Toxic Environmental Pollutants Research Articles

Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis.

The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.

Benzo[a]pyrene evokes epithelial-mesenchymal transition and pulmonary fibrosis through AhR-mediated Nrf2-p62 signaling

Benzo[a]pyrene (BaP) and its metabolic end product benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide (BPDE), are known toxic environmental pollutants. This study aimed to analyze whether sub-chronic BPDE exposure initiated pulmonary fibrosis and the potential mechanisms. In this work, male C57BL6/J mice were exposed to BPDE by dynamic inhalation exposure for 8 weeks. Our results indicated that sub-chronic BPDE exposure evoked pulmonary fibrosis and epithelial-mesenchymal transition (EMT) in mice. Both in vivo and in vitro, BPDE exposure promoted nuclear translocation of Snail. Further experiments indicated that nuclear factor erythroid 2-related factor 2 (Nrf2) and p62 were upregulated in BPDE-exposed alveolar epithelial cells. Moreover, Nrf2 siRNA transfection evidently attenuated BPDE-induced p62 upregulation. Besides, p62 shRNA inhibited BPDE-incurred Snail nuclear translocation and EMT. Mechanically, BPDE facilitated physical interaction between p62 and Snail in the nucleus, then repressed Snail protein degradation by p62-dependent autophagy-lysosome pathway, and finally upregulated transcriptional activity of Snail. Additionally, aryl hydrocarbon receptor (AhR) was activated in BPDE-treated alveolar epithelial cells. Dual-luciferase assay indicated activating AhR could bind to Nrf2 gene promoter. Moreover, pretreatment with CH223191 or α-naphthoflavone (α-NF), AhR antagonists, inhibited BPDE-activated Nrf2-p62 signaling, and alleviated BPDE-induced EMT and pulmonary fibrosis in mice. Taken together, AhR-mediated Nrf2-p62 signaling contributes to BaP-induced EMT and pulmonary fibrosis.

Long-term tributyltin exposure alters behavior, oocyte maturation, and histomorphology of the ovary due to oxidative stress in adult zebrafish

Tributyltin (TBT), an organotin endocrine-disrupting substance, is recognized as one of the important toxic environmental pollutants. The present study was carried out to investigate the toxic effects of TBT on behavior and the ovary of adult zebrafish with a focus on oxidative stress markers and oocyte maturation. Adult zebrafish were exposed to three different concentrations (125, 250, and 500 ng/L of water) of TBT for 28 days. TBT exposure produced a concentration-dependent negative effect on the body weight and behavior (anxiety-like symptoms) of adult zebrafish. Alterations in the activity of superoxide dismutase (SOD) and catalase (CAT), the total antioxidant capacity of ovarian tissue by the highest exposure level of TBT resulted in lipid peroxidation as indicated by increased malondialdehyde (MDA) level. The numbers of early-vitellogenic oocytes were significantly increased in zebrafish exposed to TBT as low as 125 ng/L. However, the numbers and size of fully-grown (mature) oocytes were significantly reduced in the highest exposure group only. Correlation between the MDA level and pre-vitellogenic oocytes in the 500 ng/L group indicated that lipid peroxidation prevented the maturation of pre-vitellogenic oocytes. TBT exposure produced significant histological changes in the ovary as evidenced by disturbed maturation of oocytes. In conclusion, TBT adversely affected the maturation of oocytes in zebrafish ovary through oxidative stress-mediated mechanisms.

Chemical health hazards and toxicity of environmental pollutants on humans, animals and others: An overview

Toxicology, rooted in ancient civilizations and evolving through pivotal historical figures like Paracelsus and Alice Hamilton, has become a multidisciplinary field encompassing various branches such as pharmacology, medical, forensic, and environmental toxicology. This exploration embarks on a journey through time and science, unravelling the intricate interplay between chemicals, pollutants, and their profound impacts on human, animal, and environmental well-being. Spanning from ancient practices like the use of hemlock in Greek capital punishment to modern-day concerns surrounding industrial chemicals and pesticides, the review delves into the mechanisms by which toxins disrupt biochemical pathways and induce organ dysfunctions. From heavy metals and pesticides persistent effects on the nervous and reproductive systems to the carcinogenic properties of polychlorinated biphenyls (PCBs), hydrocarbons, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs). The review highlights the diverse range of toxicants and their widespread impact on human health. Additionally, the review underscores the importance of proactive measures to mitigate exposure to harmful substances, advocating for the development of antidotes, bioremediation techniques, and stricter environmental regulations. By addressing the urgent need for comprehensive strategies to combat toxicological hazards, this review aims to contribute to ongoing efforts to safeguard public health and environmental sustainability in the face of evolving chemical threats.

