The blood–follicle barrier (BFB) between the blood and follicular fluid (FF) can maintain the microenvironment balance of oocyte. Boron, an exogenous environmental trace element, has been found to possibly play an important role in oocyte maturation. This study aimed to examine the distribution characteristics of boron across the BFB and find the potential effect of boron on FF microenvironment. We analyzed the concentration of boron in paired FF and serum collected from 168 women undergoing in vitro fertilization and embryo transfer in Beijing City and Shandong Province, China. To explore the potential health impact of boron enrichment in oocyte maturation, a global proteomics analysis was conducted to tentatively correlate the protein levels with the boron enrichment. Interestingly, the results showed that the concentration of boron in FF (34.5 ng/mL) was significantly higher than that in serum (22.0 ng/mL), with a median concentration ratio of 1.52. Likewise, the concentrations of boron in FF and serum were positively correlated (r = 0.446), suggesting that boron concentration in serum can represent its concentration in follicular fluid to a large extent.. This is the first time to observe the enrichment of boron in the FF to our knowledge. It is interesting to observe a total of 13 proteins, which mainly belong to immunoglobulin class, were positively correlated with boron concentration in FF. We concluded that boron, as one environmental trace element, was enriched in FF from blood validated by two area in north china, which may be involved in an increased level of immune processes of immunoglobulins.

Fine particulate matter (PM₂.₅) has been associated with risk of oral and respiratory diseases. However, the biological mechanisms of adverse oral and respiratory health response to PM₂.₅ fluctuation have not been well characterized. This study aims to explore the relationships of PM₂.₅ with airway inflammation, salivary biomarkers and buccal mucosa microbiota. We performed a panel study among 40 college students involving 4 follow-ups from August to October 2021 in Hefei, Anhui Province, China. Health outcomes included fractional exhaled nitric oxide (FeNO), salivary biomarkers [C-reactive protein (CRP), cortisol, lysozyme and alpha-amylase] and buccal mucosa microbial diversity. Linear mixed-effect models were applied to explore the cumulative impacts of PM₂.₅ on health indicators. PM₂.₅ was positively correlated with FeNO, CRP, cortisol and alpha-amylase, while negatively with lysozyme. Per 10-μg/m³ increase in PM₂.₅ was linked to maximum increments in FeNO of 10.71% (95%CI: 2.01%, 19.41%) at lag 0–24 h, in CRP of 7.10% (95%CI: 5.39%, 8.81%) at lag 0–24 h, in cortisol of 1.25% (95%CI: 0.44%, 2.07%) at lag 0–48 h, and in alpha-amylase of 2.12% (95%CI: 0.53%, 3.71%) at lag 0–24 h, while associated with maximum decrement in lysozyme of 0.53% (95%CI: 0.12%, 0.95%) at lag 0–72 h. Increased PM₂.₅ was linked to reduction in the richness and evenness of buccal microbe and o_Bacillales and o_Bacteroidales were identified as differential microbes after PM₂.₅ inhalation. Bio-information analysis indicated that immunity system pathway was the most important enriched abundant process altered by PM₂.₅ exposure. In summary, short-term PM₂.₅ exposure may impair oral and respiratory health by inducing inflammatory and stress responses, weakening immune function and altering buccal mucosa microbial diversity.

Ambient air pollutants are well-known risk factors for childhood asthma and asthma exacerbation. It is unknown whether different air pollutants individually or jointly affect pathophysiological mechanisms of asthma. In this study, we aim to integrate transcriptome and untargeted metabolome to identify dysregulated genetic and metabolic pathways that are associated with exposures to a mixture of ambient and traffic-related air pollutants among adults with asthma history. In this cross-sectional study, 102 young adults with childhood asthma history were enrolled from southern California in 2012. Whole blood transcriptome was measured with 20,869 expression signatures, and serum untargeted metabolomics including 937 metabolites were analyzed by Metabolon, Inc. Participants’ exposures to regional air pollutants (NO₂, O₃, PM₁₀, PM₂.₅) and near-roadway air pollutants averaged at one month and one year before study visit were estimated based on residential addresses. xMWAS network analysis and joint-pathway analysis were performed to identify subnetworks and genetic and metabolic pathways that were associated with exposure to air pollutants adjusted for socio-characteristic covariates. Network analysis found that exposures to air pollutants mixture were connected to 357 gene markers and 92 metabolites. One-year and one-month averaged PM₂.₅ and NO₂ were associated with several amino acids related to serine, glycine, and beta-alanine metabolism. Lower serum levels of carnosine and aspartate, which are involved in the beta-alanine metabolic pathway, as well as choline were also associated with worse asthma control (p < 0.05). One-year and one-month averaged PM₁₀ and one-month averaged O₃ were associated with higher gene expression levels of HSPA5, LGMN, CTSL and HLA-DPB1, which are involved in antigen processing and presentation. These results indicate that exposures to various air pollutants are associated with altered genetic and metabolic pathways that affect anti-oxidative capacity and immune response and can potentially contribute to asthma-related pathophysiology.

