. Our study investigates how living in and adapting to these toxic environments may affect their gut microbiomes. We compared mummichogs from a polluted area in Massachusetts with those from a non-polluted site and found significant differences in their gut microbes. Interestingly, when we raised the next generation of these fish in a lab, these differences disappeared, suggesting that the environment plays a more crucial role in shaping the gut microbiome than genetics. Understanding these changes helps shed light on how animals and their associated microbiomes adapt to pollution, which can inform conservation efforts and our broader understanding of environmental impacts on host-microbe dynamics. 

Microplastics (MPs) have been found in a diverse range of organisms across trophic levels. While a majority of the information on organismal exposure to plastics in the environment comes from gastrointestinal (GI) data, the prevalence of MP particles in other tissues is not well understood. Additionally, many studies have not been able to detect the smallest, most prevalent, MPs (1 µm - 5 mm) that are the most likely to distribute to tissues in the body. To address these knowledge gaps, MPs in the GI tract and muscle of Atlantic killifish (Fundulus heteroclitus) collected from two sites (Falmouth and Bourne) on Buzzards Bay, Cape Cod, MA were quantified down to 2 µm in size. Eight fish from Falmouth and 10 fish Bourne site were analyzed. Fourier-transform infrared spectroscopy and Raman spectroscopy were used to identify all particles. The mean concentrations of MPs in the GI tract and muscle from fish collected from Falmouth was 85.5 ± 70.2 and 11 ± 12.5 particles per gram wet weight, respectively. Fish collected from Bourne site had mean particle concentrations of 12.2 ± 18.1 and 1.69 ± 5.36 particles per gram wet weight. Of the 2,008 particles analyzed in various fish tissue samples, only 3.4% (69 particles) were identified as plastic; polymers included nylon, polyethylene, polypropylene, and polyurethane. MPs detected in the GI tract samples also tended to be more diverse in both size and polymer type than those found in the muscle. We found that MPs < 50 µm, which are often not analyzed in the literature, were the most common in both the GI tract and muscle samples. There was not a significant correlation between the MP content in the muscle compared to the GI tract, indicating that GI tract MP abundance cannot be used to predict non-GI tract tissue MP content; however, MP abundance in muscle correlated with fish total length, suggesting potential bioaccumulation of these small MPs. 

Saxitoxin (STX) is a potent neurotoxin naturally produced by dinoflagellates and cyanobacteria. STX inhibits voltage-gated sodium channels (VGSCs), affecting the propagation of action potentials. Consumption of seafood contaminated with STX is responsible for paralytic shellfish poisoning (PSP). Humans are among the species most sensitive to PSP; neurological symptoms of exposure range from tingling of the extremities to severe paralysis. The objective of this study was to determine the effects of STX exposure on developmental processes during early embryogenesis. This study was designed to test the hypothesis that early developmental exposure to STX would disrupt key processes, particularly those related to neural development. Zebrafish embryos were exposed to STX (24 or 48 pg) or vehicle (0.3 mM HCl) at 6 hours post fertilization (hpf) via microinjection. There was no overt toxicity but starting at 36 hpf there was a temporary lack of pigmentation in STX-injected embryos, which resolved by 72 hpf. Using high performance liquid chromatography, we found that STX was retained in embryos up to 72 hpf in a dose-dependent manner. Temporal transcriptional profiling of embryos exposed to 48 pg STX per embryo revealed no differentially expressed genes (DEGs) at 24 hpf, but at 36 and 48 hpf, there were 3547 and 3356 DEGs, respectively. KEGG pathway
analysis revealed significant enrichment of genes related to focal adhesion, adherens junction and regulation of
actin cytoskeleton, suggesting that cell-cell and cell-extracellular matrix interactions were affected by STX. Genes affected are critical for axonal growth and the
development of functional neural
networks. We confirmed these findings by visualizing axonal defects in transgenic zebrafish with fluorescently labeled sensory neurons. In addition, our gene expression results suggest that STX exposure affects both canonical and noncanonical functions of VGSCs. Given the fundamental role of VGSCs in both physiology and development, these findings offer valuable insights into effects of exposure to neurotoxins. 

A diversity of chemicals are intentionally added to plastics to enhance their properties and aid in manufacture. Yet, the accumulated chemical composition of these materials is essentially unknown even to those within the supply chain, let alone to consumers or recyclers. Recent legislated and voluntary commitments to increase recycled content in plastic products highlight the practical challenges wrought by these chemical mixtures, amid growing public concern about the impacts of plastic-associated chemicals on environmental and human health. In this Perspective, we offer guidance for plastics manufacturers to collaborate across sectors and critically assess their use of added chemicals. The ultimate goal is to use fewer and better additives to promote a circular plastics economy with minimal risk to humans and the environment. 