Integrated network toxicology, molecular docking, and in vivo experiments to elucidate molecular mechanism of aflatoxin B1 hepatotoxicity

Due to the rise in temperature and sea level caused by climate change, the detection rate of aflatoxin B1 (AFB1) in food crops has increased dramatically, and the frequency and severity of aflatoxicosis in humans and animals are also increasing. AFB1 has strong hepatotoxicity, causing severe liver damage and even cancer. However, the mechanism of AFB1 hepatotoxicity remains unclear. By integrating network toxicology, molecular docking and in vivo experiments, this research was designed to explore the potential hepatotoxicity mechanisms of AFB1. Thirty-three intersection targets for AFB1-induced liver damage were identified using online databases. PI3K/AKT1, MAPK, FOXO1 signaling pathways, and apoptosis were significantly enriched. In addition, the proteins of ALB, AKT1, PIK3CG, MAPK8, HSP90AA1, PPARA, MAPK1, EGFR, FOXO1, and IGF1 exhibited good affinity with AFB1. In vivo experiments, significant pathological changes occurred in the liver of mice. AFB1 induction increased the expression levels of EGFR, ERK, and FOXO1, and decreased the expression levsls of PI3K and AKT1. Moreover, AFB1 treatment caused an increase in Caspase3 expression, and a decrease in Bcl2/Bax ratio. By combining network toxicology with in vivo experiments, this study confirms for the first time that AFB1 promotes the FOXO1 signaling pathway by inactivating PI3K/AKT1 and activating EGFR/ERK signaling pathways, hence aggravating hepatocyte apoptosis. This research provides new strategies for studying the toxicity of environmental pollutants and new possible targets for the development of hepatoprotective drugs.

Hydrazide-linked perylene-based porous organic polymer: An innovative approach for removing organic dyes from aqueous solution

The presence of toxic pollutants in the aquatic environment is a significant environmental concern that requires the development of effective methods for their removal. This study focuses on applying perylene and triazine-based porous organic polymer (PT-POP) to effectively eliminate hazardous pollutants from industrial settings. Specifically, PT-POP was synthesized using two monomers, namely 3,4,9,10 perylenetetracarboxylic dianhydride (PTCDA) and 2,4,6 tris(hydrazino)-s-triazine (THTZ). The resulting PT-POP has outstanding adsorption performance and high chemical and thermal stability, making it an attractive adsorbent material. Based on the thermogravimetric analysis, it has been confirmed that PT-POP is thermally stable. The presence of aromatic rings in PT-POP is responsible for the extraordinary stability of the polymer. Then, the performance of PT-POP in the adsorption of cationic Nile blue and anionic Direct Fast Scarlet 4BS (DFS-4BS) was studied. The optimization process involves adjusting several factors, including temperature, concentration, pH, time, and adsorbent dosage. The highest adsorption capacities (qM) for the Nile blue dye and the DFS-4BS dye were 280.16 mg. g−1 and 87.50 mg. g−1, respectively. The adsorption behavior best fits the pseudo-second-order kinetic model, and the Langmuir isotherm showed the most agreement with adsorption isotherms for both. The thermodynamic study shows that the adsorption process for both dyes is spontaneous and endothermic, as evidenced by the negative value of ΔG and the positive value of ΔH. The findings show that PT-POP is more inclined toward cationic dyes due to its negative surface charge.

