Benchmarking community structure of estuarine-dependent nekton near the Aransas Pass inlet

The purpose of this study is to determine the baseline seasonal community structure of estuarine-dependent nekton (fish, shrimp, and crab) in the Aransas Pass inlet region to establish a pre-operational benchmark prior to newly proposed industrial development in this area. Many nekton occurring in coastal waters share a common estuarine-dependent life history strategy characterized by near-shore spawning in the Gulf of Mexico with larvae migrating through tidal inlets into shallow estuarine nursery habitats. Access to high-quality habitat and spawning grounds via tidal inlets is essential for the reproduction, growth, survival, and maintenance of these populations. Because 75% of commercially or recreationally important species in the Gulf are estuarine-dependent, evaluating how anthropogenic activities may impair this connection between Gulf and bay waters is critical to understanding the population dynamics in this system and how these factors may affect juvenile fish development and fishery productivity. The Aransas Pass inlet is the major tidal inlet for the region, and anthropogenic activities that may alter water chemistry, flow, and quality have the potential for significant negative impacts on the marine life using this migration corridor. The proposed industrial development of the Aransas Pass inlet region (e.g., Harbor Island) presents a critical opportunity to establish baseline community structure in the adjacent estuarine habitats. We found strong evidence that the Aransas Pass, where impacts from industrial development are likely to occur, and Packery Channel (located ~35 km south), where these impacts will likely be absent, inlets have wide-ranging differences in nekton recruitment and development at individual species and community levels. Based on the findings of this study, we recommend continued long-term monitoring in the Aransas Pass and Packery Channel inlet regions to establish baseline variability and appropriately capture planned and unplanned future natural and anthropogenic disturbances and scenarios of environmental change. Baseline studies such as this facilitate effective management plans to preserve the function of these inlet regions as nurseries and fulfill the CBBEP mission to protect and restore the health and productivity of Coastal Bend bays and estuaries while supporting continued economic growth and public use of the bays

17β-Estradiol induces changes in cytokine levels in head kidney and blood of juvenile sea bass (Dicentrarchus labrax, L., 1758)

International audienc

Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review

10.1080/10643389.2021.1915052Critical Reviews in Environmental Science and Technology52183244-328

A holistic assessment of polyethylene fiber ingestion in larval and juvenile Japanese Medaka fish

Microplastic pollution is of public concern for global environmental health, aquaculture, and fisheries. Toxicity studies have shown that microplastic ingestion may cause intestinal damage, microbiota dysbiosis, and disturb lipid and energy metabolism in fish. To determine the impact of environmentally relevant, chronic, low dose microplastic fibers on fish health, medaka larvae and juveniles were exposed to five concentrations of polyethylene (PE) fibers for 21 days through the feed. Fish growth & condition were assessed to determine the overall impact on fish health. To identify impaired energy intake, gastrointestinal tract (GIT) integrity was evaluated at the molecular and cellular levels. Microbiota analysis was performed by comparing the top 7 most abundant phyla present in both larval and juvenile fish exposed to 0, 1.5, and 3 PE fibers/fish/day. A shift in the phyla Proteobacteria and Bacteroidetes were observed. Larval samples demonstrated decreased proteobacteria abundance, while juvenile samples displayed an increase in abundance. Relative gene expression of key digestive genes from GIT tissue was quantified using real-time quantitative polymerase chain reaction. An effect on digestive gene expression potentially affecting nutrient absorption and antioxidant production was indicated via a significant decrease of solute carrier family 6 member 6 expression in larvae exposed to 6 fibers/fish/day. No significant molecular changes were observed in juvenile GIT tissue, although a non-monotonous dose-response was observed. GIT morphology was analyzed using histomorphological observations of the GIT mucus and cell types. No significant impairment of the GIT epithelial layers was observed in larvae or juveniles. To assess growth & condition, Fulton's condition factor was measured. No differences were observed in larval or juvenile growth. Comparisons of different developmental stages allowed for identifying vulnerable developmental stages for microplastic exposure; larvae were more susceptible to molecular changes, while shifts in juvenile microbial communities were similar to changes reported post-polystyrene microplastic sphere exposure. This study is one of the first to provide toxicological data on the risk of PE fiber ingestion during fish development stages. Results indicate no imminent threat to fish condition at current measured environmental levels of microplastics; however, close monitoring of vital spawning grounds for commercially important fishes is recommended

Sex-specific immunomodulatory action of the environmentalestrogen 17α-ethynylestradiol alongside with reproductive impairment in fish.

