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Nitrate reduction and iron (II) oxidation by subsurface bacteria from the Iberian Pyritic Belt: Insights into the biogeochemical cycles in this environment 伊比利亚黄铁矿带地下细菌的硝酸盐还原和铁(II)氧化:对该环境下生物地球化学循环的认识
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-12 DOI: 10.1016/j.ecoenv.2026.119990
Joelithon de Lima Costa , Jose Manuel Martínez , Nuria Rodríguez , Fabrício Motteran , Lourdinha Florêncio , Mario Takayuki Kato , Ricardo Amils , José Luis Sanz
Nitrogen and iron are central to Earth’s biogeochemical cycles. The Iberian Pyrite Belt (IPB), a vast iron reservoir, hosts extremophilic microorganisms adapted to high metal and sulfur concentrations. This study investigates two isolates from the deep IPB subsurface, Citrobacter telavivensis T1.2D-1 and Stutzerimonas stutzeri T2.31D-1, evaluating their nitrate-reducing capacity and the role of iron in denitrification, with emphasis on nitrate-dependent ferrous iron oxidation (NDFO). Both species could reduce nitrate in sucrose-, lactate-, or acetate-fed medium, while their consortium enhanced nitrate consumption and biomass production. Genome analysis revealed no genes for iron (II) oxidation, yet NDFO likely occurs, as proposed, via a heterotrophic-lithotrophic mechanism: enzymatic nitrate reduction to nitrite, followed by abiotic iron (II) oxidation that converts nitrite to nitric oxide and then to nitrous oxide. This is particularly relevant for C. telavivensis, which can perform only of the first reduction step. Experimentally, iron sometimes inhibited nitrate consumption, likely because it accumulated in crusts on bacterial cells. However, extracellular polymeric substances (EPS) production could reduce iron toxicity and allow iron to act beneficially by supporting microbial activity, as observed with sucrose supplementation. Ecologically, nitrate reducers may significantly influence IPB subsurface cycles. Even lacking iron (II) oxidation genes, these bacteria could contribute to pyrite bioleaching through: (i) chemical attack by NDFO-generated iron (III), (ii) organic acids produced by metabolism, or (iii) yet undescribed mechanisms. Overall, these findings highlight the adaptive strategies and potential environmental roles of these nitrate-reducing microorganisms in the IPB subsurface.
氮和铁是地球生物地球化学循环的核心。伊比利亚黄铁矿带(IPB)是一个巨大的铁储层,拥有适应高金属和硫浓度的嗜极微生物。本研究研究了来自IPB深层地下的两株分离菌株,Citrobacter telavivensis T1.2D-1和Stutzerimonas stutzeri T2.31D-1,评估了它们的硝酸盐还原能力和铁在反硝化中的作用,重点研究了硝酸盐依赖性亚铁氧化(NDFO)。这两种植物都能降低蔗糖、乳酸或醋酸盐培养基中的硝酸盐,而它们的联合体则能提高硝酸盐的消耗和生物量。基因组分析显示,没有铁(II)氧化的基因,但NDFO可能是通过异养-岩石营养机制发生的,正如所提出的那样:酶促硝酸盐还原为亚硝酸盐,然后是非生物铁(II)氧化将亚硝酸盐转化为一氧化氮,然后再转化为氧化亚氮。这与C. telavivensis特别相关,它只能执行第一个还原步骤。在实验中,铁有时会抑制硝酸盐的消耗,可能是因为它在细菌细胞的结痂中积累。然而,细胞外聚合物(EPS)的产生可以减少铁的毒性,并使铁通过支持微生物活动而发挥有益的作用,正如在补充蔗糖时所观察到的那样。生态上,硝酸盐还原剂可能显著影响IPB地下循环。即使缺乏铁(II)氧化基因,这些细菌也可能通过以下方式促进黄铁矿的生物浸出:(i) ndfo生成的铁的化学攻击(III), (II)代谢产生的有机酸,或(III)尚未描述的机制。总的来说,这些发现突出了这些硝酸盐还原微生物在IPB地下的适应策略和潜在的环境作用。
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引用次数: 0
Glycolytic metabolic reprogramming and mitochondrial dysfunction: A novel mechanism underlying PAEs-promoted cartilage inflammatory phenotype 糖酵解代谢重编程和线粒体功能障碍:paes促进软骨炎症表型的新机制。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-14 DOI: 10.1016/j.ecoenv.2026.120027
Lu Liu , Yongchang Chen , Wenying Lin , Mian Zheng , Tianqi Yu , Ruyan Chen , Yanru Yang , Lingling Jiao , Qinli Ruan , Jia Sun
Phthalate esters (PAEs), the most prevalent class of plasticizers, are widely acknowledged as environmental endocrine disruptors (EDCs) and have been linked to the pathogenesis of various diseases. However, their specific role and intrinsic mechanism in inducing cartilage damage in bone-related diseases remain unclear. This study aimed to clarify the correlation between PAEs and cartilage damage, and to explore their potential molecular mechanisms. The core pathological change of knee osteoarthritis (KOA) is the progressive degeneration of articular cartilage. Based on this, this study first systematically explored the association between PAEs and KOA using network toxicology combined with molecular docking technology, and screened out core regulatory molecules including MMP9, EGFR, IL-10, BCL2, and CASP3. Subsequently, verification experiments on core molecules showed that PAEs exposure could activate the CASP3 pathway to induce apoptosis of human chondrocytes and significantly promote the formation of the inflammatory phenotype of chondrocytes.
