Cigarette smoke extract (CSE), a complex mixture of compounds, contributes to a range of eye diseases; however, the underlying pathophysiological responses to tobacco smoke remain ambiguous. The purpose of the present study was to evaluate the cigarette smoke-induced phenotypic and transcriptomic changes in the corneal epithelium with a view to elucidating the likely underlying mechanism. Accordingly, for the first time, we characterized the genome-wide effects of CSE on the corneal epithelium. The ocular surface of the mice in the experimental groups was exposed to CSE for 1 h per day for a period of one week, while mice in the control group were exposed to preservative-free artificial tears. Corneal fluorescein staining, in vivo confocal microscopy and scanning electron microscopy were performed to examine the corneal ultrastructure. Transcriptome sequencing and bioinformatics analysis were performed followed by RT-qPCR to validate gene expression changes. The results indicate that CSE exposure disrupted the structural integrity of the superficial epithelium, decreased the density of microvilli, and compromised the corneal epithelial barrier intactness. RNA-seq revealed 667 differentially expressed genes, and functional analysis highlighted the enhancement of several biological processes such as antioxidant activity and the response to oxidative stress. Moreover, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that glutathione metabolism and drug metabolism cytochrome P450 were the most relevant pathways contributing to the effects of CSE on the corneal epithelium. Protein–protein interaction (PPI) network analysis illustrated that GCLC, NQO1, and HMOX1 were the most relevant nodes. In conclusion, the present study indicates that CSE exposure induces changes in the phenotype and genotype of the corneal epithelium. The antioxidant response element is essential for counteracting the effects of cigarette smoke on this tissue layer. These results shed novel insights into how cigarette smoke damages this ocular surface.

Most chemical plant wastewater contains both organic and inorganic pollutants, which are easy to diffuse along with surface runoff. The combined pollution of nonylphenol (NP) and cadmium (Cd) in soil is a serious problem that has not attracted enough attention. Based on the effects of selenium (Se) and Pseudomonas aeruginosa (P. aeruginosa) on plant and soil microbial communities, we speculated that the application of Se and P. aeruginosa in soil could improve the phytoremediation efficiency of ryegrass on contaminated soil. In this study, pot experiments with Cd and NP co-contaminated soil were conducted, and the results showed that application of P. aeruinosa alone could improve the removal rates of NP and Cd by ryegrass, and the supplementary of Se further enhanced the effect of micro-phyto remediation, with the highest removal rates of NP and Cd were 79.6% and 49.4%, respectively. The application of P. aeruginosa plus Se reduced the adsorption of Cd and NP through C–O and Si–O–Fe of the soil, changed the enzyme activity, and also affected the changing trend of the microbial community in soil. Pseudomonas, Sphingomonadales, Nitrospira, and other beneficial bacteria were enriched after a 60-day period with P. aeruginosa and Se treatment, thus promoting the removal of NP and Cd. In light of the above results, we suggest that P. aeruginosa application can efficiently facilitate the phytoremediation of ryegrass on Cd-NP co-contaminated soil, and Se supplementation in soil showed the synergistic effect on the remediation.

Fluoxetine is frequently detected in aquatic environment, and chronic FLX exposure exhibits adverse effects on aquatic communities. Its chirality makes the adverse effects more complicated. This study aimed at the enantioselective cardiotoxicity in developmental zebrafish induced by racemic (rac-)/S-/R-fluoxetine. The accumulation profiles demonstrated that biotransformation of fluoxetine to norfluoxetine occurred during rac-fluoxetine exposure, with a higher enrichment of S-norfluoxetine than R-norfluoxetine. Heart malformations including pericardial edema, circulation abnormalities, and thrombosis were observed, and enantioselective changes also occurred. According to H&E staining and Masson’s trichrome staining, the loose severity of cardiac structure and cardiac fibrosis in rac-norfluoxetine treated group was worse than that in fluoxetine treated groups. Results of toxicity-associated parameters in our homochiral enantiomers’ exposure also indicated that the toxicity induced by S-fluoxetine was more severe than R-fluoxetine. Enantioselective arrhythmia in developmental zebrafish after chiral fluoxetine exposure could be caused by myocardial fibrosis, abnormal developmental processes, and the biotransformation of fluoxetine to norfluoxetine could make that worse. Our findings can be used to assess the environmental risk of the two enantiomers of fluoxetine that induce cardiotoxicity in aquatic organisms.

