首页 > 最新文献

Ecotoxicology and Environmental Safety最新文献

英文 中文
Soluble trehalase responds to heavy metal stimulation by regulating apoptosis in Neocaridina denticulata sinensis 可溶性三卤素酶通过调节中华新鲤中的细胞凋亡对重金属刺激做出反应。
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117072
Trehalase plays an important role in insect metabolism and development by hydrolyzing blood sugar trehalose, but it seems to perform primarily an immunomodulatory function in crustaceans whose blood sugar is glucose. Metal ions as pollutants seriously affecting crustacean health, but studies on trehalase in metal immunity are still limited. In this study, a soluble trehalase (NdTre1) that could bind to multiple metals was identified from Neocaridina denticulata sinensis for investigating metal resistance. Expression profiling revealed that NdTre1 was mainly expressed in the gill and was significantly decreased following stimulation with copper (Cu²⁺) and cadmium (Cd²⁺). Transcriptomic analysis of gills revealed an increase in ecdysone synthesis after interference with NdTre1. Increased ecdysone activated the endogenous mitochondrial pathway and the mitogen activated protein kinase (MAPK) pathway to further induced apoptosis. In vitro, Escherichia coli overexpressing recombinant NdTre1 had higher survival and faster growth rates to better adapted the metal-containing medium. Overall, NdTre1 exercises an important immune function in shrimp resistance to metal stimulation by regulating apoptosis and molting. Further investigation can further explore specific response mechanisms of NdTre1 to multiple metals.
颤藻糖酶通过水解血糖颤藻糖而在昆虫的新陈代谢和发育过程中发挥重要作用,但在血糖为葡萄糖的甲壳类动物中,它似乎主要发挥免疫调节功能。金属离子作为污染物严重影响甲壳类动物的健康,但有关三卤糖酶在金属免疫方面的研究仍然有限。本研究从Neocaridina denticulata sinensis中发现了一种可与多种金属结合的可溶性三卤化酶(NdTre1),用于研究金属抗性。表达谱分析显示,NdTre1主要在鳃中表达,在铜(Cu²⁺)和镉(Cd²⁺)刺激下表达量显著下降。鳃的转录组分析表明,在干扰 NdTre1 后,蜕皮激素合成增加。增加的蜕皮激素激活了内源性线粒体途径和丝裂原活化蛋白激酶(MAPK)途径,进一步诱导细胞凋亡。在体外,过表达重组 NdTre1 的大肠杆菌存活率更高,生长速度更快,能更好地适应含金属的培养基。总之,NdTre1 通过调节细胞凋亡和蜕皮,在对虾抵抗金属刺激的过程中发挥了重要的免疫功能。进一步的研究可以进一步探索 NdTre1 对多种金属的特定响应机制。
{"title":"Soluble trehalase responds to heavy metal stimulation by regulating apoptosis in Neocaridina denticulata sinensis","authors":"","doi":"10.1016/j.ecoenv.2024.117072","DOIUrl":"10.1016/j.ecoenv.2024.117072","url":null,"abstract":"<div><div>Trehalase plays an important role in insect metabolism and development by hydrolyzing blood sugar trehalose, but it seems to perform primarily an immunomodulatory function in crustaceans whose blood sugar is glucose. Metal ions as pollutants seriously affecting crustacean health, but studies on trehalase in metal immunity are still limited. In this study, a soluble trehalase (NdTre1) that could bind to multiple metals was identified from <em>Neocaridina denticulata sinensis</em> for investigating metal resistance. Expression profiling revealed that <em>NdTre1</em> was mainly expressed in the gill and was significantly decreased following stimulation with copper (Cu²⁺) and cadmium (Cd²⁺). Transcriptomic analysis of gills revealed an increase in ecdysone synthesis after interference with <em>NdTre1</em>. Increased ecdysone activated the endogenous mitochondrial pathway and the mitogen activated protein kinase (MAPK) pathway to further induced apoptosis. <em>In vitro</em>, <em>Escherichia coli</em> overexpressing recombinant NdTre1 had higher survival and faster growth rates to better adapted the metal-containing medium. Overall, <em>NdTre1</em> exercises an important immune function in shrimp resistance to metal stimulation by regulating apoptosis and molting. Further investigation can further explore specific response mechanisms of <em>NdTre1</em> to multiple metals.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011485/pdfft?md5=69a92e969ce375403b0b923ec07cd109&pid=1-s2.0-S0147651324011485-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277789","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}
引用次数: 0
Impacts of graphene oxide contamination on a food web: Threats to somatic and reproductive health of organisms 氧化石墨烯污染对食物网的影响:对生物体和生殖健康的威胁
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117032

