Ecotoxicology and Environmental Safety最新文献

Crotonaldehyde paralyzes arteries by inducing impairment of ion channels, vascular histiocytic injury, overproduction of reactive oxygen species, mitochondrial damage, and autophagy 巴豆醛通过诱导离子通道受损、血管组织细胞损伤、活性氧过量产生、线粒体损伤和自噬来麻痹动脉

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117083

Humans are ubiquitously exposed to crotonaldehyde (CRA) endogenously and exogenously. Deeper knowledge of the pharmacological and toxicological characteristics and the mechanisms of CRA on vasculature is urgently needed for prevention of its harmfulness. The effects of acute and prolonged exposure to CRA were studied in rat isolated arteries and arterial smooth muscle cells (ASMCs). Instant exposure to CRA (1–300 μM) concentration-dependently declined the tension of pre-constricted arteries with an irreversible depression on the contractility. Prolonged exposure of rat coronary arteries (RCAs) to CRA concentration- and time-dependently depressed the arterial contractile responsiveness to various vasoconstrictors including depolarization, U46619, serotonin and Bay K8644 (an agonist of voltage-gated Ca²⁺ channels (VGCCs)). In fresh RCA ASMCs, CRA abated depolarization-induced elevation of intracellular Ca²⁺ ([Ca²⁺]_i). Electrophysiological study revealed that acute exposure to CRA depressed the functions of Ca²⁺-activated Cl^- channels (CaCCs), voltage-gated K⁺ (Kv) channels and inward rectifier K⁺ (Kir) channels in RCA ASMCs. Prolonged exposure of RCAs to CRA reduced the expressions of these ion channels in RCA ASMCs, disordered tissue frames, injured arterial cells, and increased autophagosomes in both ASMCs and endothelial cells. In rat aortic smooth muscle cells (A7r5), CRA exposure decreased the cell viability, elevated the intracellular levels of reactive oxygen species, reduced the mitochondrial membrane potential, and enhanced autophagy. Taken together, the present study for the first time portrays a clearer panoramic outline of the vascular effects and the mechanisms of CRA on arteries, demonstrates that CRA impairs arterial contractility, depresses VGCCs, CaCCs, Kv channels and Kir channels, reduces cell viability, and destroys the arterial histiocytes, and suggests that excessive oxidative stress, mitochondrial dysfunction and autophagy underlie these vascular damages. These findings are significant for the comprehensive evaluation of the vicious effects of CRA on arteries and suggest potential preventive strategies.

人类无处不在地暴露于巴豆醛（CRA）的内源性和外源性环境中。为了预防巴豆醛对血管的危害，迫切需要深入了解巴豆醛的药理毒理特征和作用机制。研究人员在大鼠离体动脉和动脉平滑肌细胞（ASMCs）中研究了急性和长期暴露于 CRA 的影响。瞬间暴露于 CRA（1-300 μM）浓度依赖性地降低了收缩前动脉的张力，并对收缩力造成了不可逆的抑制。将大鼠冠状动脉（RCA）长时间暴露于 CRA 中，其浓度和时间依赖性会抑制动脉对各种血管收缩剂（包括去极化、U46619、5-羟色胺和 Bay K8644（电压门控 Ca2+ 通道（VGCCs）激动剂））的收缩反应性。在新鲜的 RCA ASMCs 中，CRA 可抑制去极化诱导的细胞内 Ca2+ 升高（[Ca2+]i）。电生理学研究显示，急性暴露于 CRA 会抑制 RCA ASMCs 中 Ca2+ 激活的 Cl- 通道（CaCCs）、电压门控 K+ (Kv) 通道和内向整流 K+ (Kir) 通道的功能。将 RCA 长期暴露于 CRA 会降低 RCA ASMCs、紊乱组织框架和受伤动脉细胞中这些离子通道的表达，并增加 ASMCs 和内皮细胞中的自噬体。在大鼠主动脉平滑肌细胞（A7r5）中，暴露于 CRA 会降低细胞活力、升高细胞内活性氧水平、降低线粒体膜电位并增强自噬作用。综上所述，本研究首次较为清晰地勾勒出了 CRA 对动脉血管的影响及其机制，证明了 CRA 会损害动脉收缩力，抑制 VGCC、CaCC、Kv 通道和 Kir 通道，降低细胞活力，破坏动脉组织细胞，并表明过度氧化应激、线粒体功能障碍和自噬是这些血管损伤的基础。这些发现对全面评估 CRA 对动脉的恶性影响具有重要意义，并提出了潜在的预防策略。

