Ecotoxicology and Environmental Safety最新文献

{"title":"Exposure to particulate matter (PM2.5) weakens corneal defense by downregulating thrombospondin-1 and tight junction proteins","authors":"Liangliang Niu ,&nbsp;Jiamin Liu ,&nbsp;Huan Xu ,&nbsp;Binghui Liu ,&nbsp;Maomao Song ,&nbsp;Chunchun Hu ,&nbsp;Rui Jiang ,&nbsp;Xinghuai Sun ,&nbsp;Yuan Lei","doi":"10.1016/j.ecoenv.2024.117276","DOIUrl":"10.1016/j.ecoenv.2024.117276","url":null,"abstract":"<div><h3>Background</h3><div>Fine particulate matter (PM_2.5) induces ocular surface toxicity through pyroptosis, oxidative stress, autophagy, and inflammatory responses. However, the precise molecular pathways through which PM_2.5 causes corneal damage remain unclear. This study aims to investigate the underlying mechanisms by exposing human corneal epithelial cells (HCECs) to PM_2.5.</div></div><div><h3>Methods</h3><div>After the morphology and chemical composition analysis of the PM samples, we conducted both in vivo and in vitro experiments to investigate PM_2.5-induced corneal epithelial damage. We assessed corneal barrier function in HCECs using transepithelial electrical resistance (TEER) assays. To explore the molecular mechanisms of PM_2.5-induced corneal epithelial damage, we performed whole-transcriptome resequencing, quantitative RT-PCR, and western blotting in vitro. In addition, we analyzed mouse corneas exposed to concentrated ambient PM_2.5 through immunofluorescence staining to observe the resulting changes in corneal epithelial protein expression in vivo.</div></div><div><h3>Results</h3><div>Our results showed significant impairment of corneal epithelial barrier function in PM_2.5-treated HCECs, as indicated by decreased TEER values. The expression of thrombospondin-1 (THBS1) and claudin-1, both key factors for maintaining corneal epithelial barrier integrity, was markedly reduced at the gene and protein levels in both in vitro and in vivo PM_2.5 exposure models. Moreover, the levels of tight junction-associated proteins, including occludin, zonula occludens-1 (ZO-1) and ZO-2, essential components of the corneal epithelial barrier, were significantly diminished in PM_2.5-treated HCECs.</div></div><div><h3>Conclusion</h3><div>PM_2.5 exposure leads to corneal epithelium damage by disrupting tight junction proteins and THBS1 expression. These findings provide insight into potential pathways for PM_2.5-induced ocular toxicity and underscore the need for protective strategies against such environmental pollutants.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117276"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrochlorothiazide disrupts DNA damage response to exacerbate skin photosensitivity","authors":"Lei Tao ,&nbsp;Yujiao Xu ,&nbsp;Yingyue Cui ,&nbsp;Qingcheng Wei ,&nbsp;Boyang Lin ,&nbsp;Yu Cao ,&nbsp;Zhen Dai ,&nbsp;Zhi Ma ,&nbsp;Ling Zhang ,&nbsp;Aiping Shi ,&nbsp;Ling Gu ,&nbsp;Yunyao Liu","doi":"10.1016/j.ecoenv.2024.117314","DOIUrl":"10.1016/j.ecoenv.2024.117314","url":null,"abstract":"<div><div>Hydrochlorothiazide (HCTZ) is a widely utilized diuretic for the treatment of hypertension. The photosensitivity of HCTZ has been recognized for six decades, with UVA being considered the primary culprit. However, the precise molecular mechanism of HCTZ sensitizing skin to UV radiation remains unknown. In this study, we demonstrate that HCTZ exacerbates UVB-induced photosensitivity in normal skin by disrupting the DNA damage response, a crucial network responsible for maintaining epidermal homeostasis. Here, we found that HCTZ aggravates UVB-induced mouse skin damage. Through transcriptomic and proteomic profiling, we have found that the cell cycle and p53 signaling pathway may contribute to the photosensitivity caused by HCTZ. In keratinocytes, HCTZ promotes the transition from G1 to S phase and inhibits the p53 signaling pathway after exposure to UV radiation. We have found that HCTZ enhances the accumulation of DNA damage induced by UVB and impairs nucleotide excision repair (NER), which is responsible for repairing UVB-induced DNA lesions, by inhibiting the expression of NER-related genes and shortening the duration of G1 phase. Furthermore, pharmacologically inducing G1 arrest eliminates HCTZ-induced accumulation of damaged DNA. These findings unveil an unknown mechanism through which HCTZ impairs NER and interferes with UVB-induced cell cycle arrest, ultimately leading to improper response towards