To further reveal the underlying mechanism, we conducted proteomic analysis and cell experiments in human articular chondrocytes (HCs). The results showed that exposure to PAEs triggered reprogramming of glycolysis metabolism, inhibited oxidative phosphorylation, and damaged mitochondrial homeostasis. Collectively, this study provides a robust theoretical basis for understanding the inflammatory phenotypes and underlying mechanisms of chondrocyte damage driven by PAEs exposure, and further lays a foundation for the design of novel therapeutic interventions and the optimization of environmental toxicity assessment protocols targeting PAEs.
邻苯二甲酸酯(PAEs)是最普遍的一类增塑剂,被广泛认为是环境内分泌干扰物(EDCs),与多种疾病的发病机制有关。然而,它们在骨相关疾病中诱导软骨损伤的具体作用和内在机制尚不清楚。本研究旨在阐明PAEs与软骨损伤的相关性,并探讨其潜在的分子机制。膝关节骨性关节炎(KOA)的核心病理改变是关节软骨的进行性退变。基于此,本研究首先利用网络毒理学结合分子对接技术系统探索PAEs与KOA的关联,筛选出MMP9、EGFR、IL-10、BCL2、CASP3等核心调控分子。随后,核心分子的验证实验表明,PAEs暴露可激活CASP3通路诱导人软骨细胞凋亡,并显著促进软骨细胞炎症表型的形成。为了进一步揭示潜在的机制,我们在人关节软骨细胞(hc)中进行了蛋白质组学分析和细胞实验。结果表明,暴露于PAEs会引发糖酵解代谢的重编程,抑制氧化磷酸化,并破坏线粒体稳态。总的来说,本研究为理解PAEs暴露导致的炎症表型和软骨细胞损伤的潜在机制提供了坚实的理论基础,并进一步为设计针对PAEs的新型治疗干预措施和优化环境毒性评估方案奠定了基础。
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引用次数: 0
Contrasting toxicity between explosives– and chemical warfare agents–related compounds to the marine primary producer Phaeodactylum tricornutum 对比炸药和化学战剂相关化合物对海洋主要生产者三角褐指藻的毒性
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-13 DOI: 10.1016/j.ecoenv.2026.120023
João Alves Barbosa , James De Backer , Marijke Neyts , Koen Parmentier , Frédéric Laduron , Kris Geukens , Philippe François , Colin R. Janssen , Jana Asselman
Vast amounts of munitions dumped in the marine environment, have been reported to leak chemicals due to munition corrosion. The subsequent increased levels of explosives and related chemicals (E&RC), as well as chemical warfare agents and related chemicals (CWA&RC), raise risks for environmental and human health Yet, ecotoxicity data on primary producers is currently scarce. Therefore, this study investigated the acute effects of three CWA&RC (1,4-oxathiane, 1,4-dithiane, and thiodiglycol) and four E&RC (2,4,6-trinitrotoluene (TNT), tetryl, 1,3-dinitrobenzene (1,3-DNB), and picric acid) on Phaeodactylum tricornutum, a key marine diatom at the basis of the aquatic food web. Results showed that none of the three CWA&RC significantly inhibited the growth rate of Phaeodactylum tricornutum at the tested concentrations. Interestingly, picric acid stimulated growth up under the experimental conditions, suggesting a hormetic effect. TNT, tetryl, and 1,3-DNB strongly inhibited growth, with experimentally derived EC10 and EC50 values approaching environmentally relevant concentrations near dumpsites. Consequently, diatom biomass may be significantly affected by TNT, tetryl, and 1,3-DNB, potentially disturbing primary production and ocean chemistry. Future research should examine potential synergies between munition compounds and other marine pollutants, which may aggravate toxic effects, as well as consider long-term toxicity tests.