Contamination of aquatic food webs with nanomaterials poses a significant ecological and human health challenge. Ingestion of nanomaterials alongside food disrupts digestion and impairs physiological processes, with potential consequences for organism fitness and survival. Complex interactions between nanomaterials and biota further exacerbate the issue, influencing life-history strategies and ecosystem dynamics. Accumulation of nanomaterials within autotrophic and detritus-based food webs raises concerns about biomagnification, especially for top-level consumers and seafood-dependent human populations. Understanding the extent and impact of nanomaterial contamination on aquatic biota is crucial for effective mitigation strategies. To address this challenge, we conducted a comprehensive study evaluating the bioaccumulation effects of graphene oxide (GO), a commonly used nanomaterial, within an aquatic food chain. Using a gnotobiotic freshwater microcosm, we investigated the effects of micro- and nano-scale GO sheets on key organisms: green algae (Chlorella vulgaris), brine shrimp (Artemia salina), and zebrafish (Danio rerio). Two feeding regimes, direct ingestion and trophic transfer, were employed to assess GO uptake and transfer within the food web. Direct exposure involved individual organisms being exposed to either nano- or micro-scale GO sheets, while trophic transfer involved a sequential exposure pathway: algae exposed to GO sheets, artemias feeding on the algae, and zebrafish consuming the artemias. Our study provides critical insights into nanomaterial contamination in aquatic ecosystems. Physicochemical properties of GO sheets, including ζ-potential and dispersion, were influenced by salt culture media, resulting in aggregation under salt conditions. Microscopic imaging confirmed the bioaccumulation of GO sheets within organisms, indicating prolonged exposure and potential long-term effects. Notably, biodistribution analysis in zebrafish demonstrated the penetration of nano-sized GO into the intestinal wall, signifying direct interaction with vital organs. Exposure to GO resulted in increased zebrafish mortality and impaired reproductive performance, particularly through trophic transfer. These findings emphasize the urgent need to address nanomaterial contamination in aquatic food webs to protect ecosystem components and human consumers. Our study highlights the importance of developing effective mitigation strategies to preserve the integrity of aquatic ecosystems, ensure resource sustainability, and safeguard human well-being. In conclusion, our study provides crucial insights into the impact of nanomaterial pollution on aquatic biota. By recognizing the challenges posed by nanomaterial contamination and implementing targeted interventions, we can mitigate the adverse effects, preserving the integrity of aquatic ecosystems and safeguarding human health.

纳米材料对水生食物网的污染对生态和人类健康构成了重大挑战。在摄入食物的同时摄入纳米材料会扰乱消化过程并损害生理过程,从而对生物体的健康和生存造成潜在影响。纳米材料与生物群之间复杂的相互作用进一步加剧了这一问题,影响了生命史策略和生态系统动态。纳米材料在自养食物网和基于残渣的食物网中的积累引起了生物放大的担忧,尤其是对顶级消费者和依赖海产品的人类而言。了解纳米材料污染的程度及其对水生生物群的影响对于制定有效的缓解策略至关重要。为了应对这一挑战,我们开展了一项综合研究,评估常用纳米材料氧化石墨烯(GO)在水生食物链中的生物累积效应。我们利用一个非生物淡水微观世界,研究了微米级和纳米级 GO 片材对主要生物的影响:绿藻(Chlorella vulgaris)、盐水虾(Artemia salina)和斑马鱼(Danio rerio)。为了评估食物网中对 GO 的吸收和转移情况,采用了两种喂养方式,即直接摄取和营养转移。直接接触是指生物个体接触纳米级或微米级的 GO 片材,而营养转移则是指生物个体依次接触 GO 片材:藻类接触 GO 片材、蓟马以藻类为食、斑马鱼食用蓟马。我们的研究为了解水生生态系统中的纳米材料污染提供了重要依据。GO 片的物理化学特性(包括ζ电位和分散性)受到盐培养基的影响,导致其在盐条件下聚集。显微成像证实了 GO 片在生物体内的生物累积性,表明生物体长期接触 GO 片,可能会受到长期影响。值得注意的是,对斑马鱼进行的生物分布分析表明,纳米级的 GO 可渗透到肠壁,这表明 GO 可与重要器官直接相互作用。暴露于 GO 会导致斑马鱼死亡率上升,生殖能力受损,特别是通过营养传递。这些发现强调,迫切需要解决水生食物网中的纳米材料污染问题,以保护生态系统组成部分和人类消费者。我们的研究强调了制定有效的缓解策略以保护水生生态系统完整性、确保资源可持续性和保障人类福祉的重要性。总之,我们的研究提供了纳米材料污染对水生生物群影响的重要见解。通过认识纳米材料污染带来的挑战并实施有针对性的干预措施,我们可以减轻其不利影响,保护水生生态系统的完整性并保障人类健康。