DNA damage and increased skin sensitivity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117314"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chlorophenols in environment: Recent updates on pretreatment and analysis methods","authors":"Min Qian ,&nbsp;Qi An ,&nbsp;Yu Bian ,&nbsp;Meng Zhang ,&nbsp;Xue-song Feng ,&nbsp;Cheng Du","doi":"10.1016/j.ecoenv.2024.117326","DOIUrl":"10.1016/j.ecoenv.2024.117326","url":null,"abstract":"<div><div>Chlorophenols (CPs) are widely used in industries such as petrochemicals, insecticides, pharmaceuticals, synthetic dyes and wood preservatives. However, owing to the improper discharge and disposal, they have become major contaminants that are ubiquitously distributed in water, soil, and sewage sediments, posing a significant threat to ecosystems and human health. Consequently, accurate, sensitive and effective pretreatment and analysis methods for CPs are urgently required and have been actively explored in recent years. This review encompasses the pretreatment and detection methods for CPs in environmental samples from 2010 to 2024. The pretreatment methods for CPs primarily include solid-phase extraction, liquid-liquid extraction, solid-phase microextraction, liquid-phase microextraction, and QuEChERS. These methods are evolving towards more effective and environmentally friendly technologies, such as the miniaturization and automation of equipment, the development of innovative materials (including graphene, molecularly imprinted polymers, layered double hydroxides, porous organic polymers, and porous carbon), and the use of green solvents like deep eutectic solvents. Detection methods emphasize liquid chromatography-mass spectrometry, gas chromatography-mass spectrometry, sensors, and capillary electrophoresis. Advances in chromatographic columns, novel ion sources, and high-resolution mass spectrometry have significantly improved detection performance. In addition, the pros and cons of diverse techniques, critical comments and future perspectives are elaborated.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117326"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient PMs pollution, blood pressure, potential mediation by short-chain fatty acids: A prospective panel study of young adults in China","authors":"Xin Chou ,&nbsp;Miao Fang ,&nbsp;Yue Shen ,&nbsp;Cunzhong Jiang ,&nbsp;Lin Miao ,&nbsp;Liyan Yang ,&nbsp;Zexi Wu ,&nbsp;Xiangyu Yao ,&nbsp;Kunpeng Ma ,&nbsp;Kun Qiao ,&nbsp;Zhijing Lin","doi":"10.1016/j.ecoenv.2024.117316","DOIUrl":"10.1016/j.ecoenv.2024.117316","url":null,"abstract":"<div><h3>Background</h3><div>The concurrent effects of particulate matter (PM) on both blood pressure (BP) and short-chain fatty acids (SCFAs) are insufficiently explored, with limited research on the potential mediating roles of SCFAs.</div></div><div><h3>Methods</h3><div>In this prospective panel study with 4 follow-ups, we recruited 40 college students in Hefei, China, to assess the impacts of short-term exposure to PM (aerodynamic diameter ≤10 μm (PM₁₀), ≤2.5 μm (PM_2.5), and ≤1 μm (PM₁)) on BP and SCFAs, along with potential mechanisms. Real-time PM data, urinary SCFAs levels, and BP indicators were systematically collected. Linear mixed-effects models assessed the relationships between PM, SCFAs, and BP. Mediation analyses explored SCFAs’ mediating role in the PM-BP association.</div></div><div><h3>Results</h3><div>PM exposure was positively linked to BP and negatively associated with SCFAs. For a 10 μg/m³ rise in PM₁₀ at lag 0–72 h, there were notable reductions of 0.0019 % (95 %CI: −0.0028, −0.0010) in Acetic acid, 0.0262 % (-0.0369, −0.0155) in Propionic acid, and 0.0702 % (-0.1025, −0.0378) in Butyric acid. Systolic BP, diastolic BP, and mean arterial pressure (MAP) increased by 2.60 mmHg (0.96, 4.25), 2.24 mmHg (1.18, 3.31), and 2.36 mmHg (1.20, 3.53), respectively, per 10-μg/m³ rise in PM₁ at lag 0–24 h. Decreased SCFAs levels explained significant portions (24.69–31.80 %) of the elevated MAP due to PM₁₀. Stronger associations were found in females and individuals with abnormal BMI.</div></div><div><h3>Conclusions</h3><div>Our study shows that PM exposure decreases urinary SCFAs levels, which partially mediate the impact of PM on elevated BP. These findings enhance our comprehension of the pathways linking PM exposure to BP changes.