In May 2021, the M/V X-Press Pearl ship fire disaster led to the largest maritime spill of resin pellets (nurdles) and burnt plastic (pyroplastic). Field samples collected from beaches in Sri Lanka nearest to the ship comprised nurdles and pieces of pyroplastic. Three years later, the toxicity of the spilled material remains unresolved. To begin understanding its potential toxicity, solvent extracts of the nurdles and pyroplastic were screened for their bioactivity by several Attagene FACTORIAL bioassays (TF, NR, and AquaTox), which measured the activity of a combined 70 human transcription factor response elements and nuclear receptors and 6 to 7 nuclear receptors for each of three phylogenetically distinct fish species. Extracts of the pyroplastics robustly activated end points for the human aryl hydrocarbon receptor (AhR), estrogen receptor (ER), pregnane X receptor (PXR), peroxisome proliferator-activated receptor (PPAR), retinoid X receptor (RXR), and oxidative stress (NRF2) and had the potential for activation of several others. The bioactivity profile of the pyroplastics was most similar (similarity score = 0.96) to that of probable human carcinogens benzo[b]fluoranthene and benzo[k]fluoranthene despite the extracts being a complex mixture of thousands of compounds. The activity diminished only slightly for extracts of pyroplastic collected eight months after the spill. The AquaTox FACTORIAL bioassay measured the activation of ERα, ERβ, androgen receptor (AR), PPARα, PPARγ, and RXRβ for human, zebrafish (Danio rerio), Japanese medaka (Oryzias latipes), and rainbow trout (Oncorhynchus mykiss), revealing species-specific sensitivities to the chemicals associated with the pyroplastics. These findings provide needed information to guide long-term monitoring efforts, make hazard assessments of the spilled material, and direct further research on pyroplastic, an emerging global contaminant. 

Abstract Harmful algal blooms (HABs) produce neurotoxins that affect human health. Developmental exposure of zebrafish embryos to the HAB toxin domoic acid (DomA) causes myelin defects, loss of reticulospinal neurons, and behavioral deficits. However, it is unclear whether DomA primarily targets myelin sheaths, leading to the loss of reticulospinal neurons, or reticulospinal neurons, causing myelin defects. Here, we show that while exposure to DomA at 2 dpf did not reduce the number of oligodendrocyte precursors prior to myelination, it led to fewer myelinating oligodendrocytes that produced shorter myelin sheaths and aberrantly wrapped neuron cell bodies. DomA-exposed larvae lacked Mauthner neurons prior to the onset of myelination, suggesting that axonal loss is not secondary to myelin defects. The loss of the axonal targets may have led oligodendrocytes to inappropriately myelinate neuronal cell bodies. Consistent with this, GANT61, a GLI1/2 inhibitor that reduces oligodendrocyte number, caused a reduction in aberrantly myelinated neuron cell bodies in DomA-exposed fish. Together, these results suggest that DomA initially alters reticulospinal neurons and the loss of axons causes aberrant myelination of nearby cell bodies. The identification of initial targets and perturbed cellular processes provides a mechanistic understanding of how DomA alters neurodevelopment, leading to structural and behavioral phenotypes. 

Abstract Harmful algal blooms produce potent neurotoxins that accumulate in seafood and are hazardous to human health. Developmental exposure to the harmful algal bloom toxin, domoic acid (DomA), has behavioral consequences well into adulthood, but the cellular and molecular mechanisms of DomA developmental neurotoxicity are largely unknown. To assess these, we exposed zebrafish embryos to DomA during the previously identified window of susceptibility and used the well-known startle response circuit as a tool to identify specific neuronal components that are targeted by exposure to DomA. Exposure to DomA reduced startle responsiveness to both auditory/vibrational and electrical stimuli, and even at the highest stimulus intensities tested, led to a dramatic reduction of one type of startle (short latency c-starts). Furthermore, DomA-exposed larvae had altered kinematics for both types of startle responses tested, exhibiting shallower bend angles and slower maximal angular velocities. Using vital dye staining, immunolabelling, and live imaging of transgenic lines, we determined that while the sensory inputs were intact, the reticulospinal neurons required for short latency c-starts were absent in most DomA-exposed larvae. Furthermore, axon tracing revealed that DomA-treated larvae also showed significantly reduced primary motor neuron axon collaterals. Overall, these results show that developmental exposure to DomA targets large reticulospinal neurons and motor neuron axon collaterals, resulting in measurable deficits in startle behavior. They further provide a framework for using the startle response circuit to identify specific neural populations disrupted by toxins or toxicants and to link these disruptions to functional consequences for neural circuit function and behavior.