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1. Epigenetic inheritance of DNA methylation changes in fish living in hydrogen sulfide–rich springs

   https://doi.org/10.1073/pnas.2014929118  

   Kelley, Joanna L.; Tobler, Michael; Beck, Daniel; Sadler-Riggleman, Ingrid; Quackenbush, Corey R.; Arias Rodriguez, Lenin; Skinner, Michael K. (June 2021, Proceedings of the National Academy of Sciences)

   Environmental factors can promote phenotypic variation through alterations in the epigenome and facilitate adaptation of an organism to the environment. Although hydrogen sulfide is toxic to most organisms, the fish Poecilia mexicana has adapted to survive in environments with high levels that exceed toxicity thresholds by orders of magnitude. Epigenetic changes in response to this environmental stressor were examined by assessing DNA methylation alterations in red blood cells, which are nucleated in fish. Males and females were sampled from sulfidic and nonsulfidic natural environments; individuals were also propagated for two generations in a nonsulfidic laboratory environment. We compared epimutations between the sexes as well as field and laboratory populations. For both the wild-caught (F0) and the laboratory-reared (F2) fish, comparing the sulfidic and nonsulfidic populations revealed evidence for significant differential DNA methylation regions (DMRs). More importantly, there was over 80% overlap in DMRs across generations, suggesting that the DMRs have stable generational inheritance in the absence of the sulfidic environment. This is an example of epigenetic generational stability after the removal of an environmental stressor. The DMR-associated genes were related to sulfur toxicity and metabolic processes. These findings suggest that adaptation of P. mexicana to sulfidic environments in southern Mexico may, in part, be promoted through epigenetic DNA methylation alterations that become stable and are inherited by subsequent generations independent of the environment. 

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2. Accumulation of Nanoplastics in Biomphalaria glabrata Embryos and Transgenerational Developmental Effects

   https://doi.org/10.3390/environments12010028  

   Martin, Leisha; Armendarez, Carly; Merrill, Mackenzie; Huang, Chi; Xu, Wei (January 2025, Environments)

   (1) Background: Nanoplastics are emerging environmental pollutants with potential toxic effects on aquatic organisms. This study investigates the toxicity of NPs in Biomphalaria glabrata, a freshwater snail species widely used as a bioindicator species in ecotoxicology studies.; (2) Methods: We exposed three generations (F0–F2) of B. glabrata snail embryos to different sizes of polystyrene nanoparticles and assessed responses.; (3) Results: We observed severe effects on F0 to F2 B. glabrata embryos, including size-dependent (30 to 500 nm) increases in mortality rates, size and dosage-dependent (1 to 100 ppm) effects on hatching rates with concentration-dependent toxicity in the 30 nm exposure group. The F2 generation embryos appear to be most responsive to detoxification (CYP450) and pollutant metabolism (HSP70) at 48-h-post-treatment (HPT), while our developmental marker (MATN1) was highly upregulated at 96-HPT. We also report a particle-size-dependent correlation in HSP70 and CYP450 mRNA expression, as well as enhanced upregulation in the offspring of exposed snails. We also observed significant reductions in hatching rates for F2.; (4) Conclusions: These findings indicate that F2 generation embryos appear to exhibit increased stress from toxic substances inherited from their parents and grandparents (F1 and F0). This study provides valuable insights into the impact of plastic particulate pollution on multiple generations and highlights the importance of monitoring and mitigating plastic waste. 

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3. Emerging investigator series: linking chemical transformations of silver and silver nanoparticles in the extracellular and intracellular environments to their bio-reactivity

   https://doi.org/10.1039/c9en00710e  

   Minghetti, Matteo; Dudefoi, William; Ma, Qing; Catalano, Jeffrey G. (October 2019, Environmental Science: Nano)