{"title":"Impacts of graphene oxide contamination on a food web: Threats to somatic and reproductive health of organisms","authors":"","doi":"10.1016/j.ecoenv.2024.117032","DOIUrl":"10.1016/j.ecoenv.2024.117032","url":null,"abstract":"<div><p>Contamination of aquatic food webs with nanomaterials poses a significant ecological and human health challenge. Ingestion of nanomaterials alongside food disrupts digestion and impairs physiological processes, with potential consequences for organism fitness and survival. Complex interactions between nanomaterials and biota further exacerbate the issue, influencing life-history strategies and ecosystem dynamics. Accumulation of nanomaterials within autotrophic and detritus-based food webs raises concerns about biomagnification, especially for top-level consumers and seafood-dependent human populations. Understanding the extent and impact of nanomaterial contamination on aquatic biota is crucial for effective mitigation strategies. To address this challenge, we conducted a comprehensive study evaluating the bioaccumulation effects of graphene oxide (GO), a commonly used nanomaterial, within an aquatic food chain. Using a gnotobiotic freshwater microcosm, we investigated the effects of micro- and nano-scale GO sheets on key organisms: green algae (Chlorella vulgaris), brine shrimp (Artemia salina), and zebrafish (Danio rerio). Two feeding regimes, direct ingestion and trophic transfer, were employed to assess GO uptake and transfer within the food web. Direct exposure involved individual organisms being exposed to either nano- or micro-scale GO sheets, while trophic transfer involved a sequential exposure pathway: algae exposed to GO sheets, artemias feeding on the algae, and zebrafish consuming the artemias. Our study provides critical insights into nanomaterial contamination in aquatic ecosystems. Physicochemical properties of GO sheets, including ζ-potential and dispersion, were influenced by salt culture media, resulting in aggregation under salt conditions. Microscopic imaging confirmed the bioaccumulation of GO sheets within organisms, indicating prolonged exposure and potential long-term effects. Notably, biodistribution analysis in zebrafish demonstrated the penetration of nano-sized GO into the intestinal wall, signifying direct interaction with vital organs. Exposure to GO resulted in increased zebrafish mortality and impaired reproductive performance, particularly through trophic transfer. These findings emphasize the urgent need to address nanomaterial contamination in aquatic food webs to protect ecosystem components and human consumers. Our study highlights the importance of developing effective mitigation strategies to preserve the integrity of aquatic ecosystems, ensure resource sustainability, and safeguard human well-being. In conclusion, our study provides crucial insights into the impact of nanomaterial pollution on aquatic biota. By recognizing the challenges posed by nanomaterial contamination and implementing targeted interventions, we can mitigate the adverse effects, preserving the integrity of aquatic ecosystems and safeguarding human health.</p></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011084/pdfft?md5=d6d34b36d779fc8f17219adb56e21c02&pid=1-s2.0-S0147651324011084-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243155","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}
引用次数: 0
Establishment of tumor microenvironment following bisphenol A exposure in the testis 睾丸接触双酚 A 后肿瘤微环境的建立。
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117071
Although detrimental roles of bisphenol A (BPA) in xenoestrogen target organs, testis and epididymis, and male fertility are well-documented, disruption of the immune privilege system in the male reproductive tract following BPA exposure remains poorly understood. Therefore, this study aimed to explore the precise mechanisms of BPA in interfering immune privilege in the testis on RNA sequencing results. CD-1 male mice were daily treated no-observed-adverse-effect (NOAEL, 5 mg BPA/kg BW) and lowest-observed-adverse-effects (LOAEL, 50 mg BPA/kg BW) of BPA by oral gavage for 6 weeks. Following the LOAEL exposure, the expression of immune response-associated transcripts was upregulated in the testis. Moreover, BPA switch the testicular microenvironment to tumor friendly through the recruitment of tumor associated macrophages (TAMs), which can produce both anti- and pro-inflammatory cytokines, such as TNF-α, TLR2, IL-10, and CXCL9. Number of testicular blood vessels were approximately 2-times increased by upregulation of matrix metallopeptidase 2 in TAMs and upregulation of AR expression in the nucleus of Leydig cells. Moreover, we found that the tumor-supportive environment can also be generated even though NOAEL BPA concentration due to the individual’s variability in cancer susceptibility.