Tributyltin (TBT) is a widely used organotin compound around the world and was frequently detected in surface waters, which would pose risk to aquatic organisms. However, the mechanisms of TBT-induced toxicity is not full clear. The present study investigated the effects of the tributyltin (TBT) on the blood parameters, immune responses and thyroid hormone system in zebrafish. Fish were exposed to sublethal concentrations of TBT (10 ng/L, 100 ng/L and 300 ng/L) for 6 weeks. The effects of long-term exposure to TBT on blood parameters (NH3, ammonia; GLU, glucose; TP, total proteins; CK, creatine kinase; ALT, alanine aminotransferase; AST, aspartate aminotransferase), immune responses (Lys, lysozyme; IgM, immunoglobulin M) and some indexes related thyroid hormone system (T3, 3,5,3′-triiodothyronine; T4, thyroxine) were measured in zebrafish, as well as the expression of genes related to immune responses and thyroid hormone system. Based on the results, the physiological-biochemical responses was significantly enhanced with an increase in TBT concentration, reflected by the abnormal blood indices, dysregulation of endocrine system and immunotoxicity in zebrafish under TBT stress. The present study greatly extends our understanding of adverse effects of TBT on aquatic organisms.

Global climate change (GCC) significantly affects aquatic ecosystems. Continual use of pyrethroid insecticides results in contamination of these ecosystems and concurrent GCC raises the potential for synergistic effects. Resistance to pyrethroids has been documented in Hyalella azteca, a common epibenthic amphipod and model organism. Resistant H. azteca can bioconcentrate elevated amounts of pyrethroids and represent a threat to consumers via trophic transfer. In the present study, a predator of H. azteca, the inland silverside (Menidia beryllina), was used to examine the impacts of GCC on pyrethroid bioaccumulation via trophic transfer from resistant prey organisms. M. beryllina were fed ¹⁴C-permethrin dosed pyrethroid-resistant H. azteca for 14 days at three salinities (6, 13 and 20 practical salinity units (PSU)) and two temperatures (18 and 23 °C). Fish were analyzed for total body residues, percent parent compound and percent metabolites. Gene expression in liver and brain tissue were evaluated to assess whether dietary bioaccumulation of permethrin would impact detoxification processes, metabolism, and general stress responses. M. beryllina bioaccumulated significant amounts of permethrin across all treatments, ranging from 39 to 557 ng g⁻¹ lipid. No statistically significant effect of temperature was found on total bioaccumulation. Salinity had a significant effect on total bioaccumulation, owing to greater bioaccumulation at 6 PSU compared to 13 and 20 PSU, which may be due to alterations to xenobiotic elimination. Permethrin bioaccumulation and the interaction with temperature and salinity elicited significant transcriptional responses in genes relating to detoxification, growth, development, and immune response. Given the increased prevalence of pesticide-resistant aquatic invertebrates, GCC-induced alterations to temperature and salinity, and the predicted increase in pesticide usage, these findings suggest trophic transfer may play an important role in pesticide bioaccumulation and effects in predatory fish.

As ubiquitous, persistent organic pollutants, polycyclic aromatic hydrocarbons (PAHs) have adverse impacts on human health. Phenanthrene (Phe) is one of the most abundant PAHs in the environment. However, the long-term effects of exposure to environmental level of Phe on the kidneys and the potential mechanisms are unclear. T helper (Th) cells, a subtype of CD4⁺ T cells that play a central role in the renal immune microenvironment. In this study, male mice were chronically exposed to 5, 50, and 500 ng/kg bw Phe every other day for total 210 days. Those results indicated that environmental Phe exposure caused kidney hypertrophy, injury and fibrosis in the mice. Chronic, long-term environmental level of Phe exposure did not significantly alter the innate immune response but induced adaptive immune response changes (Th1/Th2 related cytokines release), causing a type 1 immune response in the 5 ng/kg bw Phe group and a type 2 immune response in the high dose groups (50 and 500 ng/kg bw). This study provides novel insights into the roles of adaptive immune response in long-term PAH exposure-induced chronic kidney injury and fibrosis, which is beneficial for further understanding the potential health hazards of PAHs and providing new avenues for immune intervention strategies to alleviate PAHs toxicity.