Transcriptomic and biochemical analysis of metabolic remodeling in Bacillus subtilis MSC4 under Benzo[a]pyrene stress

Polyaromatic benzo[a]pyrene (B[a]P) is a toxic carcinogenic environmental pollutant, and the use of microorganisms to remediate B[a]P contamination is considered to be one of the most effective strategies. However, there is still a gap in studying the metabolic remodeling of microorganisms under B[a]P stress. In this study, our systematically investigated the effects of B[a]P on the metabolism of Bacillus subtilis MSC4 based on transcriptomic, molecular and biochemical analyses. The results showed that in response to B[a]P stress, MSC4 formed more biofilm matrix and endospores, the structure of the endospores also was changed, which led to a reduction in their resistance and made them more difficult to germinate. In addition to an increase in glycolysis activity, the activities of tricarboxylic acid cycle, pentose phosphate pathway and the electron transport chain were decreased. B[a]P stress forced MSC4 to strengthen arginine synthesis, urea cycle, and urea decomposition, meanwhile, synthesize more ribonucleotides. The activity of DNA replication, transcription activities and the expression of multiple ribosomal protein genes were reduced. Moreover, all of the reported enzymes involved in B[a]P degradation showed decreased transcript abundance, and the degradation of B[a]P caused significant up-regulation of the gene expression of the acid inducible enzyme OxdC and the synthesis of acetoin. In addition, the cytotoxicity of B[a]P to bacteria was directly displayed in four aspects: increased intracellular level of reactive oxygen species (ROS), elevated cell membrane permeability, up-regulation of the cell envelope stress-sensing two-component system LiaRS, and downregulation of siderophores biosynthesis. Finally, B[a]P also caused morphological changes in the cells, with some cells exhibiting significant deformation and concavity. These findings provide effective research directions for targeted improvement the cellular activity of B[a]P-degrading strains, and is beneficial for further application of microorganisms to remediate B[a]P -contaminated soils.

Isoliquiritin counteracts cadmium-induced intestinal damage in mice through enhancing intestinal barrier function and inhibiting apoptosis

Cadmium (Cd), a crucial toxic environmental pollutant, can induce damage to many organs, especially the gastrointestinal tract. Isoliquiritin (ISO), a critical flavonoid glycoside compound isolated from Glycyrrhiza uralensis, has anti-inflammatory, anticancer, antioxidant and other pharmaceutical value. However, the potential roles of ISO in Cd-induced intestinal damage have not been reported yet. This study aimed to research the beneficial effects of ISO on Cd-induced intestinal damage and identify its underlying mechanisms. Our results showed that ISO reduced inflammation by suppressing the production of pro-inflammatory cytokines and the activity of serum Lipopolysaccharide (LPS) in mice with Cd exposure. In terms of mechanism, ISO administration protected the intestinal barrier function through increasing the expression of tight junction proteins and Muc2. Furthermore, ISO could significantly suppress Cd-induced intestinal apoptosis and activation of NLRP3 inflammasome. Interestingly, inhibiting the activation of NLRP3 by nigericin completely blocking the effect of ISO on apoptosis. Most importantly, ISO markedly abrogated Cd-induced cell damage and NLRP3 inflammasome activation in vitro. Taken together, these findings suggest that ISO reduces Cd-induced intestinal damage by increasing the goblet cells, improving intestinal barrier, suppressing NLRP3 inflammasome activation and inhibiting apoptosis, which may offer a novel strategy against the toxic effects of heavy metals.

Molecular engineering of a new method for effective removal of cadmium from water

Cadmium (Cd) is a widespread and highly toxic environmental pollutant, seriously threatening animal and plant growth. Therefore, monitoring and employing robust tools to enrich and remove Cd from the environment is a major challenge. In this work, by conjugating a fluorescent indicator (CCP) with a functionalized glass slide, a special composite material (CCPB) was constructed to enrich, remove, and monitor Cd2+ in water rapidly. Then Cd2+ could be effectively eluted by immersing the Cd-enriched CCPB in an ethylenediaminetetraacetic acid (EDTA) solution. With this, the CCPB was continuously reused. Its recovery of Cd2+was above and below 100 % after multiple uses by flame atomic absorption spectrometry (FAAS), which was excellent for practical use in enriching and removing Cd2+ in real aqueous samples. Therefore, CCPB is an ideal material for monitoring, enriching, and removing Cd2+ in wastewater, providing a robust tool for future practical applications of Cd enrichment and removal in the environment.