Although many polymers are known by their toxicity, we know nothing about the impact of polyethylene glycol (PEG) on anurofauna. Its presence in different products and disposal in aquatic environments turn assessments about its impact on amphibians an urgent matter. Accordingly, we tested the hypothesis that short-time exposure (72 h) of tadpoles belonging to the species Physalaemus cuvieri (Anura, Leptodactylidae) to PEG induces oxidative stress and neurotoxicity on them. We observed that polymer uptake in P. cuvieri occurred after exposure to 5 and 10 mg/L of PEG without inducing changes in their nitrite levels neither at the levels of substances reactive to thiobarbituric acid. However, hydrogen peroxide and reactive oxygen species production was higher in animals exposed to PEG, whose catalase and superoxide dismutase levels were not enough to counterbalance the production of these reactive species. Therefore, this finding suggests physiological changes altering REDOX homeostasis into oxidative stress. In addition, the increased activity of acetylcholinesterase and butyrylcholinesterase, and reduction in superficial neuromasts, confirmed PEG’s neurotoxic potential. To the best of our knowledge, this is the first report on PEG’s biological impact on a particular amphibian species. The study has broadened the understanding about ecotoxicological risks associated with water pollution by these polymers, as well as motivated further investigations on its impacts on amphibians’ health and on the dynamics of their natural populations.

Numerous studies have established that acute or chronic exposure to environmental pollutants like particulate matter (PM) leads to the development of accelerated aging related pathologies including pulmonary and cardiovascular diseases, and thus air pollution is one of the major global threats to human health. Air pollutant particulate matter 2.5 (PM₂.₅)-induced cellular dysfunction impairs tissue homeostasis and causes vascular and cardiopulmonary damage. To test a hypothesis that elevated plasminogen activator inhibitor-1 (PAI-1) levels play a pivotal role in air pollutant-induced cardiopulmonary pathologies, we examined the efficacy of a drug-like novel inhibitor of PAI-1, TM5614, in treating PM₂.₅-induced vascular and cardiopulmonary pathologies. Results from biochemical, histological, and immunohistochemical studies revealed that PM₂.₅ increases the circulating levels of PAI-1 and thrombin and that TM5614 treatment completely abrogates these effects in plasma. PM₂.₅ significantly augments the levels of pro-inflammatory cytokine interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF), and this also can be reversed by TM5614, indicating its efficacy in amelioration of PM₂.₅-induced increases in inflammatory and pro-thrombotic factors. TM5614 reduces PM₂.₅-induced increased levels of inflammatory markers cluster of differentiation 107 b (Mac3) and phospho-signal transducer and activator of transcription-3 (pSTAT3), adhesion molecule vascular cell adhesion molecule 1 (VCAM1), and apoptotic marker cleaved caspase 3. Longer exposure to PM₂.₅ induces pulmonary and cardiac thrombosis, but TM5614 significantly ameliorates PM₂.₅-induced vascular thrombosis. TM5614 also reduces PM₂.₅-induced increased blood pressure and heart weight. In vitro cell culture studies revealed that PM₂.₅ induces the levels of PAI-1, type I collagen, fibronectin (Millipore), and sterol regulatory element binding protein-1 and 2 (SREBP-1 and SREBP-2), transcription factors that mediate profibrogenic signaling, in cardiac fibroblasts. TM5614 abrogated that stimulation, indicating that it may block PM₂.₅-induced PAI-1 and profibrogenic signaling through suppression of SREBP-1 and 2. Furthermore, TM5614 blocked PM₂.₅-mediated suppression of nuclear factor erythroid related factor 2 (Nrf2), a major antioxidant regulator, in cardiac fibroblasts. Pharmacological inhibition of PAI-1 with TM5614 is a promising therapeutic approach to control air pollutant PM₂.₅-induced cardiopulmonary and vascular pathologies.

Methane emitted by insects is considered to be an important source of atmospheric methane. Here we report the stimulation of methane emission in the cockroach Periplaneta americana and termite Coptotermes chaohuensis, insects with abundant methanogens, by neonicotinoids, insecticides widely used to control insect pests. Cycloxaprid (CYC) and imidacloprid (IMI) caused foregut expansion in P. americana, and increased the methane emission. Antibiotics mostly eliminated the effects. In P. americana guts, hydrogen levels increased and pH values decreased, which could be significantly explained by the gut bacterium community change. The proportion of several bacterium genera increased in guts following CYC treatment, and two genera from four could generate hydrogen. Hydrogen is a central intermediate in methanogenesis. All increased methanogens in both foregut and hindgut used hydrogen as electron donor to produce methane. Besides, the up-regulation of mcrA, encoding the enzyme for the final step of methanogenesis suggested the enhanced methane production ability in present methanogens. In the termite, hydrogen levels in gut and methane emission also significantly increased after neonicotinoid treatment, which was similar to the results in P. americana. In summary, neonicotinoids changed bacterium community in P. americana gut to generate more hydrogen, which then stimulated gut methanogens to produce and emit more methane. The finding raised a new concern over neonicotinoid applications, and might be a potential environmental risk associated with atmospheric methane.