据报道,倾倒在海洋环境中的大量弹药由于弹药腐蚀而泄漏化学物质。随后爆炸物和相关化学品(e&rc)以及化学战剂和相关化学品(cwa&rc)的水平增加,增加了对环境和人类健康的风险。然而,关于初级生产者的生态毒性数据目前很少。因此,本研究考察了三种cwarc(1,4-草甘烷、1,4-二硫烷和硫代二甘醇)和四种e&rc(2,4,6-三硝基甲苯(TNT)、四基、1,3-二硝基苯(1,3- dnb)和苦味酸)对三角褐藻(Phaeodactylum tricornutum)的急性效应。结果表明,3种CWA&;RC在不同浓度下均未显著抑制三角褐指藻的生长速度。有趣的是,在实验条件下,苦味酸刺激了生长,表明了一种激效效应。TNT、四乙基和1,3- dnb强烈抑制生长,实验得出的EC10和EC50值接近垃圾场附近的环境相关浓度。因此,硅藻生物量可能受到TNT、四酰和1,3- dnb的显著影响,可能干扰初级生产和海洋化学。今后的研究应审查弹药化合物与其他可能加重毒性作用的海洋污染物之间的潜在协同作用,并考虑进行长期毒性试验。
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引用次数: 0
Corrigendum to “Polyethylene microplastics trigger osteosarcoma progression via ITGA5/FAPα/LGMN cancer promoting complex: A novel environmental cancer promoting mechanism” [Ecotoxicol. Environ. Saf. 305 (2025) 119207] “聚乙烯微塑料通过ITGA5/FAPα/LGMN促癌复合体引发骨肉瘤进展:一种新的环境促癌机制”的更正[Ecotoxicol]。环绕。[f]. 305(2025) 119207。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-10 DOI: 10.1016/j.ecoenv.2026.120014
Weilin Zhang, Shengbang Huang, Kuize Liu, Dao Feng, Jinguo Liang, Zhencong Li, Boyuan Zhou, Zhiwen Dai, Zhongwei Wang, Jinsong Wei
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引用次数: 0
Erratum to “Perfluorooctane sulfonate induces joint inflammation to trigger osteoarthritis through the YAP1/IκBα signaling pathway” [Ecotoxicol. Environ. Saf. 312 (2026) 119961] “全氟辛烷磺酸通过YAP1/ i - κ b α信号通路诱导关节炎症引发骨关节炎”[Ecotoxicol]。环绕。科学通报,2012(5):391 - 391。
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-11 DOI: 10.1016/j.ecoenv.2026.120021
Huiying Guo , Jieruo Li , Guiwang Shen , Zifeng Wu , Hengyu Liao , Zhiyu Huang , Xiaofei Zheng , Zhengang Zha , Jinshao Ye , Jie Yang
{"title":"Erratum to “Perfluorooctane sulfonate induces joint inflammation to trigger osteoarthritis through the YAP1/IκBα signaling pathway” [Ecotoxicol. Environ. Saf. 312 (2026) 119961]","authors":"Huiying Guo ,&nbsp;Jieruo Li ,&nbsp;Guiwang Shen ,&nbsp;Zifeng Wu ,&nbsp;Hengyu Liao ,&nbsp;Zhiyu Huang ,&nbsp;Xiaofei Zheng ,&nbsp;Zhengang Zha ,&nbsp;Jinshao Ye ,&nbsp;Jie Yang","doi":"10.1016/j.ecoenv.2026.120021","DOIUrl":"10.1016/j.ecoenv.2026.120021","url":null,"abstract":"","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120021"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Per- and polyfluoroalkyl substances and cardiovascular disease: A mechanistic and epidemiological synthesis 全氟和多氟烷基物质与心血管疾病:机理和流行病学综合
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-14 DOI: 10.1016/j.ecoenv.2026.119901
Xiaoxi Yang , Xuemei Li , Xingqiang Li , Hongyan Zhang , Ce Wang , Xinyue Chen
Per- and polyfluoroalkyl substances (PFAS) are globally persistent pollutants increasingly implicated in adverse cardiovascular outcomes. Although research on PFAS toxicity has expanded rapidly, existing literature remains fragmented, with limited integration across exposure science, epidemiological evidence, molecular mechanisms, and mitigation strategies. Current reviews typically provide broad summaries of PFAS toxicity but seldom focus specifically on cardiovascular disease (CVD) or the mechanistic pathways underlying PFAS-induced cardiovascular injury. Moreover, the rapid emergence of short-chain and replacement PFAS introduces additional uncertainty regarding their