New Y0.045Ni0.045Fe2.91O4 nanowires decorated over mesoporous silica for crystal violet removal: Response surface methodology optimization, kinetics, and isothermal studies

Recently, there has been considerable interest in developing an efficient, easily separable, cost-effective, and environmentally friendly catalyst for treating toxic environmental pollutants. In this study, we successfully designed yttrium–nickel-doped magnetite nanowires (Y0.045Ni0.045Fe2.91O4) and their mesoporous silica (MS)-coated composite (Y0.045Ni0.045Fe2.91O4/MS) using a simple coprecipitation method. The resulting composite demonstrated effective adsorption and photocatalytic degradation of crystal violet (CV) dye under sunlight. Various instrumental characterization techniques were employed to assess the nanowires' morphological, chemical, and surface functional properties and their composite. The existence of metal–oxygen bonds in Y0.045Ni0.045Fe2.91O4 within the 500–800 cm−1 range was verified through FTIR analysis. According to the Brunauer–Emmett–Teller analysis, the composite exhibited a surface area of 285 m2/g, a pore volume of 0.436 cm³/g, and an average pore width of 5 nm. The composite's high surface area and mesoporous nature underscored its porous structure, confirming its enhanced adsorption capacity for contaminants. High resolution XPS spectrum justified the presence of surface silanol groups (Si–OH) which are responsible for adsorption phenomena. Photocatalytic experiments revealed that Y0.045Ni0.045Fe2.91O4 nanowires and their composites achieved 89% and 90% degradation rates for CV dye within 60 and 10 min, respectively. The removal efficiency was assessed under optimized conditions of pH (8), dose (15 mg), time (60 and 10 min), and concentration (10 mg/L). Statistical analysis revealed that pH significantly impacted CV dye removal because functional group activation varied at different pH values. To elucidate the adsorption mechanism and kinetics, the Temkin isotherm model and pseudo-second-order kinetics model (R2 = 1.996 mg min−1) were the best fit for the composite. Furthermore, approximately 99% of the nanowires were magnetically separated from the reaction mixture in an external magnetic field. The demonstrated synergy of efficient adsorption–photocatalysis, coupled with easy recovery, suggests that innovatively designed nanomaterials are optimal for the water remediation of organic pollutants in wastewater.

Neo-construction of a SO2-tunable near-infrared ratiometric fluorescent probe for high-fidelity diagnosis and evaluation hazards of Cd2+-induced liver injury

Cadmium-contaminated water and food are seriously hazardous to the human health, especially liver injury. To understand the entanglement relationship between cadmium ion (Cd2+)-induced liver injury and the biomarker sulfur dioxide (SO2), a reliable bioanalytical tool is urgently needed, detecting SO2 to diagnose and evaluate the extent of liver injury in vivo. Herein, based on the Förster resonance energy transfer (FRET) mechanism, a novel SO2-tunable NIR ratiometric fluorescent probe (SMP) was developed, it was used to diagnose and treat liver injury induced by Cd2+ in biosystems. Specifically, it was constructed by conjugating a NIR dicyanoisophorone with a NIR benzopyranate as the donor and acceptor, respectively, and the ratiometric response of SO2- regulated by the Michael addition reaction. In addition, SMP exhibits rapid reaction time (<15 s), two well-resolved emission peaks (68 nm) with less cross-talk between channels for high imaging resolution, superior selectivity, and low limit of detection (LOD=80.3 nM) for SO2 detection. Impressively, SMP has been successfully used for intracellular ratiometric imaging of Cd2+-induced SO2 and diagnostic and therapeutic evaluation in liver injury mice models with satisfactory results. Therefore, SMP may provide a powerful molecular tool for revealing the occurrence and development relationship between SO2 and Cd2+-induced liver injury. Environmental ImplicationCadmium ions are one of the well-known toxic environmental pollutants, which are enriched in the human body through inhalation of cadmium-contaminated air or from the food chain, leading to damage in various organs, especially liver injury. Therefore, we developed a novel fluorescent probe that can specifically detect SO2 in Cd2+-induced liver injury, which is critically important for the diagnosis and evaluation of Cd2+-induced liver injury diseases. The specific detection of SO2 of this probe has been successfully demonstrated in live HepG2 cells and Cd2+-induced liver injury mice.

Neurological risks arising from the bioaccumulation of heavy metal contaminants: A focus on mercury.