Estrogenic endocrine disrupting chemicals (EEDCs) are present ubiquitously in sediments and aquatic ecosystems worldwide. The detrimental impact of EEDCs on the reproduction of wildlife is widely recognized. Increasing evidence shows the immunosuppressive effects of EEDCs in vertebrates. Yet, no studies have considered concomitantly EEDC-induced impacts on reproductive impairment and immune suppression in vivo, which are deemed essential for risk assessment and environmental monitoring. In this study, EE2 was used as a representative EEDC, for parallel evaluation of EEDC-induced immune suppression (immune marker gene expression, leukocyte numbers, host resistance assay, and immune competence index) and reproductive impairment (estrogen responsive gene expression, fecundity, fertilization success, hatching success, and reproductive competence index) in an established fish model (marine medaka Oryzias melastigma), considering sex-specific induction and adaptation and recovery responses under different EE2 exposure scenarios. The findings in marine medaka reveal distinct sex differences in the EE2-mediated biological responses. For female fish, low concentration of exogenous EE2 (33 ng/L) could induce hormesis (immune enhancement), enable adaptation (restored reproduction) and even boost fish resistance to bacterial challenge after abatement of EE2. However, a prolonged exposure to high levels of EE2 (113 ng/L) not only impaired F0 immune function, but also perturbed females recovering from reproductive impairment, resulting in a persistent impact on the F1 generation output. Thus, for female fish, the exposure concentration of EE2 is more critical than the dose of EE2 in determining the impacts of EE2 on immune function and reproduction. Conversely, male fish are far more sensitive than females to the presence of low levels of exogenous EE2 in water and the EE2-mediated biological impacts are clearly dose-dependent. It is also evident in male fish that direct contact of EE2 is essential to sustain impairments of immune competence and reproductive output as well as deregulation of immune function genes in vivo. The immunomodulatory pathways altered by EE2 were deciphered for male and female fish, separately. Downregulation of hepatic tlr3 and c3 (in female) and tlr3, tlr5 and c3 (in male) may be indicative of impaired fish immune competence. Taken together, impaired immune competence in the EE2-exposed fish poses an immediate thread on the survival of F0 population. Impaired reproduction in the EE2-exposed fish can directly affect F1 output. Parallel evaluation of immune competence and reproduction are important considerations when assessing the risk of sublethal levels of EE2/EEDCs in aquatic environments

Assessment of parental beno[a]pyrene exposure-induced cross-generational neurotoxicity and changes in offspring sperm DNA methylome in medaka fish

Previous studies have revealed that DNA methylation changes could serve as potential genomic markers for environmental benzo[a]pyrene (BaP) exposure and intergenerational inheritance of various physiological impairments (e.g. obesity and reproductive pathologies). As a typical aromatic hydrocarbon pollutant, direct BaP exposure has been shown to induce neurotoxicity. To unravel the inheritance mechanisms of the BaP-induced bone phenotype in freshwater medaka, we conducted whole-genome bisulfte sequencing of F1 sperm and identifed 776 differentially methylated genes (DMGs). Ingenuity pathway analysis revealed that DMGs were signif cantly enriched in pathways associated with neuronal development and function. Therefore, it was hypothesized that parental BaP exposure (1 μg/l, 21 days) causes offspring neurotoxicity. Furthermore, the possibility for sperm methylation as an indicator for a neu rotoxic phenotype was investigated. The F0 adult brains and F1 larvae were analyzed for BaP-induced direct and inherited toxicity. Acetylcholinesterase activity was signifcantly reduced in the larvae, together with decreased swimming velocity. Molecular analysis revealed that the marker genes associated with neuron development and growth (alpha1-tubulin, mbp, syn2a, shh, and gap43) as well as brain development (dlx2, otx2, and krox-20) were universally downregulated in the F1 larvae (3 days post-hatching). While parental BaP exposure at an environmentally relevant concentration could induce neurotoxicity in the developing larvae, the brain function of the exposed F0 adults was unaffected. This indicates that developmental neurotoxicity in larvae may result from impaired neuronal devel opment and differentiation, causing delayed brain growth. The present study demonstrates that the possible adverse health effects of BaP in the environment are more extensive than currently understood. Thus, the possibility of multigenerational BaP toxicity should be included in environmental risk assessments.This work was supported by funding from the Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou) (SMSEGL20SC02) and the National Natural Science Foundation of China (No. 41977371). Dr F.S. was supported by the National Institute of Environmental Health Sciences of the National Institutes of Health under award number 1R15ES032936-01

The role of DNA methylation on gene expression in the vertebrae of ancestrally benzo[a]pyrene exposed F1 and F3 male medaka

Benzo[a]pyrene (BaP) is ubiquitously present in the aquatic environment and has been identified as a bone toxicant. Previous studies have demonstrated that ancestral BaP exposure can cause transgenerational bone deformities in fish. Transgenerational effects are thought to be caused by heritable epigenetic changes, such as DNA methylation, histone modification, and non-coding RNAs. To investigate the role of DNA methylation in BaP-induced transgenerational skeletal deformities and the related transcriptomic changes in deformed vertebrae, we examined the vertebrae of male F1 and F3 medaka fish using high-throughput RNA sequencing (RNA-seq) and whole-genome bisulphite sequencing (WGBS). The histological results revealed that osteoblast numbers at the vertebral bone decreased in the BaP-derived F1 and F3 adult males in comparison with the control group. Differentially methylated genes (DMGs) associated with osteoblastogenesis (F1 and F3), chondrogenesis (F1 and F3), and osteoclastogenesis (F3) were identified. However, RNA-seq data did not support the role of DNA methylation in the regulation of genes involved in skeletogenesis since there was very little correlation between the level of differential methylation and gene expression profiles related to skeletogenesis. Although DNA methylation plays a major role in the epigenetic regulation of gene expression, the dysregulation of vertebral gene expression patterns observed in the current study is most likely to be mediated by histone modification and miRNAs. Notably, RNA-seq and WGBS data indicated that genes related to nervous system development are more sensitive to ancestral BaP exposure, indicating a more complex transgenerational phenotype in response to ancestral BaP exposure