Microcystis aeruginosa (MA) is a primary hazardous cyanobacteria species in aquatic ecosystems that can produce microcystin-LR (MC-LR), which harms aquatic animals. The intestine is an important target tissue for MA and MC-LR. In this study, we investigated the effects of MA and MC-LR exposure on the intestinal microbiota variation and immune responses of Litopenaeus vannamei. Shrimp were experimentally exposed to MA and MC-LR for 72 h. The results showed that both MA and MC-LR exposure caused marked histological variation and apoptosis characteristics and increased oxidative stress in the intestine. Furthermore, the relative expression levels of antimicrobial peptide genes (ALF, Crus, Pen-3) decreased, while those of pro-inflammatory cytokines (MyD88, Rel, TNF-a), a pattern-recognition receptor (TLR4) and a mediator of apoptosis (Casp-3) increased. MA and MC-LR exposure also caused intestinal microbiota variation, including decreasing microbial diversity and disturbing microbial composition. Specifically, the relative abundance of Proteobacteria decreased in the two stress groups; that of Bacteroidetes decreased in the MA group but increased in the MC-LR group, while Tenericutes varied inversely with Bacteroidetes. Our results indicate that MA and MC-LR exposure causes intestinal histopathological and microbiota variations and induces oxidative stress and immune responses in L. vannamei. In conclusion, this study reveals the negative effects of MA and MC-LR on the intestinal health of shrimp, which should be considered in aquaculture.

Both microplastics and persistent organic pollutants (POPs) are ubiquitously present in natural water environment, posing a potential threat to aquatic organisms. While it has been suggested that the immune responses of aquatic organisms could be hampered by exposure to microplastics and POPs, the synergistic immunotoxic impact of these two types of pollutants remain poorly understood. In addition, little is known about the mechanism behind the immunotoxic effect of microplastics. Therefore, in the present study, the immunotoxicity of microplastics and two POPs, benzo[a]pyrene (B[a]P) and 17β-estradiol (E2), were investigated alone or in combination in a bivalve species, Tegillarca granosa. Evident immunotoxicity, as indicated by alterations of haemocyte count, blood cell composition, phagocytic activity, intracellular content of ROS, concentration of Ca²⁺ and lysozyme, and lysozyme activity, was revealed for both microplastics and the two POPs examined. In addition, the expression of six immune-, Ca²⁺ signalling-, and apoptosis-related genes was significantly altered by exposure of clams to the contaminants studied. Furthermore, the toxicity of POPs was generally aggravated by smaller microplastics (500 nm) and mitigated by larger ones (30 μm). This size dependent effect on POP toxicity may result from size dependent interactions between microplastics and POPs. Data obtained in this study also indicate that similar to exposure to B[a]P and E2, exposure to microplastics may hamper the immune responses of clams through a series of interdependent physiological and molecular processes.

Microcystis aeruginosa is one of the main species of cyanobacteria that causes water blooms. M. aeruginosa can release into the water several types of microcystins (MCs), which are harmful to aquatic organisms and even humans. However, few studies have investigated the hepatotoxicity of M. aeruginosa itself in zebrafish in environments that simulate natural aquatic systems. The objective of this study was to evaluate the hepatotoxicity of M. aeruginosa in adult zebrafish (Danio rerio) after short-term (96 h) exposure and to elucidate the potential underlying mechanisms. Distinct histological changes in the liver, such as enlargement of the peripheral nuclei and sinusoids and the appearance of fibroblasts, were observed in zebrafish grown in M. aeruginosa culture. In addition, antioxidant enzyme activity was activated and protein phosphatase (PP) activity was significantly decreased with increasing microalgal density. A proteomic analysis revealed alterations in a number of protein pathways, including ribosome translation, immune response, energy metabolism and oxidative phosphorylation pathways. Western blot and real-time PCR analyses confirmed the results of the proteomic analysis. All results indicated that M. aeruginosa could disrupt hepatic functions in adult zebrafish, thus highlighting the necessity of ecotoxicity assessments for M. aeruginosa at environmentally relevant densities.

Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl2O3) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl2O3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg−1·day−1 nAl2O3 for 3 weeks. It was observed that exposure to nAl2O3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl2O3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl2O3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17.