This study investigated the concentrations of heavy metals in the water sources of the upstream region of the Huangpu River, the Yangtze River Estuary, and various areas in Shanghai, as well as the heavy metal concentrations in the blood of Shanghai residents. It aimed to analyze the heavy metal elements absorbed by the human body and the resulting pathological effects. The results revealed that surface water primarily contains five heavy metals: copper (Cu), lead (Pb), zinc (Zn), arsenic (As), and mercury (Hg), while water sediments primarily contain seven heavy metals: Cu, cadmium (Cd), Pb, chromium (Cr), Zn, As, and Hg. The main heavy metals present in the human body are Pb, Hg, As, and Cd. By reviewing previous articles, it was found that heavy metal concentrations in human blood are higher than those in surface water, suggesting uncertainties in the heavy metal content of surface water and its tendency to settle at the bottom. Furthermore, a comparison of heavy metal content in sediments revealed that Hg is the most readily absorbed heavy metal by the human body and is also a toxic environmental pollutant. Within the cell, Hg is highly toxic to mitochondria and may cause oxidative stress and neurodegenerative disease. This study concludes that water sediments serve as the major source of pollution in the human body and pose significant health risks, thereby necessitating the implementation of effective preventive measures.

A long non-coding RNA associated with H3K7me3 methylation negatively regulates OsZIP16 transcription under cadmium stress

Cadmium (Cd) is a toxic environmental pollutant, posing a high risk to crop production and human health. However, the genetic mechanisms for regulation of Cd accumulation in crops are poorly understood. In this study, we functionally identified a novel long non-coding RNA (lncRNA, TCONS_00502780) that repressed a locus encoding an uncharacterized metal transporter ZIP16 (ZRT/IRT-like Protein) in rice. LncRNA-OsZIP16 (L16) is resident in the antisense strand of OsZIP16. Both L16 and OsZIP16 were transcriptionally expressed during the life cycle, but under Cd stress the L16 transcription was repressed, whereas the OsZIP16 expression was upregulated. OsZIP16 is localized to the endoplasmic reticulum. Knocking out OsZIP16 by CRISPR-Cas9 (C16) resulted in Cd sensitivity, manifested by reduced plant growth and intense cellular damage with a slightly higher Cd translocation from roots to shoots, suggesting that OsZIP16 expression is required for rice growth and development under Cd stress. Conversely, OsZIP16 constitutive overexpression (OE16) lines displayed a growth phenotype compatible to the wide-type with lower Cd translocation ratio from roots to shoots. L16 knock-down lines by RNA interference (L16-R) showed a similar phenotype to the OE16 lines, while the L16 overexpression (L16-OE) lines were phenotypically similar to the C16 lines. The OsZIP16 transcription was upregulated in the L16-R lines but downregulated in the L16-OE lines. Using an antibody against the trimethylation of histone H3 lysine 27 (H3K27me3) followed by chromatin immunoprecipitation (ChIP), we found the reduced H3K27me3 methylation marks surrounding the OsZIP16 gene under Cd stress. Further examination of H3K27me3 in the L16-R lines revealed that the methylation levels were also significantly lower than those in WT. Taken together, these data suggest that the L16 could negatively regulate the OsZIP16 transcriptional expression through an epigenetic mechanism for rice adaption to Cd stress.

Two red/blue-emitting fluorescent probes for quick, portable, and selective detection of thiophenol in food, soil and plant samples, and their applications in bioimaging

Thiophenol (PhSH), which is widely used in many industries, poses significant health risks owing to its acute toxicity and irritating effects. Thus, the detection of PhSH is crucial for ensuring environmental and food safety. There is significant room for improvement in the sensing properties of the reported analytical methods, such as response time, detection limit, selectivity, and portable detection. Herein, we present two new red/blue fluorescence-emissive sensors (NS1 and NS2) for PhSH detection. After reacting with PhSH, NS1 exhibited a low detection limit (66.7 nM), red emission, fast response time of just 10 s, and large Stokes shift (240 nm). NS2 could detect PhSH with a low detection limit (75.8 nM), fast response time of 20 s, and blue emission. The noticeable color response and portability of the two probes made them suitable for on-site detection of PhSH in various samples, such as water, soil, plant, food samples, and living cells. Moreover, it has been shown that these probes could be used to determine PhSH content in smartphone applications, thin layer chromatography kits, and polysulfone capsule kits. Prepared probes have low cytotoxicity and show good permeability in tested living cells, which is important for early diagnosis, disease research, and emergency analysis. Compared with other studies, the proposed approach has remarkable advantages in terms of detection limit, portability, response time, and low cytotoxicity. Thus, it meets the crucial demand for ensuring health, environmental and food safety, and adherence to regulatory standards.