尽管双酚 A(BPA)对异雌激素靶器官、睾丸和附睾以及男性生育能力的有害作用已得到充分证实,但人们对暴露于双酚 A 后男性生殖道免疫特权系统的破坏仍然知之甚少。因此,本研究旨在根据 RNA 测序结果探索双酚 A 干扰睾丸免疫特权的确切机制。研究人员对 CD-1 雄性小鼠进行了为期 6 周的口服双酚 A 暴露试验,每天分别给予小鼠无不良效应水平(NOAEL,5 毫克双酚 A/千克体重)和最低不良效应水平(LOAEL,50 毫克双酚 A/千克体重)的双酚 A 暴露剂量。暴露于最低观测不良效应水平后,睾丸中与免疫反应相关的转录本表达上调。此外,双酚 A 通过招募肿瘤相关巨噬细胞(TAMs)将睾丸微环境转换为肿瘤友好环境,TAMs 可产生抗炎和促炎细胞因子,如 TNF-α、TLR2、IL-10 和 CXCL9。通过上调 TAMs 中的基质金属肽酶 2 和上调 Leydig 细胞核中 AR 的表达,睾丸血管的数量增加了约 2 倍。此外,我们还发现,由于个体对癌症的易感性不同,即使无观测不良效应水平双酚 A 浓度也会产生肿瘤支持环境。
{"title":"Establishment of tumor microenvironment following bisphenol A exposure in the testis","authors":"","doi":"10.1016/j.ecoenv.2024.117071","DOIUrl":"10.1016/j.ecoenv.2024.117071","url":null,"abstract":"<div><div>Although detrimental roles of bisphenol A (BPA) in xenoestrogen target organs, testis and epididymis, and male fertility are well-documented, disruption of the immune privilege system in the male reproductive tract following BPA exposure remains poorly understood. Therefore, this study aimed to explore the precise mechanisms of BPA in interfering immune privilege in the testis on RNA sequencing results. CD-1 male mice were daily treated no-observed-adverse-effect (NOAEL, 5 mg BPA/kg BW) and lowest-observed-adverse-effects (LOAEL, 50 mg BPA/kg BW) of BPA by oral gavage for 6 weeks. Following the LOAEL exposure, the expression of immune response-associated transcripts was upregulated in the testis. Moreover, BPA switch the testicular microenvironment to tumor friendly through the recruitment of tumor associated macrophages (TAMs), which can produce both anti- and pro-inflammatory cytokines, such as TNF-α, TLR2, IL-10, and CXCL9. Number of testicular blood vessels were approximately 2-times increased by upregulation of matrix metallopeptidase 2 in TAMs and upregulation of AR expression in the nucleus of Leydig cells. Moreover, we found that the tumor-supportive environment can also be generated even though NOAEL BPA concentration due to the individual’s variability in cancer susceptibility.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011473/pdfft?md5=ff1d109885af135076cecfdccf14677a&pid=1-s2.0-S0147651324011473-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277781","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}
引用次数: 0
Microplastic ingestion induces energy loss on the copepod Tigriopus koreanus 微塑料摄入导致韩国桡足类 Tigriopus koreanus 的能量损失。
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117056
In marine environments, exposure to microplastics threaten various organisms. A large portion of MPs may be bioavailable to copepods, and ingesting MPs has been reported to induce various adverse effects, including increased mortality, developmental retardation, and decreased reproduction. Adverse effects of MPs on these important processes of copepods may be induced by the obstructive effects of the ingested MPs on energy acquisition. However, few studies have explored the biological effects of MPs on copepods in terms of energy budgets. Therefore, we analyzed ATP (adenosine triphosphate) levels, enzyme activities, swimming distances, and excretion rates in marine copepods (Tigriopus koreanus) that have ingested polystyrene microplastics. Our results indicate that the ingestion of MPs may prevent adequate acquisition of nourishment and lead the copepods into a vicious circle in the respect to energetic burden. Our study provides biochemical evidence for a reduction in the energy budget of copepods due to MPs ingestion. Further, this study increases our understanding of the risks of microplastics, by providing advanced evidences of their effects on marine primary consumer.