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引用次数: 0

Polystyrene nanoplastics mediate skeletal toxicity through oxidative stress and the BMP pathway in zebrafish (Danio rerio) 聚苯乙烯纳米塑料通过氧化应激和 BMP 通路介导斑马鱼（Danio rerio）的骨骼毒性

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117096

The widespread presence of micro(nano)plastics (MNPs) has generated public concern. Studies have indicated that MNPs can accumulate in mammalian bones; however, research on the skeletal toxicity and underlying molecular mechanisms of MNPs in aquatic organisms remains limited. We subjected zebrafish embryos to three varying levels (1, 10, 100 μg/mL) of polystyrene nanoplastics (PSNPs) exposure over a period of 7 days in our research. The results revealed that PSNPs significantly reduced the body length and hatching rate of zebrafish, leading to skeletal deformities. mRNA level analysis showed significant upregulation of sp7, sparc, and smad1 genes transcription by PSNPs. Moreover, PSNPs markedly downregulated the mRNA levels associated with runx2a, bmp2a, and bmp4. Further investigations demonstrated that PSNPs dramatically increased ROS levels in zebrafish larvae, with significant downregulation of transcription levels of sod1 and cat genes, resulting in a sharp increase in transcription levels of apoptosis-related regulatory genes bcl-2 and bax. Furthermore, PSNPs led to a marked rise in Caspase 3 activity in zebrafish larvae, suggesting the initiation of apoptosis. PSNPs also notably inhibited alkaline phosphatase (AKP) activity. Compared to a 4-day exposure, a 7-day exposure to PSNPs intensified abnormalities across multiple indicators. In summary, our research indicates that PSNPs cause significant oxidative stress in zebrafish larvae, resulting in apoptosis. Moreover, PSNPs disrupt the transcription of genes related to skeletal development through the bone morphogenetic protein (BMP) pathway, further disrupting skeletal development processes and ultimately resulting in skeletal deformities in zebrafish larvae. This study provides new insights into the skeletal toxicity of MNPs.

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引用次数: 0

Effect of the residual levofloxacin on hydroponic vegetables with sewage treatment plant tailwater: Microbial community, discharge risk and control strategy 残留左氧氟沙星对使用污水处理厂尾水的水培蔬菜的影响：微生物群落、排放风险和控制策略

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117087

Tailwater-based hydroponic vegetable is a promising strategy for domestic wastewater recycling. However, the effect of residual antibiotics on the hydroponic vegetable system and the relation between hydroponic culture parameters and the residual water quality are still unclear. Here, the typical antibiotic Levofloxacin (LVFX) was employed, and the effect of LVFX (5 mg/L) on the residual water quality, plant growth and microbial community of water spinach hydroponic culture system were investigated under different hydraulic residence times (HRT). Obvious toxic effects on water spinach were observed, and the highest removal rate of LVFX (about 6 %) and TN (25.67±1.43 %) was observed when HRT was 7 days. Hydroponic culture increased the microbial abundance, diversity, and microbial community stability. To optimize the hydroponic culture, actual sewage plant tailwater spiked with 20 μg/L LVFX, along with three common planting substrates (sponge, ceramsite, and activated carbon) were used for the hydroponic culture of lettuce (seasonal reasons). The inhibition effect of LVFX on the removal of NO₃^--N and TN was observed even as the LVFX concentration decreased significantly (from 14.62 ± 0.44 μg/L to 0.65 ± 0.07 μg/L). The best growth situation of lettuce and removal rates of NH₄⁺-N, NO₃^--N, TN, especially LVFX (up to 95.65 ± 0.54 %) were observed in the activated carbon treated group. The overall results indicate the negative effect of residual antibiotics on the hydroponic vegetable systems, and adding activated carbon as substrate is an effective strategy for supporting plant growth and controlling discharged risk.