Breast milk-mediated exposure to dioxins and antigen in infancy enhances antigen-specific antibody production capacity in adulthood in mice.

The immune system is sensitive to many chemicals. Among dioxin compounds, 2,3,7,8-tetrachlorodizenzo-p-dioxin (TCDD) is the most toxic environmental pollutant. The effects of perinatal maternal exposure to dioxins may persist into childhood. However, there have been no reports to date on the effects of exposure to dioxins during infancy, when the immune organs are developing. Therefore, we investigated the effects of TCDD and antigen exposure during lactation on immune function, especially antibody production capacity, in adult mice. Beginning the day after delivery, lactating mothers were orally administered TCDD or a mixture of TCDD and ovalbumin (OVA) daily for 4 weeks, until the pups were weaned. At 6 weeks of age, progeny mice were orally administered OVA daily for 10 weeks, while non-progeny mice were orally administered OVA or a mixture of TCDD and OVA daily for 10 weeks. Production of serum OVA-specific IgG was examined weekly. The amount of TCDD transferred from the mother to the progeny via breast milk was determined by measuring TCDD in the gastric contents of the progeny. A trend toward increasing IgA titer was observed in TCDD-treated mice, and production of IgE was observed only in progeny whose mothers were treated with TCDD and OVA. The results suggest that exposure to TCDD and OVA in breast milk can affect immune function in newborns.

Measurement of the absorption cross-sections of sulfur compounds in the 180-270 nm region considering nonlinear effects.

Sulfur compounds (SO2, CS2, H2S and OCS) are common toxic pollutants in the atmospheric environment, and the absorption spectroscopy technique can indeed help to realize online monitoring of their concentrations. However, nonlinear effects that occur during absorption spectroscopy measurements have a serious impact on the measurement of the absorption cross-sections (ACSs) of sulfur compounds, leading to serious deviations in both the substance absorption properties and concentrations obtained based on ACS analysis. In this paper, the maximum effective ACSs of sulfur compounds in the linear region are obtained by considering the influence of nonlinear effects and eliminating interference factors such as oxygen and photolysis. In addition, the nonlinear effects are found to be greatly attenuated in spectra with broad band absorption characteristics by comparing the oscillatory absorption spectra before and after the differential treatment and by comparing the change in the oscillatory ACS with the broad band ACS. The experimental results show that the effective ACSs of SO2, CS2, H2S, and OCS with a resolution of 0.23 nm are 14.15 × 10-18 cm2 per molecule, 5.61 × 10-16 cm2 per molecule, 7.09 × 10-18 cm2 per molecule, and 3.20 × 10-19 cm2 per molecule, respectively. So far, it is the largest ACS obtained at room temperature and atmospheric pressure, which is of great significance for online measurement of sulfur compounds.

Transcriptome analysis during 4-vinylcyclohexene diepoxide exposure-induced premature ovarian insufficiency in mice.

The occupational chemical 4-Vinylcyclohexene diepoxide (VCD) is a reproductively toxic environmental pollutant that causes follicular failure, leading to premature ovarian insufficiency (POI), which significantly impacts a woman's physical health and fertility. Investigating VCD's pathogenic mechanisms can offer insights for the prevention of ovarian impairment and the treatment of POI. This study established a mouse model of POI through intraperitoneal injection of VCD into female C57BL/6 mice for 15 days. The results were then compared with those of the control group, including a comparison of phenotypic characteristics and transcriptome differences, at two time points: day 15 and day 30. Through a comprehensive analysis of differentially expressed genes (DEGs), key genes were identified and validated some using RT-PCR. The results revealed significant impacts on sex hormone levels, follicle number, and the estrous cycle in VCD-induced POI mice on both day 15 and day 30. The DEGs and enrichment results obtained on day 15 were not as significant as those obtained on day 30. The results of this study provide a preliminary indication that steroid hormone synthesis, DNA damage repair, and impaired oocyte mitosis are pivotal in VCD-mediated ovarian dysfunction. This dysfunction may have been caused by VCD damage to the primordial follicular pool, impairing follicular development and aggravating ovarian damage over time, making it gradually difficult for the ovaries to perform their normal functions.