在海洋环境中,接触微塑料会对各种生物造成威胁。据报道,摄入微塑料会导致各种不利影响,包括死亡率上升、发育迟缓和繁殖能力下降。MPs对桡足类这些重要过程的不利影响可能是由摄入的MPs对能量获取的阻碍作用引起的。然而,很少有研究从能量预算的角度探讨 MPs 对桡足类的生物影响。因此,我们分析了摄入聚苯乙烯微塑料的海洋桡足类(Tigriopus koreanus)的三磷酸腺苷(ATP)水平、酶活性、游泳距离和排泄率。我们的研究结果表明,摄入聚苯乙烯微塑料可能会阻碍桡足类获得充足的营养,并导致它们在能量负担方面陷入恶性循环。我们的研究提供了生化证据,证明桡足类因摄入 MPs 而导致能量预算减少。此外,这项研究通过提供微塑料对海洋初级消费者影响的先进证据,加深了我们对微塑料风险的理解。
{"title":"Microplastic ingestion induces energy loss on the copepod Tigriopus koreanus","authors":"","doi":"10.1016/j.ecoenv.2024.117056","DOIUrl":"10.1016/j.ecoenv.2024.117056","url":null,"abstract":"<div><div>In marine environments, exposure to microplastics threaten various organisms. A large portion of MPs may be bioavailable to copepods, and ingesting MPs has been reported to induce various adverse effects, including increased mortality, developmental retardation, and decreased reproduction. Adverse effects of MPs on these important processes of copepods may be induced by the obstructive effects of the ingested MPs on energy acquisition. However, few studies have explored the biological effects of MPs on copepods in terms of energy budgets. Therefore, we analyzed ATP (adenosine triphosphate) levels, enzyme activities, swimming distances, and excretion rates in marine copepods (<em>Tigriopus koreanus</em>) that have ingested polystyrene microplastics. Our results indicate that the ingestion of MPs may prevent adequate acquisition of nourishment and lead the copepods into a vicious circle in the respect to energetic burden. Our study provides biochemical evidence for a reduction in the energy budget of copepods due to MPs ingestion. Further, this study increases our understanding of the risks of microplastics, by providing advanced evidences of their effects on marine primary consumer.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011321/pdfft?md5=4d43c13cc977aece5858726ae3ded14f&pid=1-s2.0-S0147651324011321-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277787","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}
引用次数: 0
Microcystin-LR induces histopathological injury and cell apoptosis in the hepatopancreas of white shrimp, Litopenaeus vannamei 微囊藻毒素-LR诱导南美白对虾肝胰腺组织病理学损伤和细胞凋亡
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117059
Microcystin-LR (MC-LR), a common hepatotoxin produced by bloom-forming cyanobacteria, presents a serious threat to the health of aquatic animals. In this study, we studied the impact of MC-LR on hepatopancreas histopathology, enzyme activity, transcriptome, and apoptosis of Litopenaeus vannamei. Thus, shrimp postlarvae (1.63 ± 0.5 g) exposed to MC-LR at 500 μg/kg caused morphological lesions in the histology of the shrimp hepatopancreas, which exhibited swollen, lighter coloration and unclear edges. Moreover, MC-LR significantly altered the hepatopancreas enzyme activities such as the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), acid phosphatase (ACP), alkaline phosphatase (AKP) and lysozyme (LZM), including the state of apoptosis in hepatopancreas. From the RNA-seq analysis of the hepatopancreas, a total of 728 differentially expressed genes (DEGs) were identified, and their functions in MC-LR treatment group were involved in cellular processes, metabolic processes, biological regulation, cellular components, catalytic activity and binding. The metabolic pathways primarily associated with the DEGs included reactive oxygen species, glycerophospholipid metabolism and the phospholipase D signaling pathway. Overall, q-PCR results indicated that MC-LR led to significant changes in multiple apoptosis genes of shrimp hepatopancreas. This study expand the understanding of the effect of microcystin-LR on commercially farmed crustaceans.