基于尾水的水培蔬菜是一种很有前景的生活污水循环利用策略。然而，残留抗生素对水培蔬菜系统的影响以及水培培养参数与残留水质之间的关系仍不清楚。本文采用典型抗生素左氧氟沙星（LVFX），研究了在不同水力停留时间（HRT）下，左氧氟沙星（5 mg/L）对蕹菜水培系统残留水质、植物生长和微生物群落的影响。水力停留时间为 7 天时，LVFX 的去除率最高（约 6%），TN 的去除率最高（25.67±1.43%）。水培提高了微生物丰度、多样性和微生物群落稳定性。为了优化水培，实际污水厂尾水中添加了 20 μg/L LVFX，并使用三种常见的种植基质（海绵、陶瓷石和活性炭）对生菜进行水培（季节原因）。即使 LVFX 浓度显著降低（从 14.62 ± 0.44 μg/L 降至 0.65 ± 0.07 μg/L），也能观察到 LVFX 对去除 NO3-N 和 TN 的抑制作用。活性炭处理组的莴苣生长状况最好，NH4+-N、NO3--N、TN，尤其是 LVFX 的去除率最高（达 95.65 ± 0.54 %）。总体结果表明，残留抗生素对水培蔬菜系统有负面影响，而添加活性炭作为基质是支持植物生长和控制排放风险的有效策略。

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引用次数: 0

Taraxasterol attenuates zearalenone-induced kidney damage in mice by modulating oxidative stress and endoplasmic reticulum stress 蒲公英甾醇通过调节氧化应激和内质网应激减轻玉米赤霉烯酮诱发的小鼠肾损伤

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117093

Taraxasterol is one of the bioactive ingredients from traditional Chinese herb Taraxacum, which exhibits multiple pharmacological activities and protective effects. However, the underlying influence and mechanism of its use against kidney damage caused from zearalenone (ZEA) remain unexplored. The ZEA-induced kidney damage model of mice was established by feeding diets containing ZEA (2 mg/kg), and taraxasterol (5 and 10 mg/kg) was administered by gavage for 28 days. Results demonstrated taraxasterol increased average daily gain (ADG) and average daily feed intake (ADFI), reduced feed-to-gain ratio (F/G) and kidney index of mice induced by ZEA. Taraxasterol alleviated histopathological changes of kidney, reduced ZEA residue and the levels of blood urea nitrogen (BUN), uric acid (UA), and creatinine (CRE). Concurrently, taraxasterol reduced the contents of oxidative stress indicator reactive oxygen species (ROS) and malondialdehyde (MDA), and increased the activities of antioxidant enzymes catalase (CAT), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px). Further, taraxasterol up-regulated the mRNA and protein expression of nuclear factor erythroid-2-related factor 2 (Nrf2), GSH-Px, NAD(P)H quinone oxidoreductase 1 (NQO1), and heme oxygenase-1 (HO-1), and down-regulated the mRNA and protein expression of KELCH like ECH associated protein (Keap1) in Nrf2/Keap1 pathway. Taraxasterol down-regulated the mRNA and protein expression of immunoglobulin binding protein (Bip), C/EBP homologous protein (CHOP), Bcl-2 associated X (Bax), cysteine protease (Caspase)-12, and Caspase-3, and up-regulated B-cell lymphoma 2 (Bcl-2) expression in endoplasmic reticulum stress pathway. This study suggests that taraxasterol attenuates ZEA-induced mouse kidney damage through the modulation of Nrf2/Keapl pathway to play antioxidant role and endoplasmic reticulum stress pathway to enhance anti-apoptotic ability. It will provide a basis for taraxasterol as a potential drug to prevent and treat ZEA-induced kidney damage.

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引用次数: 0

Dietary Aflatoxin G1 exposure causes an imbalance between pulmonary tissue-resident alveolar macrophages and monocyte-derived macrophages in both mother and offspring mice 膳食中黄曲霉毒素 G1 的暴露会导致母鼠和子鼠肺组织驻留的肺泡巨噬细胞与单核细胞衍生的巨噬细胞之间的失衡