Fructose-stabilized DNA-copper nanoclusters as a nanoprobe for the one-pot fluorometric detection of mercury ions

Mercury ion (Hg2+) is a highly toxic environmental pollutant, particularly harmful to human health, necessitating the development of analytical techniques with advanced performance to monitor its presence. Herein, we demonstrate the utility of fructose-stabilized DNA-copper nanoclusters (Fru@DNA-CuNCs) as a stable nanoprobe for the sensitive detection of Hg2+ with a simplified procedure. Upon interaction with Hg2+, the fluorescence of Fru@DNA-CuNCs undergoes rapid quenching, which was caused by metallophilic interactions promoting electron transfer between Hg and Cu, changing the electron configuration of nanoclusters. This nanoprobe exhibits exceptional sensitivity, with a detection limit of 2.49 nM for Hg2+ detection, and the detection process costs less than 20 min. Importantly, unlike other unstable CuNCs analogs, the incorporation of fructose enhances the stability of the Fru@DNA-CuNCs, which can maintain its performance for Hg2+ detection after being stored for up to 4 weeks. This robustness makes it suitable for Hg2+ monitoring without specialized and centralized facilities. To our knowledge, this is the first attempt to explore the analytical application of Fru@DNA-CuNCs, providing a facile, rapid, and stable synthetic biology-based sensing technique for Hg2+ monitoring.

Selenomethionine alleviates decabromodiphenyl ether-induced oxidative stress and ferroptosis via the NRF2/GPX4 pathway in the chicken brain

Decabromodiphenyl ether (BDE209) is a toxic environmental pollutant that can cause neurotoxicity, behavioral abnormalities, and cognitive impairment in animals. However, the specific mechanisms of BDE209-induced neurological injury and effective preventative and therapeutic interventions are lacking. Even though selenomethionine (Se-Met) has a significant detoxification effect and protects the nervous system, it remains unclear whether Se-Met can counteract the toxic effects of BDE209. For the in vivo test, we randomly divided 60 1-week-old hy-line white variety chicks into the Con, BDE209, Se-Met, and BDE209 +Se-Met groups. In vitro experiments were performed, exposing chick embryo brain neurons to BDE209, Se-Met, N-Acetylcysteine (NAC, a ROS inhibitor), and RSL3 (a GPX4 inhibitor). We demonstrated that BDE209 induced oxidative stress and ferroptosis in the chicken brain, which mainly manifested as mitochondrial atrophy, cristae breakage, increased Fe2+ and MDA content, decreased antioxidant enzyme activity, and the inhibition of the NRF2/GPX4 signaling pathway in the brain neurons. However, Se-Met supplementation reversed these changes by activating the NRF2/GPX4 pathway, reducing mitochondrial damage, enhancing antioxidant enzyme activity, and alleviating ferroptosis. This study provides insight into the mechanism of BDE209-related neurotoxicity and suggests Se-Met as an effective preventative and control measure against BDE209 poisoning.

Evaluation of alternate hosts for recombinant expression of a reductive dehalogenase

Organohalides are recalcitrant, toxic environmental pollutants. Reductive dehalogenase enzymes (RDases) found in organohalide respiring bacteria (OHRB) utilise organohalides as electron acceptors for cellular energy and growth, producing lesser-halogenated compounds. Consequently, microbial reductive dehalogenation via organohalide respiration represents a promising solution for clean-up of organohalide pollutants. Dehalobacter sp. UNSWDHB is an OHRB capable of respiring highly toxic chloroform (CF) and converting it to dichloromethane (DCM). TmrA has been identified as an RDase responsible for this conversion and different strategies for generation of functional recombinant TmrA is the focus of this article. In this study, TmrA was recovered from inclusion bodies expressed in E. coli and refolded in the presence of FeCl3, Na2S and cobalamin to yield functional enzyme. TmrA has been previously expressed in a soluble and functional form in the corrinoid-producing Bacillus megaterium. Using a fractional experimental design for cultivation and induction combined with purification under anaerobic conditions resulted in substantially higher activity of recombinant and native TmrA than previously reported. TmrA was then expressed in a soluble and active form in Shimwellia blattae. Co-expression with two different putative chaperone proteins from the original host did not increase the level of soluble expression in S. blattae, however activity assays showed that removing the TAT signal from TmrA increases the dechlorination activity compared to when the TAT signal is present. Finally, TmrA was successfully expressed in a soluble and active form in the H2-oxidizing C. necator H16, a novel host for the expression of RDases.