cardiovascular relevance. To address these gaps, this review provides a comprehensive and mechanistically focused synthesis of PFAS exposure and CVD. A literature search through November 2025 identified eligible epidemiological, clinical, and experimental studies evaluating PFAS, including legacy compounds (Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonate (PFHxS), and perfluorononanoic acid (PFNA)) and emerging PFAS, and their associations with hypertension, blood pressure variation, vascular dysfunction, atherosclerosis, arrhythmias, cardiac injury, and cardiovascular mortality. Studies using serum or plasma biomarkers, drinking-water contamination records, cord blood measurements, and advanced mixture-modeling approaches were included. Extracted evidence encompassed exposure assessment, cardiovascular endpoints, mechanistic pathways, and potential therapeutic or risk-mitigating strategies. Across studies, PFAS exposure was consistently associated with modest but meaningful increases in systolic and diastolic blood pressure, higher risks of hypertension and gestational hypertensive disorders, impaired endothelial function, greater carotid intima-media thickness, and increased CVD incidence and mortality. Mechanistic evidence converges on several key pathways, including endothelial dysfunction, oxidative stress, inflammation, renin–angiotensin system activation, epithelial sodium channel upregulation, dyslipidemia, and placental vascular impairment linked to developmental programming. Vulnerable populations, including women, individuals with metabolic disorders, and those with impaired kidney function, exhibit heightened susceptibility. By integrating evidence across exposure science, epidemiology, mechanistic toxicology, and emerging intervention research, this review advances current understanding of PFAS-related cardiovascular toxicity and supports informed public health policy, clinical risk assessment, and regulatory decision-making.
全氟烷基和多氟烷基物质(PFAS)是全球持久性污染物,与心血管不良后果的关系日益密切。尽管对PFAS毒性的研究迅速扩大,但现有文献仍然零散,暴露科学、流行病学证据、分子机制和缓解策略之间的整合有限。目前的综述通常提供了PFAS毒性的广泛总结,但很少特别关注心血管疾病(CVD)或PFAS诱导心血管损伤的机制途径。此外,短链和替代PFAS的迅速出现给它们与心血管的相关性带来了额外的不确定性。为了解决这些空白,本综述提供了PFAS暴露和CVD的全面和机械集中的综合。截至2025年11月的文献检索确定了评估PFAS的合格流行病学、临床和实验研究,包括传统化合物(全氟辛酸(PFOA)、全氟辛烷磺酸(PFOS)、全氟己烷磺酸(PFHxS)和全氟壬酸(PFNA))和新出现的PFAS,以及它们与高血压、血压变化、血管功能障碍、动脉粥样硬化、心律失常、心脏损伤和心血管死亡率的关系。包括使用血清或血浆生物标志物、饮用水污染记录、脐带血测量和先进的混合建模方法的研究。提取的证据包括暴露评估、心血管终点、机制途径和潜在的治疗或风险缓解策略。在所有研究中,PFAS暴露始终与收缩压和舒张压的适度但有意义的升高、高血压和妊娠高血压疾病的高风险、内皮功能受损、颈动脉内膜-中膜厚度增大、CVD发病率和死亡率增加相关。机制证据集中在几个关键途径上,包括内皮功能障碍、氧化应激、炎症、肾素-血管紧张素系统激活、上皮钠通道上调、血脂异常和与发育程序相关的胎盘血管损伤。易感人群,包括妇女、代谢紊乱者和肾功能受损者,表现出更高的易感性。通过整合暴露科学、流行病学、机制毒理学和新兴干预研究的证据,本综述推进了目前对pfas相关心血管毒性的理解,并支持知情的公共卫生政策、临床风险评估和监管决策。
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引用次数: 0
A One Health framework integrating teratogenic risk and ecological assessment in freshwaters 整合淡水致畸风险和生态评估的“同一个健康”框架
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-14 DOI: 10.1016/j.ecoenv.2026.120015
Giulia Cesarini , Massimiliano Scalici , Marco Colasanti , Federica Spani