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117082

Aflatoxin G₁ (AFG₁) is a mycotoxin commonly found in agricultural products, including dried fruits, meat, and milk products. Oral AFG₁ administration induced tumor necrosis factor (TNF)-α-dependent chronic pulmonary inflammation, promoting AFG₁-induced damage in alveolar epithelial cell, which is associated with lung adenocarcinoma. Pulmonary macrophages may be divided into tissue-resident alveolar macrophages (TRAMs) and monocyte-derived macrophages (MoMs), which involve in chronic lung inflammation. However, whether these macrophages contribute to AFG₁-induced chronic pulmonary inflammation remains unknown. In this study, we found oral AFG₁ administration disrupted the balance between TRAMs and MoMs, increasing MoMs infiltration and decreasing the number of TRAMs. AFG₁ upregulated TNF-α expression in MoMs, but downregulated sialic acid binding Ig-like lectin F (Siglec-F) expression in TRAMs. Inhibition of TNF-α-dependent inflammation rescued the imbalance between TRAMs and MoMs in AFG₁-treated lung tissues. Additionally, AFG₁ stimulated MoMs differentiation to the proinflammatory M1 phenotype in vitro. Using a specific in vitro TRAM model, AFG₁ downregulated Siglec-F and the M2 phenotypic markers arginase 1 and YM1, and upregulated the M1 phenotypic markers IL-6, iNOS and TNF-α, altering the TRAMs phenotype to the pro-inflammatory M1 phenotype in vitro. Additionally, mouse maternal dietary exposure to AFG₁ caused an imbalance in pulmonary macrophages, decreasing TRAMs and increasing MoMs population in offspring, which was associated with proliferative lesions in the alveolar septa. Thus, dietary AFG₁ exposure triggered an imbalance in pulmonary macrophages in both mother and offspring mice, and induced pro-inflammatory phenotypic alterations, which contributed to AFG₁-induced chronic lung inflammation. These results provide clues to how AFG₁-induced immunotoxicity and genotoxicity in humans might be prevented.

黄曲霉毒素 G1（AFG1）是一种常见于干果、肉类和奶制品等农产品中的霉菌毒素。口服 AFG1 可诱导肿瘤坏死因子（TNF）-α 依赖性慢性肺部炎症，促进 AFG1 诱导的肺泡上皮细胞损伤，这与肺腺癌有关。肺巨噬细胞可分为组织驻留肺泡巨噬细胞（TRAMs）和单核细胞衍生巨噬细胞（MoMs），它们参与了慢性肺部炎症。然而，这些巨噬细胞是否参与了 AFG1 诱导的慢性肺部炎症仍是未知数。本研究发现，口服 AFG1 会破坏 TRAMs 和 MoMs 之间的平衡，增加 MoMs 的浸润，减少 TRAMs 的数量。AFG1会上调MoMs中TNF-α的表达，但会下调TRAMs中与硅铝酸结合的Ig样凝集素F（Siglec-F）的表达。抑制 TNF-α 依赖性炎症可以缓解 AFG1 处理的肺组织中 TRAMs 和 MoMs 之间的失衡。此外，AFG1 还能刺激 MoMs 在体外向促炎 M1 表型分化。利用特定的体外 TRAM 模型，AFG1 下调了 Siglec-F 以及 M2 表型标志物精氨酸酶 1 和 YM1，并上调了 M1 表型标志物 IL-6、iNOS 和 TNF-α，从而改变了体外 TRAMs 表型，使其变为促炎 M1 表型。此外，小鼠母体膳食暴露于 AFG1 会导致肺巨噬细胞失衡，后代中 TRAMs 数量减少，MoMs 数量增加，这与肺泡间隔的增殖性病变有关。因此，膳食AFG1暴露会引发母鼠和子鼠肺巨噬细胞的失衡，并诱导促炎症表型的改变，从而导致AFG1诱导的慢性肺炎症。这些结果为如何预防AFG1诱导的人类免疫毒性和遗传毒性提供了线索。

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引用次数: 0

Exploring the mechanisms of organic fertilizers on Cd bioavailability in rice fields: Environmental behavior and effect factors 探索有机肥对水稻田镉生物利用率的影响机制：环境行为和影响因素

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117094

The problem of paddy Cadmium (Cd) contamination is currently the focus of global research. Earlier researches have confirmed that utilization of organic fertilizers regulates Cd chemical fraction distribution by increases organic bound Cd. However, environmental behaviours of organic fertilizers in paddy are still lack exploration. Here, we critical reviewed previous publications and proposed a novel research concept to help us better understand it. Three potential impact pathways of utilization of organic fertilizers on the bioavailability of Cd are presented: (i) use of organic fertilizers changes soil physicochemical properties, which directly affects Cd bioavailability by changing chemical form of Cd(II); (ii) use of organic fertilizers increases soil nutrient content, which indirectly regulates Cd supply and bioaccumulation through ion adsorption and competition for ion-transport channels between nutrients and Cd; and (iii) use of organic fertilizers increases activity of microorganisms and efflux of rice root exudates, which indirectly affects Cd bioavailability of through complexation and sequestration of these organic materials with Cd. Meanwhile, dissolved organic matter (DOM) in the rhizosphere of rice is believed to be the key to revealing the effects of organic fertilizers on Cd. DOM is capable of adsorption and complexation-chelation reactions with Cd and the fractionation of Cd(II) is regulated by DOM. Molecular mass, chemical composition, major functional groups and reaction sequence of DOM determine the formation and solubilization of DOM-Cd complexes.