   The fish intestine is an important barrier for environmental toxicants, including metals and metal nanoparticles. Tracking chemical transformation at the interface between the intestinal epithelium and the intestinal lumen can inform us about chemicals' bio-reactivity and toxicity but is challenging due to the lack of appropriate models. To allow for such investigations, a model of the fish intestine derived from rainbow trout ( Oncorhynchus mykiss ), the RTgutGC cell line, was used. Cells were exposed to silver nitrate (AgNO 3 ) or citrate coated silver nanoparticles (cit-AgNPs) in Leibovitz's L-15 medium without amino acids and vitamins (L-15/ex), which allowed the determination of the extracellular silver species using a chemical equilibrium model. X-ray absorption spectroscopy (XAS) was used to track intracellular silver speciation. Cellular toxicity, silver accumulation, and metallothionein (MT) mRNA levels were also measured. Cells accumulated the same concentrations of silver when exposed to equimolar amounts ( i.e. 1, 5 and 10 μM) of AgNO 3 or cit-AgNPs. However, AgNO 3 was shown to be more toxic than cit-AgNPs. Intracellular silver speciation changed over time in both exposure series. After 1 hour, intracellular silver speciation was dominated by chloride complexation in both exposures. After 24 and 72 hours of exposure to cit-AgNPs, ∼7% of silver was complexed to cysteine, whereas the remaining silver was AgNPs. In cells exposed to AgNO 3 for 72 hours, 97% of Ag was complexed to cysteine. A significant increase, compared to controls, in metallothionein mRNA levels at 24 and 72 hours of exposure to AgNO 3 and cit-AgNPs can explain the formation of Ag–cysteine complexes. In summary, these data show that silver chloride species are bioavailable and that complexation to cysteine scavenges intracellular dissolved silver ions, thus preventing toxicity. Silver nanoparticles present a similar but attenuated toxic response to AgNO 3 . Thus, at least in acute exposures, existing risk assessment for dissolved silver species could be protective for nanosilver. 

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4. Silver Nanoparticles Stable to Oxidation and Silver Ion Release Show Size-Dependent Toxicity In Vivo

   https://doi.org/10.3390/nano11061516  

   Cunningham, Brittany; Engstrom, Arek M.; Harper, Bryan J.; Harper, Stacey L.; Mackiewicz, Marilyn R. (June 2021, Nanomaterials)

   null (Ed.)

   Silver nanoparticles (AgNPs) are widely used in commerce, however, the effect of their physicochemical properties on toxicity remains debatable because of the confounding presence of Ag+ ions. Thus, we designed a series of AgNPs that are stable to surface oxidation and Ag+ ion release. AgNPs were coated with a hybrid lipid membrane comprised of L-phosphatidylcholine (PC), sodium oleate (SOA), and a stoichiometric amount of hexanethiol (HT) to produce oxidant-resistant AgNPs, Ag–SOA–PC–HT. The stability of 7-month aged, 20–100 nm Ag–SOA–PC–HT NPs were assessed using UV–Vis, dynamic light scattering (DLS), and inductively coupled plasma mass spectrometry (ICP-MS), while the toxicity of the nanomaterials was assessed using a well-established, 5-day embryonic zebrafish assay at concentrations ranging from 0–12 mg/L. There was no change in the size of the AgNPs from freshly made samples or 7-month aged samples and minimal Ag+ ion release (<0.2%) in fishwater (FW) up to seven days. Toxicity studies revealed AgNP size- and concentration-dependent effects. Increased mortality and sublethal morphological abnormalities were observed at higher concentrations with smaller nanoparticle sizes. This study, for the first time, determined the effect of AgNP size on toxicity in the absence of Ag+ ions as a confounding variable. 

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5. Zinc Finger Readers of Methylated DNA

   https://doi.org/10.3390/molecules23102555  

   Hudson, Nicholas O.; Buck-Koehntop, Bethany A. (October 2018, Molecules)

   DNA methylation is a prevalent epigenetic modification involved in regulating a number of essential cellular processes, including genomic accessibility and transcriptional outcomes. As such, aberrant alterations in global DNA methylation patterns have been associated with a growing number of disease conditions. Nevertheless, the full mechanisms by which DNA methylation information is interpreted and translated into genomic responses is not yet fully understood. Methyl-CpG binding proteins (MBPs) function as important mediators of this essential process by selectively reading DNA methylation signals and translating this information into down-stream cellular outcomes. The Cys2His2 zinc finger scaffold is one of the most abundant DNA binding motifs found within human transcription factors, yet only a few zinc finger containing proteins capable of conferring selectivity for mCpG over CpG sites have been characterized. This review summarizes our current structural understanding for the mechanisms by which the zinc finger MBPs evaluated to date read this essential epigenetic mark. Further, some of the biological implications for mCpG readout elicited by this family of MBPs are discussed. 

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