In addition to endocrine disruption, bisphenol A (BPA) is known to induce inflammation through the activation of nuclear factor-κB (NF-κB). However, detailed studies on the mechanism of NF-κB activation by BPA have not been sufficiently conducted. In the present study, we observed that low concentrations of BPA (≤1 μM) upregulated the release of proinflammatory mediators, including nitric oxide (NO) and prostaglandin E₂ (PGE₂), as well as proinflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-12, and IL-6. Molecular modeling predicted that BPA docked with the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) complex activates downstream molecules including myeloid differentiation primary response 88 (MyD88) and IL-1 receptor-associated kinase 4 (IRAK-4) and results in the upregulation of the NF-κB signaling pathway. Additionally, BPA increased morphological abnormalities and mortality in zebrafish larvae and enhanced the dispersal of macrophages and neutrophils in the whole body, thereby causing an endotoxemia-like disorder. However, a specific TLR4 inhibitor, TLR4-IN-C34, mitigated BPA-induced mortality and morphological abnormalities, which indicates that the TLR4/MD2 complex is a molecular target of BPA-induced immunotoxicity. Collectively, our results indicate that low concentrations of BPA, which is a potential agonist of the TLR4/MD2 complex, can intensify the immune response and eventually cause an endotoxemia-like disorder.

An increase in polycyclic aromatic hydrocarbon (PAH) pollution poses significant challenges to human and ecosystem health in the Three Gorges Reservoir (TGR) of the Yangtze River. Based on the combination of PAH analysis with qPCR and high-throughput sequencing of bacteria, 32 topsoil samples collected from 16 sites along the TGR were used to investigate the distribution and biodegradation pathways of PAHs in the water-level-fluctuation zone (WLFZ). The results indicated that the concentrations of PAHs were 43.8–228.2 and 30.8–206.3 ng/g soil (dry weight) under the high- and low-water-level (HWL and LWL) conditions, respectively. The PAH concentration in urban areas was higher than that in rural areas. Under both the HWL and LWL conditions, the abundance of the bamA gene, a biomarker of anaerobic PAH biodegradation, was significantly higher than that of the ring-hydroxylating-dioxygenase (RHD) gene, a biomarker of aerobic PAH biodegradation. The abundance of the bamA gene was significantly positively correlated with PAHs (R² = 0.8), and the biodegradation percentage of PAHs incubated anaerobically was greater than that in the aerobically incubated microcosm experiments. These data implicated a key role of the anaerobic pathway in PAH biodegradation. Co-occurrence network analysis suggested that anaerobic Anaerolineaceae, Dechloromonas, Bacteroidetes_vadin HA17 and Geobacter were key participants in the biodegradation of PAHs. The diversity analysis of functional bacteria based on the bamA gene and microcosm experiments further demonstrated that nitrate was the primary electron acceptor for PAH biodegradation. These findings provide a new perspective on the mechanism of PAH biodegradation in the TGR and knowledge that can be used to develop strategies for environmental management.

The spread of antibiotic resistance genes (ARGs) is a global environmental issue. Dissolved biochar is more likely to contact bacteria in water, producing ecological risks. This study explored the effects of dissolved biochar on ARGs transfer in bacteria. Conjugative transfer efficiency was significantly different following treatment with different types of dissolved biochar. Typically, humic acid-like substance in dissolved biochar can significantly improve the transfer efficiency of ARGs between bacteria. When the concentration of dissolved biochar was ≤10 mg biochar/mL, humic acid-like substance substantially promoted ARGs transfer. An increase in dissolved biochar concentration weakened the ARGs transfer from humic acid-like substance. The inhibitory effects of small-molecule matters dominated, decreasing conjugative transfer frequency. At a concentration of 100 mg biochar/mL, the conjugative transfer efficiency of all treatments was lower than that of control. Compared with corn straw dissolved biochar, there were more transconjugants in pine sawdust dissolved biochar. Following treatment with 10 mg biochar/mL pine sawdust dissolved biochar, the number of transconjugants was at its maximum; approximately 7.3 folds higher than the control. We also explored mechanisms by which dissolved biochar impacts conjugative transfer. Due to the complex composition of dissolved biochar, its effects on the expression of conjugative transfer-related genes were also dynamic. This study investigates the ecological risk of biochar and guides its scientific application.

Current understanding of biochar's effect on antibiotic resistance genes (ARGs) in soil is limited, and whether the effect could change after long-term field aging remains largely unknown. In this study, we employed high-throughput quantitative PCR to assess the effect of biochar amendment on soil resistome as affected by three years of field aging. Application of fresh biochar significantly elevated the number and abundance of ARGs in the manured soil, but did not show such effect under pakchoi cultivation. The presence of aged biochar caused a marked reduction of ARGs only in the planted manured soil. Results of principal coordinate analysis and structural equation modeling indicate that biochar's effect on soil ARG profile was changed by field aging through altering soil microbial composition. These results highlight the necessity of considering aging effect of biochar during its on-farm application to mitigate soil antibiotic resistance.