水稻镉（Cd）污染问题是目前全球研究的焦点。早期的研究已经证实，有机肥的使用会增加有机结合镉，从而调节镉化学组分的分布。然而，有机肥在水稻中的环境行为仍缺乏研究。在此，我们对以前的文献进行了批判性的回顾，并提出了一个新的研究概念，以帮助我们更好地理解这一问题。本文提出了利用有机肥对镉的生物利用率的三种潜在影响途径：(i) 施用有机肥改变土壤理化性质，通过改变镉（II）的化学形态直接影响镉的生物利用率；(ii) 施用有机肥增加土壤养分含量，通过离子吸附和养分与镉之间的离子传输通道竞争间接调节镉的供应和生物累积；(iii) 施用有机肥会增加微生物的活性和水稻根系渗出液的外流，通过这些有机物与镉的络合和固碳作用，间接影响镉的生物利用率。同时，水稻根圈中的溶解有机物（DOM）被认为是揭示有机肥对镉影响的关键。DOM 能够与 Cd 发生吸附和络合-螯合反应，Cd(II) 的分馏受 DOM 的调节。DOM 的分子质量、化学成分、主要官能团和反应顺序决定了 DOM-Cd 复合物的形成和溶解。

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引用次数: 0

Potential toxicity of carbonaceous nanomaterials on aquatic organisms and their alleviation strategies: A review 碳质纳米材料对水生生物的潜在毒性及其缓解策略：综述

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-23 DOI: 10.1016/j.ecoenv.2024.117019

Carbonaceous nanomaterials (CNMs) are widely used in electronics, biomedicine, agriculture, environmental remediation, and catalysis due to their excellent biocompatibility, high reactivity, and high specific surface area. However, the extensive applications of CNMs cause their inevitable release into water, which may result in toxic effects on the aquatic ecological environment and organisms. CNMs can cause lipid peroxidation damage and neurotoxicity in aquatic organisms, affecting embryo hatching and larval morphology. The effects of CNMs on aquatic organisms vary depending on their structures and physicochemical properties, as well as the species, age, and tolerance of the tested organisms. The above uncertainties have increased the difficulty of exploring the impact of carbonaceous nanomaterials on the toxicity of aquatic organisms to a certain extent. Solving these issues is of great significance and reference value for promoting the research and safe utilization of carbon nanomaterials. Therefore, a systematic review of the effects of potential toxicity of carbonaceous nanomaterials on aquatic organisms and their alleviation strategies is needed. This paper firstly summarizes the toxic effects of commonly used CNMs (i.e., carbon nanotubes, graphene, and fullerene) on different aquatic organisms, which include developmental toxicity, behavioral and metabolic toxicity, reproductive toxicity, and organ toxicity. Then the main mechanisms of CNMs to aquatic organisms are further explored, and the methods to reduce the toxicity of CNMs are also summarized. Finally, the current challenges and future perspectives for studying CNM toxicity to aquatic organisms are proposed.

碳质纳米材料（CNMs）具有良好的生物相容性、高反应活性和高比表面积，因此被广泛应用于电子、生物医学、农业、环境修复和催化等领域。然而，氯化萘甲烷的广泛应用不可避免地会将其释放到水中，从而对水生生态环境和生物产生毒性影响。氯化萘甲烷可对水生生物造成脂质过氧化损伤和神经毒性，影响胚胎孵化和幼虫形态。氯化萘甲烷对水生生物的影响因其结构和理化性质以及受测生物的种类、年龄和耐受性而异。上述不确定性在一定程度上增加了探讨碳质纳米材料对水生生物毒性影响的难度。解决这些问题对于促进碳纳米材料的研究和安全利用具有重要的意义和参考价值。因此，有必要系统综述碳纳米材料对水生生物潜在毒性的影响及其缓解策略。本文首先概述了常用碳纳米材料（即碳纳米管、石墨烯和富勒烯）对不同水生生物的毒性效应，包括发育毒性、行为和代谢毒性、生殖毒性和器官毒性。然后进一步探讨了 CNMs 对水生生物的主要作用机制，并总结了降低 CNMs 毒性的方法。最后，提出了研究氯化萘对水生生物毒性的当前挑战和未来展望。