微囊藻毒素-LR(MC-LR)是一种由蓝藻藻华产生的常见肝脏毒素,严重威胁水生动物的健康。在本研究中,我们研究了 MC-LR 对凡纳滨对虾肝胰腺组织病理学、酶活性、转录组和细胞凋亡的影响。结果表明,对虾幼体(1.63 ± 0.5 g)暴露于浓度为 500 μg/kg 的 MC-LR 后,对虾肝胰腺组织发生形态病变,表现为肿胀、颜色变浅、边缘不清。此外,MC-LR明显改变了肝胰腺酶活性,如谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、酸性磷酸酶(ACP)、碱性磷酸酶(AKP)和溶菌酶(LZM)的水平,包括肝胰腺的凋亡状态。通过对肝胰腺的RNA-seq分析,共鉴定出728个差异表达基因(DEGs),这些基因在MC-LR治疗组中的功能涉及细胞过程、代谢过程、生物调控、细胞组分、催化活性和结合。与 DEGs 主要相关的代谢途径包括活性氧、甘油磷脂代谢和磷脂酶 D 信号通路。总体而言,q-PCR结果表明,MC-LR导致对虾肝胰脏多个凋亡基因发生显著变化。这项研究拓展了人们对微囊藻毒素-LR对商业养殖甲壳类动物影响的认识。
{"title":"Microcystin-LR induces histopathological injury and cell apoptosis in the hepatopancreas of white shrimp, Litopenaeus vannamei","authors":"","doi":"10.1016/j.ecoenv.2024.117059","DOIUrl":"10.1016/j.ecoenv.2024.117059","url":null,"abstract":"<div><div>Microcystin-LR (MC-LR), a common hepatotoxin produced by bloom-forming cyanobacteria, presents a serious threat to the health of aquatic animals. In this study, we studied the impact of MC-LR on hepatopancreas histopathology, enzyme activity, transcriptome, and apoptosis of <em>Litopenaeus vannamei</em>. Thus, shrimp postlarvae (1.63 ± 0.5 g) exposed to MC-LR at 500 μg/kg caused morphological lesions in the histology of the shrimp hepatopancreas, which exhibited swollen, lighter coloration and unclear edges. Moreover, MC-LR significantly altered the hepatopancreas enzyme activities such as the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), acid phosphatase (ACP), alkaline phosphatase (AKP) and lysozyme (LZM), including the state of apoptosis in hepatopancreas. From the RNA-seq analysis of the hepatopancreas, a total of 728 differentially expressed genes (DEGs) were identified, and their functions in MC-LR treatment group were involved in cellular processes, metabolic processes, biological regulation, cellular components, catalytic activity and binding. The metabolic pathways primarily associated with the DEGs included reactive oxygen species, glycerophospholipid metabolism and the phospholipase D signaling pathway. Overall, q-PCR results indicated that MC-LR led to significant changes in multiple apoptosis genes of shrimp hepatopancreas. This study expand the understanding of the effect of microcystin-LR on commercially farmed crustaceans.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011357/pdfft?md5=09331c6e86aede4403634e9c9765cd20&pid=1-s2.0-S0147651324011357-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277786","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}
引用次数: 0
Bisphenol H exposure disrupts Leydig cell function in adult rats via oxidative stress-mediated m6A modifications: Implications for reproductive toxicity 暴露于双酚 H 会通过氧化应激介导的 m6A 修饰破坏成年大鼠的睾丸细胞功能:对生殖毒性的影响
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117061
Bisphenol H (BPH) has emerged as a potential alternative to bisphenol A (BPA), which has been curtailed for use due to concerns over its reproductive and endocrine toxicity. This study investigates whether BPH exerts antiandrogenic effects by impairing Leydig cell function, a critical component in testosterone production. We administered orally BPH to adult male rats at doses of 0, 1, 10, and 100 mg/kg/day for 7 days. Notably, BPH treatment resulted in a dose-dependent reduction in testicular testosterone levels, with significant decreases observed at ≥ 1 mg/kg/day. Additionally, BPH affected the expression of key genes involved in steroidogenesis and cholesterol metabolism, including Nr5a1, Nr3c4, Lhcgr, Scarb1, and Star, at higher doses (10 and/or 100 mg/kg/day). The study also revealed alterations in antioxidant gene expression (Sod2 and Cat) and modulation of m6A-related genes (Ythdf1–3 and Foxo3) and their proteins. Through MeRIP-qPCR analysis, we identified increased m6A modifications in Scarb1 and Star genes following BPH exposure. In vitro experiments with primary Leydig cells confirmed that BPH enhanced oxidative stress and diminished testosterone production, which were partially mitigated by antioxidant vitamin E supplementation and Ythdf3 knockdown. Meanwhile, simultaneous administration of BPH and vitamin E to primary Leydig cells partially counteracted BPH-induced alterations in the Ythdf3 expression. Our findings underscore a novel mechanism by which BPH disrupts Leydig cell function through the oxidative stress-m6A modification-autophagy pathway, raising concerns about its potential reproductive toxicity.