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117316"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenium protects mouse spermatogonia against ivermectin-induced apoptosis by alleviating endoplasmic reticulum stress in vitro","authors":"Daniel Chavez Varias,&nbsp;Sung-Hwan Moon,&nbsp;Seung Hee Shin,&nbsp;Buom-Yong Ryu","doi":"10.1016/j.ecoenv.2024.117307","DOIUrl":"10.1016/j.ecoenv.2024.117307","url":null,"abstract":"<div><div>Ivermectin (IVM) is a widely used anthelmintic in human and veterinary medicine. However, the increasing use of IVM raises concerns about its potential harm against non-targeted organisms. This study demonstrates a novel mechanism where IVM triggers apoptosis via endoplasmic reticulum (ER) stress in GC-1 spg <em>in vitro</em>. The inhibitory effects of selenium (Se) against the toxicological mechanism were also explored. IVM dose-dependently induces oxidative stress, dysregulated Ca²⁺ levels, and intracellular protein aggregation. Increased mitochondria-associated ER membrane (MAM) activity through Glucose-regulated Protein 75 (Grp75) overloads the mitochondria with Ca²⁺, causing mitochondrial dysfunction. These simultaneous stressors lead to unfolded protein response and apoptosis. Se reverses all these subcellular events by promoting the expression of selenoprotein-encoding genes to maintain the ER and redox homeostasis. The testis-enriched Glutathione Peroxidase 4 (<em>Gpx4</em>) and the testis-specific Selenoprotein V (<em>Selenov</em>) are only upregulated in the IVM and Se co-treatment group, suggesting their potential role in stress response. These findings confirm that toxic doses of IVM lead to programmed cell death in type B spermatogonia through redox imbalance-associated ER stress. This study provides valuable insights into refining male reproductive toxicity evaluation, targeting of ER stress to protect male germ cells, and maintaining male fertility from IVM-induced toxicity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117307"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MANF inhibits NLRP3 inflammasome activation by competitively binding to DDX3X in paraquat-stimulated alveolar macrophages","authors":"Yi Pu ,&nbsp;Siying Han ,&nbsp;Jie Chen ,&nbsp;Zhenning Liu","doi":"10.1016/j.ecoenv.2024.117331","DOIUrl":"10.1016/j.ecoenv.2024.117331","url":null,"abstract":"<div><div>NLRP3 inflammasome activation in macrophages is involved in paraquat-induced acute lung injury (ALI). MANF exerts an inhibitory effect against inflammation and cell death. The aim of this study was to investigate the role of MANF in paraquat-stimulated alveolar macrophages and the potential mechanism. Paraquat-induced ALI mouse model was established by intraperitoneally injection of 30 mg/kg of paraquat. The lung pathological changes were observed by hematoxylin and eosin staining. The expression of MANF/DDX3X/NLRP3/Caspase-1 in mice lung macrophages was evaluated by double immunofluorescence staining and western blot. NLRP3 inflammasome activation and pro-inflammatory cytokines (IL-1β and IL-18) in paraquat-stimulated macrophage transfected with MANF overexpression plasmid (pcDNA3.1-MANF) or siRNA-MANF were measured by Western blot. The protein–protein interaction of MANF/DDX3X/NLRP3 was verified by Co-immunoprecipitation. As a result, MANF/DDX3X/NLRP3/Caspase-1 were upregulated in alveolar macrophages of paraquat-induced ALI in mice. In paraquat-stimulated alveolar macrophages, upregulation of MANF and DDX3X were also observed, accompanied by NLRP3 inflammasome activation. In addition, overexpression of MANF inhibited NLRP3 inflammasome activation in paraquat-stimulated alveolar macrophages. In contrast, knockdown of MANF aggravated NLRP3 inflammasome activation. Co-immunoprecipitation results revealed that DDX3X could bind to MANF and NLRP3, but MANF could not bind to NLRP3 in paraquat-stimulated alveolar macrophages. Furthermore, Co-immunoprecipitation of truncated three fragments of DDX3X confirmed MANF can interact with the helicase core of DDX3X which is the binding site for NLRP3. Taken together, MANF exerted a protective effect against paraquat-induced cytotoxicity by inhibiting the NLRP3 inflammasome activation in macrophages via competitive binding to the helicase core of DDX3X.