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引用次数: 0

Association between exposure to organophosphate esters metabolites and sarcopenia prevalence: A cross-sectional study using NHANES data 有机磷酸酯代谢物暴露与肌少症患病率之间的关系：利用 NHANES 数据进行的横断面研究。

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-21 DOI: 10.1016/j.ecoenv.2024.117041

Organophosphate esters (OPEs) are an emerging group of environmental pollutants linked to numerous health concerns, and their increasing prevalence in the environment is alarming. However, the impact of OPEs exposure on sarcopenia, a condition characterized by muscle loss and weakness, remains unknown. In this study, the connection between urinary metabolites of OPEs and the occurrence of sarcopenia was investigated using data from the National Health and Nutrition Examination Survey (NHANES) covering a period from 2011 to 2018. The analysis found that two specific urinary metabolites, Dibutyl phosphate (DBUP) and Bis (2-chloroethyl) phosphate (BCEP), were positively correlated with an increased risk of sarcopenia. Among these metabolites, DBUP had the highest contribution to sarcopenia development according to weighted quantile sum (WQS) model analysis. Additionally, it was observed that inflammation mediated the relationship between urinary exposure to DBUP/BCEP and the prevalence of sarcopenia. Overall, this research emphasizes the role of OPEs in the progression of sarcopenia, prompting concerns regarding their potential impact on health and advocating for further prospective investigations into their correlation with the risk of developing sarcopenia.

有机磷酸酯（OPEs）是一类新出现的环境污染物，与众多健康问题有关，其在环境中日益普遍的程度令人担忧。然而，暴露于 OPEs 对肌肉疏松症（一种以肌肉流失和虚弱为特征的疾病）的影响仍然未知。在这项研究中，研究人员利用美国国家健康与营养调查（NHANES）涵盖 2011 年至 2018 年期间的数据，调查了尿液中 OPEs 代谢物与肌肉疏松症发生率之间的联系。分析发现，磷酸二丁酯（DBUP）和磷酸二（2-氯乙基）酯（BCEP）这两种特定的尿液代谢物与肌肉疏松症风险的增加呈正相关。根据加权量化总和（WQS）模型分析，在这些代谢物中，DBUP对肌少症的发生影响最大。此外，研究还发现，炎症介导了尿液中的 DBUP/BCEP 暴露与肌肉疏松症发病率之间的关系。总之，这项研究强调了 OPE 在肌肉疏松症发展过程中的作用，引起了人们对其对健康的潜在影响的关注，并提倡对其与患肌肉疏松症风险的相关性进行进一步的前瞻性研究。

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引用次数: 0

Cardamonin inhibits silicosis development through the PI3K-AKT signaling pathway 白豆蔻素通过 PI3K-AKT 信号通路抑制矽肺病的发展。

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-21 DOI: 10.1016/j.ecoenv.2024.117067

Silicosis is one of the most severe occupational diseases characterized by inflammatory cell infiltration, fibroblasts activation, and fibrosis in the lung. However, specific drug treatments are lacking. Cardamonin (CDM) has been reported to possess antitumor, anti-inflammatory/fibrotic effects. While, the effect of CDM on the progression of silicosis remains unknown. In this study, we established a SiO₂-M stimulated fibroblast cell model, and explored the antifibrotic effect of CDM and the related molecular mechanism using WB, RT-qPCR, and immunofluorescence. The results indicate that CDM inhibits SiO₂-M-induced fibroblast activation, proliferation, and migration. Furthermore, a silicosis mouse model was established through injecting silica suspension intratracheally. The results revealed that CDM retards the progression of pulmonary fibrosis. The RNA sequencing results suggest that the antifibrotic effect of CDM may be mediated by the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. In conclusion, the results of this study demonstrate that CDM inhibits the development of silicosis via the PI3K-AKT signaling pathway, which could provide guidance for the development of drugs for silicosis treatment.