Freshwater ecosystems face mixture-dominated pressures that often elude conventional monitoring. We assessed eight rivers in Latium (Central Italy) to jointly evaluate ecological status and teratogenic risk within a One Health perspective. We combined in-situ physico-chemical measurements and elemental profiling by inductively coupled plasma mass spectrometry (ICP-MS; including the rare-earth tracer gadolinium) with two biological lines of evidence: benthic diatom assemblages to derive the Intercalibration Common Metric Index (ICMi) and screen teratological valves, and the Hydra vulgaris regeneration assay summarized as the Teratogenic Risk Index (TRI), with behavioural endpoints. Environmental conditions were heterogeneous, with eutrophication and high organic load at some sites. ICMi classified Almone and Arrone as Poor, Marta and Sacco as Good, and Mignone, Aniene, Tevere and Ninfa as High. TRI indicated Very High teratogenic risk at Almone; High at Marta, Sacco and Tevere; Low at Arrone, Mignone and Aniene; and No risk at Ninfa. Diatom teratologies were detected at all sites and peaked at Tevere. ICMi showed a negative association with gadolinium (r = -0.76, p < 0.05), whereas TRI and ICMi were not correlated. These results demonstrate that ecological status and teratogenic hazard need not converge. TRI captured organism-level developmental and neuro-functional impairment at low doses and in complex mixtures, even where ICMi was Good/High. Integrating organism- and community-level indicators with targeted chemistry offers a sensitive, cost-effective framework to flag hotspots, prioritize monitoring of emerging contaminants, and support risk management under the Water Framework Directive.
淡水生态系统面临着以混合物为主的压力,而传统的监测方法往往无法做到这一点。我们评估了拉蒂姆(意大利中部)的八条河流,以“同一个健康”视角共同评估生态状况和致畸风险。我们通过电感耦合等离子体质谱(ICP-MS,包括稀土示踪剂钆)将现场物理化学测量和元素谱分析与两个生物证据线结合起来:底栖硅藻组合,得出了Intercalibration Common Metric Index (ICMi)和筛选致畸风险,以及水螅再生试验,总结为致畸风险指数(TRI),具有行为终点。环境条件不均匀,部分站点富营养化,有机负荷高。ICMi将Almone和arone分类为“差”,Marta和Sacco分类为“好”,Mignone, Aniene, Tevere和Ninfa分类为“高”。TRI提示Almone有极高致畸风险;在玛尔塔、萨科和提维尔高中;洛在阿罗内、米尼奥内和阿涅内;在尼法没有风险。在所有地点均检测到硅藻致畸,并在Tevere达到峰值。ICMi与钆呈负相关(r = -0.76,p <; 0.05),而TRI与ICMi不相关。这些结果表明,生态状况和致畸危害不需要趋同。在低剂量和复杂混合物中,即使在ICMi为好/高的情况下,TRI也捕获了生物体水平的发育和神经功能损伤。将生物和社区层面的指标与目标化学结合起来,提供了一个敏感的、具有成本效益的框架,可以标记热点,优先监测新出现的污染物,并支持水框架指令下的风险管理。
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引用次数: 0
Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice 反复吸入聚苯乙烯纳米塑料可诱导小鼠持续肺损伤和纤维化
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-12 DOI: 10.1016/j.ecoenv.2026.120007
Zhiyang Han , Luan Wang , Xiang Li , Yumeng Dai , Xinyu Guan , Zhencheng Su , Xu Li , Xiujuan Wang , Tiegang Li , Mingkai Xu
Atmospheric nanoplastics represent an emerging environmental health concern, as their small size and physicochemical properties facilitate unintentional inhalation. However, their pulmonary toxicity under repeated exposure and following exposure cessation remains poorly understood. Here, polystyrene nanoplastics (PS-NPs) with different particle sizes (25, 100, and 500 nm) were intratracheally instilled into C57BL/6 mice at doses of 1 and 5 mg/kg body weight, three times per week for four weeks (exposure period, EXP), followed by a two-week post-exposure period (PEP). A ddH₂O-treated group was included