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117331"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142637903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine exposure is associated with targeted impairments in primordial follicle phenotype in cultured neonatal mouse ovaries","authors":"Sara M. Idrees,&nbsp;Sarah L. Waite,&nbsp;Sofia Granados Aparici ,&nbsp;Mark A. Fenwick","doi":"10.1016/j.ecoenv.2024.117302","DOIUrl":"10.1016/j.ecoenv.2024.117302","url":null,"abstract":"<div><div>The ovarian reserve consists of a limited supply of primordial follicles (PFs), each containing an oocyte surrounded by a layer of granulosa cells (GCs). PFs are relatively quiescent and must remain viable for a long period, thereby making them susceptible to environmental and lifestyle influences. Given the widespread prevalence of e-cigarette use, this study aimed to investigate the effects of nicotine and its metabolite cotinine in a mouse model and to elucidate the mechanisms by which nicotine influences the ovarian reserve. Neonatal ovaries were cultured for 7-days in nicotine or cotinine reflective of concentrations in plasma of e-cigarette users. From histological evaluation, nicotine or cotinine had no impact on the number of PFs or early growing follicles; however, the medium (15 ng/ml) and high (45 ng/ml) concentrations of nicotine (but not cotinine) caused a small reduction in oocyte and GC size within PFs relative to controls (0 ng/ml; both <em>P</em>&lt;0.01). These morphological effects were not associated with changes in immunofluorescent markers of apoptosis (active caspase-3) or proliferation (Pcna), but were associated with increased gH2AX in PF oocytes, indicative of DNA damage and repair. RNA-sequencing of cultured ovaries exposed to nicotine (45 ng/ml) relative to control (0 ng/ml), revealed a suite of differentially expressed candidates, as well as numerous gene ontology biological processes associated with increased DNA damage, metabolism, respiration and immune function, alongside suppression of meiosis, cell adhesion, differentiation and morphogenesis. Findings from this study indicate that direct nicotine exposure has a limited effect on the quantity of PFs, but importantly highlights a range of processes that could impinge on the quality of the ovarian reserve.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"288 ","pages":"Article 117302"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142637923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acetylation of FOXO1 is involved in cadmium-induced rat kidney injury via mediating autophagosome-lysosome fusion blockade and autophagy inhibition","authors":"Yingxin Ruan ,&nbsp;Yang Xue ,&nbsp;Pengyu Zhang ,&nbsp;Junya Jia","doi":"10.1016/j.ecoenv.2024.117253","DOIUrl":"10.1016/j.ecoenv.2024.117253","url":null,"abstract":"<div><div>Cadmium (Cd), a potentially toxic elements, has the potential to cause harm to the kidneys. Studies has demonstrated that autophagosome-lysosome fusion blockade and consequent autophagy inhibition is related to Cd-induced kidney injury. Studies indicate that acetylation of forkhead box protein O1 (FOXO1) as a transcriptional factor of lysosomal and autophagy genes, but its roles in Cd-exposed kidney tissues remains unclear till now. Therefore, the present study was conducted to elucidate this issue. Data found that Cd enhances the acetylation level of FOXO1 and inhibits the expression level of silent information regulator 1 (Sirt1, deacetylase of FOXO1). Pharmacological activation of Sirt1 (SRT2104 treatment) decreases Cd-increased acetylation level of FOXO1, enhances Cd-inhibited transcription level of Ras-related protein 7 (Rab7), restores Cd-blocked fusion of autophagosome and lysosome, and alleviates Cd-induced autophagy inhibition. Moreover, data corroborated that inhibiting the acetylation level of FOXO1 is conductive to mitigating Cd-induced kidney injury. Collectively, these results demonstrate that acetylation of FOXO1 mediates the autophagosome-lysosome fusion blockade and autophagy inhibition during Cd-induced kidney injury, while regulating the acetylation level of FOXO1 may be a potential mechanism of treating nephrotoxicity after Cd exposure.