矽肺病是最严重的职业病之一，其特征是炎症细胞浸润、成纤维细胞活化和肺部纤维化。然而，目前还缺乏特效药物治疗。据报道，白豆蔻素（CDM）具有抗肿瘤、抗炎和抗纤维化的作用。但是，CDM 对矽肺病进展的影响仍然未知。本研究建立了二氧化硅-M刺激成纤维细胞模型，并利用WB、RT-qPCR和免疫荧光等方法探讨了CDM的抗纤维化作用及其相关分子机制。结果表明，CDM 可抑制 SiO2-M 诱导的成纤维细胞活化、增殖和迁移。此外，还通过气管内注射二氧化硅悬浮液建立了矽肺小鼠模型。结果显示，CDM 可延缓肺纤维化的进展。RNA 测序结果表明，CDM 的抗纤维化作用可能是由磷脂肌醇 3- 激酶/蛋白激酶 B（PI3K/AKT）信号通路介导的。总之，本研究结果表明，CDM可通过PI3K-AKT信号通路抑制矽肺的发展，这为开发治疗矽肺的药物提供了指导。

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引用次数: 0

How does increasing temperature affect the toxicity of bisphenol A on Cryptomonas ovata and its consumer Daphnia magna? 温度升高如何影响双酚 A 对卵隐杆线虫及其消费者大型蚤的毒性？

IF 6.2 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2024-09-21 DOI: 10.1016/j.ecoenv.2024.117090

The global rise in plastic production has led to significant plastic deposition in aquatic ecosystems, releasing chemical compounds as plastics degrade. Among these, bisphenol A (BPA) is a major global concern due to its endocrine-disrupting effects and widespread presence in aquatic environments. Furthermore, the toxicity of BPA on aquatic organisms can be modulated by global change stressors such as temperature, which plays an essential role in the metabolism of organisms, including the degradation and accumulation of toxic compounds. In this study, we aimed to understand how temperature can modulate the toxic effect of BPA on a phytoplankton species (Cryptomonas ovata) and how this effect can be transferred to its herbivorous consumer (Daphnia magna). To do this, we first determined the sensitivity of C. ovata over a BPA gradient (0–10 mg L⁻¹). Subsequently, we experimentally determined how the increase in temperature (+5ºC) could modify the toxic effect of BPA on the physiology, metabolism and growth of the phytoplankton. Finally, we investigated how this effect transferred to the growth rate of D. magna through food. Our results show a negative effect of BPA on C. ovata from 5 mg BPA L⁻¹, affecting its photosynthetic yield of photosystem II, net primary production, respiration, and growth. This effect was accelerated when the temperature was higher. Additionally, the growth rate of D. magna also decreased when fed on C. ovata grown in the presence of BPA and high temperature. Our results indicate that high temperature can accelerate the toxic effects of BPA on organisms located at the base of the food web and this effect could be transferred to higher levels through food.

全球塑料产量的增加导致大量塑料沉积在水生生态系统中，并在塑料降解过程中释放出化学物质。其中，双酚 A（BPA）因其干扰内分泌的作用和广泛存在于水生环境中而成为全球关注的焦点。此外，双酚 A 对水生生物的毒性可受温度等全球变化胁迫因素的调节，而温度在生物的新陈代谢（包括有毒化合物的降解和积累）中起着至关重要的作用。在这项研究中，我们旨在了解温度如何调节双酚 A 对浮游植物物种（卵形隐单胞菌）的毒性效应，以及这种效应如何转移到其食草性消费者（大型蚤）身上。为此，我们首先确定了 C. ovata 对双酚 A 梯度（0-10 毫克/升）的敏感性。随后，我们通过实验确定了温度的升高（+5ºC）如何改变双酚 A 对浮游植物的生理、新陈代谢和生长的毒性影响。最后，我们研究了这种影响如何通过食物转移到大型蚤的生长速度上。我们的结果表明，5 毫克双酚 A L-1 的双酚 A 对 C. ovata 有负面影响，影响其光合产物光系统 II、净初级生产量、呼吸作用和生长。温度越高，这种影响越明显。此外，以在双酚 A 和高温条件下生长的 C. ovata 为食，D. magna 的生长速度也会下降。我们的研究结果表明，高温会加速双酚 A 对食物网底层生物的毒性影响，这种影响会通过食物转移到更高的层次。

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引用次数: 0