as the control. PS-NPs accumulated extensively in the lungs and translocated to the heart, liver, spleen, and kidneys. Notably, inhaled nanoplastics sustained in lung tissue after PEP. Exposure to PS-NPs disrupted the alveolar epithelial barrier, induced inflammation, and oxidative stress in lung tissue, altered lung function, led to pulmonary fibrosis, and reduced peripheral white blood cell counts. These toxic effects were particle size-dependent, with smaller particles inducing greater toxicity. Moreover, adverse effects sustained during PEP, indicating that PS-NPs–induced injury was not readily reversible in the short term. Furthermore, our results suggest that macrophage polarization is involved in the progression of PS-NPs–induced pulmonary fibrosis. These findings demonstrate that repeated inhalation exposure to PS-NPs can induce sustained pulmonary injury, with incomplete recovery observed during PEP, highlighting potential respiratory health concerns associated with airborne nanoplastics.
大气纳米塑料代表了一个新兴的环境健康问题,因为它们的小尺寸和物理化学性质便于无意吸入。然而,它们在反复暴露和停止暴露后的肺毒性仍然知之甚少。本研究将不同粒径(25、100和500 nm)的聚苯乙烯纳米塑料(PS-NPs)以1和5 mg/kg体重的剂量经气管注入C57BL/6小鼠,每周3次,持续4周(暴露期,EXP),然后进行两周的暴露后期(PEP)。以ddH₂处理组为对照组。PS-NPs在肺部广泛积聚,并转移到心脏、肝脏、脾脏和肾脏。值得注意的是,PEP后吸入的纳米塑料在肺组织中持续存在。暴露于PS-NPs破坏肺泡上皮屏障,诱导肺组织炎症和氧化应激,改变肺功能,导致肺纤维化,降低外周血白细胞计数。这些毒性作用与颗粒大小有关,颗粒越小毒性越大。此外,PEP期间的不良反应持续存在,表明ps - nps诱导的损伤在短期内不易逆转。此外,我们的研究结果表明巨噬细胞极化参与了ps - nps诱导的肺纤维化的进展。这些研究结果表明,反复吸入PS-NPs可诱导持续肺损伤,PEP期间观察到不完全恢复,突出了与空气传播纳米塑料相关的潜在呼吸健康问题。
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引用次数: 0
Heat priming protects oyster gills from subsequent lethal heat stress: Histopathology and apoptosis evidence in Crassostrea angulata 热启动保护牡蛎鳃免受随后的致死热应激:角长牡蛎的组织病理学和细胞凋亡证据
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-13 DOI: 10.1016/j.ecoenv.2026.120026
Wenxin Chen , Ziqiang Han , Qingxiang Xu , Yikun He , Sang Van Vu , Tong Li , Huayong Que
Acquired thermotolerance (heat priming) enables organisms to withstand lethal heat stress after prior sublethal exposure. While documented in bivalves through survival analyses, histological mechanisms in gills—their primary environmental interface—remain unclear. This study investigated heat priming effects on Crassostrea angulata gills using four experimental groups: control, sublethal, priming (sublethal + lethal), and lethal. Histopathology (HE staining and SEM) and apoptosis (TUNEL) were analyzed under varying thermal regimes. Lethal stress induced more than 20% gill shrinkage (vs. control) with elevated mucus cell counts, while SEM revealed exacerbated filament breakage and ciliary loss. Priming pretreatment significantly reduced filament contraction and mitigated structural damage. TUNEL-positive cell density peaked in the lethal group, showing an eightfold increase over priming at 48 h, whereas priming and sublethal groups exhibited comparable level. These findings indicate that heat priming synergistically alleviates both mechanical damage (gill shrinkage/filament disruption) and TUNEL-detected cell-death signals during subsequent lethal stress. The study establishes a tissue-level foundation for understanding acquired thermotolerance in oysters.