双酚 H(BPH)已成为双酚 A(BPA)的潜在替代品,而双酚 A 因其生殖和内分泌毒性问题已被限制使用。本研究探讨了 BPH 是否会通过损害睾酮生成过程中的一个关键环节--莱伊底格细胞的功能来发挥抗雄激素作用。我们以 0、1、10 和 100 毫克/千克/天的剂量给成年雄性大鼠口服 BPH,连续 7 天。值得注意的是,BPH 会导致睾丸睾酮水平呈剂量依赖性下降,当剂量≥ 1 毫克/千克/天时,睾酮水平会显著下降。此外,BPH还会影响参与类固醇生成和胆固醇代谢的关键基因的表达,包括Nr5a1、Nr3c4、Lhcgr、Scarb1和Star,剂量越高(10和/或100毫克/千克/天),影响越大。研究还揭示了抗氧化基因(Sod2 和 Cat)表达的改变以及 m6A 相关基因(Ythdf1-3 和 Foxo3)及其蛋白质的调节。通过 MeRIP-qPCR 分析,我们发现 BPH 暴露后 Scarb1 和 Star 基因中的 m6A 修饰增加。原代髓质细胞的体外实验证实,BPH 会增强氧化应激并减少睾酮的产生,而补充抗氧化剂维生素 E 和敲除 Ythdf3 可部分缓解这一现象。同时,给原代Leydig细胞同时服用BPH和维生素E可部分抵消BPH诱导的Ythdf3表达变化。我们的研究结果强调了一种新的机制,即BPH通过氧化应激-m6A修饰-自噬途径破坏Leydig细胞的功能,从而引起了人们对其潜在生殖毒性的关注。
{"title":"Bisphenol H exposure disrupts Leydig cell function in adult rats via oxidative stress-mediated m6A modifications: Implications for reproductive toxicity","authors":"","doi":"10.1016/j.ecoenv.2024.117061","DOIUrl":"10.1016/j.ecoenv.2024.117061","url":null,"abstract":"<div><div>Bisphenol H (BPH) has emerged as a potential alternative to bisphenol A (BPA), which has been curtailed for use due to concerns over its reproductive and endocrine toxicity. This study investigates whether BPH exerts antiandrogenic effects by impairing Leydig cell function, a critical component in testosterone production. We administered orally BPH to adult male rats at doses of 0, 1, 10, and 100 mg/kg/day for 7 days. Notably, BPH treatment resulted in a dose-dependent reduction in testicular testosterone levels, with significant decreases observed at ≥ 1 mg/kg/day. Additionally, BPH affected the expression of key genes involved in steroidogenesis and cholesterol metabolism, including <em>Nr5a1</em>, <em>Nr3c4</em>, <em>Lhcgr</em>, <em>Scarb1</em>, and <em>Star</em>, at higher doses (10 and/or 100 mg/kg/day). The study also revealed alterations in antioxidant gene expression (<em>Sod2</em> and <em>Cat</em>) and modulation of m6A-related genes (<em>Ythdf1–3</em> and <em>Foxo3</em>) and their proteins. Through MeRIP-qPCR analysis, we identified increased m6A modifications in <em>Scarb1</em> and <em>Star</em> genes following BPH exposure. <em>In vitro</em> experiments with primary Leydig cells confirmed that BPH enhanced oxidative stress and diminished testosterone production, which were partially mitigated by antioxidant vitamin E supplementation and <em>Ythdf3</em> knockdown. Meanwhile, simultaneous administration of BPH and vitamin E to primary Leydig cells partially counteracted BPH-induced alterations in the <em>Ythdf3</em> expression. Our findings underscore a novel mechanism by which BPH disrupts Leydig cell function through the oxidative stress-m6A modification-autophagy pathway, raising concerns about its potential reproductive toxicity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011370/pdfft?md5=deb84c34f4559eb824ac62ee3ab18d5f&pid=1-s2.0-S0147651324011370-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277776","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}
引用次数: 0
Exploring the impact of estrogenic endocrine disruptors on cervical cancer progression: A transcriptome analysis and prognostic model development 探索雌激素内分泌干扰物对宫颈癌进展的影响:转录组分析和预后模型的建立
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117025