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117253"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzophenone-3 exposure induced apoptosis via impairing mitochondrial function in human chondrocytes","authors":"Ye Yang ,&nbsp;Rui Gao ,&nbsp;Zhenyu Zhu,&nbsp;Wenfeng Xiao,&nbsp;Jing Wang,&nbsp;Wenxia Zhao,&nbsp;Yingjun Li","doi":"10.1016/j.ecoenv.2024.117286","DOIUrl":"10.1016/j.ecoenv.2024.117286","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a chronic joint disease affecting millions of adults worldwide, characterized by degeneration of articular cartilage. Many environmental risk factors contribute to OA development. Benzophenone-3 (BP-3), a commonly used ultraviolet filter in personal care products, has been positively associated with OA risk. However, it remains unclear whether and how BP-3 induces toxic effects on articular chondrocytes and promote OA development. This study aims to investigate the damage of BP-3 at environmentally relevant concentrations to human chondrocytes, as well as potential mechanisms linking BP-3 with injury of chondrocytes. Notably, BP-3 significantly inhibited cell viability, induced apoptosis, and up-regulated matrix metalloproteinase (MMP) 1 and 13 which mediated cartilage degradation in C28/I2 human normal chondrocytes. Moreover, the function of mitochondria was impaired and oxidative stress occurred in BP-3 exposure groups, evidenced by elevation of reactive oxygen species (ROS) generation, reduction of mitochondrial membrane potential, decrease of ATP production and inhibition of mitochondrial respiratory chain complex I, II, III and IV. Meanwhile, BP-3 caused mitochondrial cristae vague and formation of autophagosomes. PTEN induced putative kinase 1/E3 ubiquitin protein ligase (PINK1/Parkin) pathway was also activated by BP-3. Addition of autophagy inhibitor, 3-Methyladenine (3-MA), suppressed PINK1/Parkin-mediated mitophagy, but increased BP-3-induced expression of MMP1 and 13, as well as exacerbated BP-3-induced apoptosis, suggesting mitophagy may exert a chondroprotective effect and partially alleviate apoptosis induced by this compound. In brief, BP-3 exposure may increase OA risk via inducing apoptosis and increasing breakdown of extracellular matrix in chondrocytes, and mitochondrial dysfunction and mitophagy may play a crucial role in the mechanisms of BP-3-induced toxicity to articular chondrocytes.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117286"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between bisphenol A and paraben exposure, oxidative stress, and the activity of outer hair cells in the cochlea in children with hearing loss","authors":"Chia-Huang Chang ,&nbsp;Chun-Ting Lu ,&nbsp;Tai-Ling Chen ,&nbsp;Hsin-Chang Chen ,&nbsp;Wen-Chi Pan ,&nbsp;Chen-Wei Chang ,&nbsp;Yu-Chun Chen ,&nbsp;Yu-Lin Yu","doi":"10.1016/j.ecoenv.2024.117310","DOIUrl":"10.1016/j.ecoenv.2024.117310","url":null,"abstract":"<div><div>This study aimed to determine the associations of childhood exposure to bisphenol A (BPA) and parabens (PBs) with oxidative stress and the activity of outer hair cells (OHCs) in the cochlea of children with hearing loss (HL). A total of 641 children were enrolled in this cross-sectional study. Urinary concentrations of BPA and four PBs including methyl paraben (MP), ethyl paraben (EP), propyl paraben (PP), and butyl paraben (BP) were quantified by using liquid chromatography–tandem mass spectrometry (LC/MSMS). Four urinary biomarkers of oxidative stress, 8-hydroxy-2′-deoxyguanosine (8-OHdG), 8-nitroguanine (8-NO₂Gua), 4-hydroxynonenal mercapturic acid (HNE-MA), and 8-isoprostaglandin F2α (8-iso-PGF_2α), were measured using high-performance liquid chromatography-electrospray ionization mass spectrometry. Hearing tests were conducted by an audiologist in the audiometric test room, and the results were confirmed by an otolaryngologist. The activity of OHCs in the cochlea was measured by distortion product otoacoustic emissions (DPOAEs). The associations of BPA/PB exposure and oxidative stress with the activity of OHCs at different frequencies were evaluated in the multivariable linear regression models. There were 91 children with HL, for an incidence of approximately 14.2 %. There was a significant negative association between the presence of EP (1.5 K Hz, 3 K Hz) or PP (2 K Hz) or 8-OHdG (1 K Hz, 1.5 K Hz, 2 K Hz) and the activity of OHCs in the left ear. Significant results were also observed for BPA (2 K Hz), MP (1 K Hz, 1.5 K Hz, 2 K Hz), EP (3 K Hz), and 8-OHdG (2 K Hz) in the right ear. This study revealed that exposure to BPA/PBs reduces the activity of OHCs, especially at middle frequencies, in children.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"287 ","pages":"Article 117310"},"PeriodicalIF":6.2,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142610868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}