Acute polyethylene microplastic (PE-MPs) exposure activates the intestinal mucosal immune network pathway in adult zebrafish (Danio rerio).

Polyethylene is one of the most important plastic types with the highest consumption in the world. Plastics are prone to photodegradation and turn into microplastics, which are magnified as they move across trophic levels. Microplastics would be able to penetrate into lymph even cross cell membranes, causing harm to the lymphatic and/or circulatory systems, accumulating in secondary organs, and impacting the immune system and cell health. The objective of this study was to test that the activation of the intestinal immune network might be caused by disruption of intestinal microbiota after exposure to different polyethylene microplastics (PE-MPs) concentrations (1, 10, 100, and 1000 µg/mL) in adult zebrafish (Danio rerio) for 7 days. The concentrations of PE-MPs (100 and 1000 µg/mL) exposure decreased the goblet cell coverage. The intestinal microbial diversity index (Shannon and Simpson) was increased at 100 and 1000 µg/mL PE-MPs concentrations. The relative abundance of intestinal dominant microbiota phylum Proteobacteria and Actinobacteria increased significantly (P < 0.05); however, phylum Fusobacteria decreased significantly (P < 0.05). The relative abundance of intestinal microbiota at level of genera showed varying degrees of elevation such as Acinetobacter (6.31-fold), Plesiomonas (4.80-fold), Flavobacterium (10.54-fold) and Pseudomonas (5.17-fold) in 1000 µg/mL PE-MPs. Intestinal innate immunity-complement C3 and C4 content first increased and then declined in a dose-dependent manner. Expression of genes from the intestinal immune network for mucosal immunoglobulin production were increased also in a dose-dependent manner. The expression of immune-related genes (pigr, il10 and ighv4-5) were positively correlated with the relative abundance of genera Plesiomonas. In conclusion, PE-MPs increase the infection probability in the intestinal mucosa by altering the abundance of intestinal dominant microbiota at the level of phylum. PE-MPs exposure activated the intestinal immune network pathway for mucosal immunoglobulin production at a concentration of 100 or 1000 µg/mL for 7 days.

Effects of Per- and Polyfluoroalkyl Substance Mixtures on the Susceptibility of Larval American Bullfrogs to Parasites.

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants known to adversely affect health and development in many taxa. Although PFAS generally occur as mixtures in the environment, little is known about the effects of PFAS mixtures on organisms compared to single chemical exposures. Moreover, PFAS exposure in nature occurs alongside biotic factors such as parasitism. Even though host-parasite interactions are common in natural systems, there is little information about how PFAS affect these interactions. Here, we examined the effects of PFAS mixtures on the susceptibility of larval American bullfrogs (Rana catesbeiana) to echinostomes. Our PFAS treatments included perfluorooctanesulfonic acid (PFOS) at 4 and 10 ppb, two mixtures without PFOS as a component at 6 and 10 ppb total PFAS, and a mixture containing PFOS at 10 ppb total PFAS. We found that a 62-day PFAS exposure increased parasite loads by 42-100% in all treatments relative to the control. Additionally, we found that the singular exposure to PFOS increased parasite loads by ∼40% compared to a mixture containing PFOS suggesting antagonism among PFAS in mixtures. Our results highlight the need for further investigation into the effects of PFAS mixtures on organisms and how PFAS affect common ecological interactions.

The combined effect of Macondo oil and corexit on sheepshead minnow (Cyprinodon variegatus) during early development.

During the 2010 Deepwater Horizon (DWH), oil spill an estimated 800 million L oil and 7.9 million L dispersant entered the environment. The potential adverse effects of the oil-dispersant mixture are poorly understood. The aim of this study was to investigate the impacts of this mixture on early development of sheepshead minnow (Cyprinodon variegatus), a small-bodied estuarine fish commonly found in the area affected by the DWH spill. Embryos were exposed to a chemically enhanced water accommodated fraction (CEWAF; 10:1 mixture of Macondo oil; Corexit 9500) for 48 hr, after which organisms were maintained in uncontaminated water for an additional 8 days. Impacts were assessed on embryonic (heart rate, development of eye pigmentation, embryonic movement measured) and larval (time to hatch, larval survival, standard length, and cyp1a gene expression) development. No significant alterations were found in survival, time to hatch or cyp1a at the end of the experiment. However, CEWAF induced significant decreases in heart rate of embryos, delayed development of eye pigmentation, reduced embryonic movement, and diminished standard length. These results indicate potential sublethal adverse consequences attributed to CEWAF exposure during early development, even in the absence of maintained cyp1a induction or survival rate, potentially affecting the fitness of organisms later in life.

Vascular toxicity of silver nanoparticles to developing zebrafish (Danio rerio).

Nanoparticles (NPs, 1-100 nm) can enter the environment and result in exposure to humans and other organisms leading to potential adverse health effects. The aim of the present study is to evaluate the effects of early life exposure to polyvinylpyrrolidone-coated silver nanoparticles (PVP-AgNPs, 50 nm), particularly with respect to vascular toxicity on zebrafish embryos and larvae (Danio rerio). Previously published data has suggested that PVP-AgNP exposure can inhibit the expression of genes within the vascular endothelial growth factor (VEGF) signaling pathway, leading to delayed and abnormal vascular development. Here, we show that early acute exposure (0-12 h post-fertilization, hpf) of embryos to PVP-AgNPs at 1 mg/L or higher results in a transient, dose-dependent induction in VEGF-related gene expression that returns to baseline levels at hatching (72 hpf). Hatching results in normoxia, negating the effects of AgNPs on vascular development. Interestingly, increased gene transcription was not followed by the production of associated proteins within the VEGF pathway, which we attribute to NP-induced stress in the endoplasmic reticulum (ER). The impaired translation may be responsible for the observed delays in vascular development at later stages, and for smaller larvae size at hatching. Silver ion (Ag(+)) concentrations were < 0.001 mg/L at all times, with no significant effects on the VEGF pathway. We propose that PVP-AgNPs temporarily delay embryonic vascular development by interfering with oxygen diffusion into the egg, leading to hypoxic conditions and ER stress.