获得性热耐受性(热启动)使生物体在先前的亚致死暴露后能够承受致命的热应激。虽然通过生存分析记录了双壳类动物,但鳃的组织学机制(它们的主要环境界面)仍不清楚。本研究采用对照组、亚致死组、热启动(亚致死+致死)组和致死组研究热启动对角长牡蛎鳃的影响。在不同的热环境下分析组织病理学(HE染色和SEM)和细胞凋亡(TUNEL)。致死应激诱导超过20%的鳃收缩(与对照组相比),粘液细胞计数升高,而扫描电镜显示纤维断裂和纤毛丢失加剧。预处理显著减少纤维收缩和减轻结构损伤。tunel阳性细胞密度在致死组达到峰值,在48 h时比启动组增加了8倍,而启动组和亚致死组表现出相当的水平。这些发现表明,在随后的致死应激中,热启动协同缓解了机械损伤(鳃收缩/细丝断裂)和tunel检测到的细胞死亡信号。该研究为理解牡蛎获得性耐热性奠定了组织水平的基础。
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引用次数: 0
Survival over growth: Accelerated bursa of Fabricius development enhances immune resilience in heavy metal-exposed tree sparrows 生存高于生长:法氏囊的加速发育增强了重金属暴露的树麻雀的免疫弹性
IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-15 Epub Date: 2026-03-12 DOI: 10.1016/j.ecoenv.2026.120004
Yue Shen, Zhaocun Lin, Yuquan Miao, Ming Zhang, Wenya Zhang, Yingmei Zhang
The bursa of Fabricius (BF), a regressive lymphoid organ unique to avian species, plays a pivotal role in early immune defense post-hatching: it not only mediates innate immune responses but also provides a microenvironment necessary for B-cell maturation, thereby playing an indispensable role in the development and functional maturation of the avian adaptive immune system. Life history theory predicts energy allocation trade-offs in response to environmental challenges, which often suppresses costly processes like immunity to prioritize survival. This study investigated effects of long-term environmental heavy metal pollution on these trade-offs and BF development in the tree sparrow (Passer montanus). Contrary to the paradigm of stress-induced immunosuppression, we found that despite significant impairments in body condition and growth rate, nestlings from a polluted site exhibited enhanced BF development. This was demonstrated through three key phenotypic adaptations: (1) an increased BF coefficient, (2) accelerated follicular development and histological maturation, and (3) increased B-lymphocyte density and migration to the spleen. Nestlings from a polluted site also displayed enhanced innate immunity and antioxidant defenses. An Integrated Biological Response (IBR) model suggested a strategic energy reallocation where investment in growth was suppressed to prioritize immune organ development and function. These findings provide a novel perspective on adaptive life-history strategies, demonstrating that birds can prioritize immune resilience to persist in contaminated environments at a cost to somatic development.
法氏囊(bursa of Fabricius, BF)是鸟类特有的退行性淋巴器官,在孵化后的早期免疫防御中起着关键作用:它不仅介导先天免疫应答,还提供b细胞成熟所需的微环境,因此在鸟类适应性免疫系统的发育和功能成熟中起着不可或缺的作用。生命史理论预测了能量分配的权衡,以应对环境挑战,这通常会抑制昂贵的过程,如优先考虑生存的免疫力。本研究探讨了长期环境重金属污染对树雀(Passer montanus)这些权衡和BF发育的影响。与应激诱导免疫抑制的范式相反,我们发现,尽管受到污染的雏鸟身体状况和生长速度明显受损,但来自污染地点的雏鸟表现出增强的BF发育。这通过三个关键的表型适应来证明:(1)BF系数增加,(2)卵泡发育和组织学成熟加速,(3)b淋巴细胞密度增加和向脾脏迁移。来自污染地区的雏鸟也表现出增强的先天免疫和抗氧化防御能力。综合生物反应(IBR)模型表明,在抑制生长投资以优先考虑免疫器官发育和功能的战略能量重新分配中。这些发现为适应性生活史策略提供了一个新的视角,表明鸟类可以优先考虑免疫弹性,以维持在污染环境中,以牺牲体细胞发育为代价。
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Ecotoxicology and Environmental Safety
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