Cervical cancer is the fourth most common cancer among women globally. The detrimental health effects of estrogenic endocrine disruptors (EED), such as bisphenol A (BPA) and phthalates, are recognized, but their role in cervical cancer progression remains unclear. To investigate this, a transcriptome analysis using bioinformatics was conducted. The Comparative Toxicogenomics Database (CTD) identified estrogen-responsive genes (ERGs) associated with EED. Cervical cancer expression and clinical data were sourced from The Cancer Genome Atlas (TCGA). The limma package identified differentially expressed ERGs (DERGs), which were further analyzed for molecular mechanisms through enrichment analysis. LASSO regression developed a prognostic risk score model, and COX analysis identified prognostic biomarkers. ssGSEA assessed immune tumor infiltration, and Autodock performed molecular docking. A total of 217 DERGs were linked to endocrine resistance, estrogen signaling, and the cell cycle. The prognostic risk score and nomogram based on DERGs were highly predictive of cervical cancer prognosis and could serve as independent risk factors. The risk score influenced the tumor immune microenvironment by affecting immune cell presence. SCARA3 and FASN emerged as independent prognostic factors, with molecular docking confirming strong binding between EED and FASN. DERGs can aid in creating a reliable prognostic model and predicting overall survival in cervical cancer patients, offering new insights into the impact of EED on cancer progression and highlighting environmental factors related to cancer risks and development.

宫颈癌是全球妇女第四大常见癌症。双酚 A(BPA)和邻苯二甲酸盐等雌激素内分泌干扰物(EED)对健康的有害影响已得到公认,但它们在宫颈癌进展中的作用仍不清楚。为了研究这个问题,我们利用生物信息学进行了转录组分析。比较毒物基因组学数据库(CTD)确定了与 EED 相关的雌激素反应基因(ERGs)。宫颈癌表达和临床数据来自癌症基因组图谱(TCGA)。limma软件包确定了差异表达的ERGs(DERGs),并通过富集分析进一步分析了其分子机制。ssGSEA评估免疫肿瘤浸润,Autodock进行分子对接。共有217个DERGs与内分泌抗性、雌激素信号转导和细胞周期有关。基于 DERGs 的预后风险评分和提名图对宫颈癌的预后有很高的预测性,可作为独立的风险因素。风险评分通过影响免疫细胞的存在来影响肿瘤免疫微环境。SCARA3和FASN成为独立的预后因素,分子对接证实了EED与FASN之间的强结合。DERGs有助于建立可靠的预后模型和预测宫颈癌患者的总生存期,为EED对癌症进展的影响提供了新的见解,并突出了与癌症风险和发展相关的环境因素。
{"title":"Exploring the impact of estrogenic endocrine disruptors on cervical cancer progression: A transcriptome analysis and prognostic model development","authors":"","doi":"10.1016/j.ecoenv.2024.117025","DOIUrl":"10.1016/j.ecoenv.2024.117025","url":null,"abstract":"<div><p>Cervical cancer is the fourth most common cancer among women globally. The detrimental health effects of estrogenic endocrine disruptors (EED), such as bisphenol A (BPA) and phthalates, are recognized, but their role in cervical cancer progression remains unclear. To investigate this, a transcriptome analysis using bioinformatics was conducted. The Comparative Toxicogenomics Database (CTD) identified estrogen-responsive genes (ERGs) associated with EED. Cervical cancer expression and clinical data were sourced from The Cancer Genome Atlas (TCGA). The limma package identified differentially expressed ERGs (DERGs), which were further analyzed for molecular mechanisms through enrichment analysis. LASSO regression developed a prognostic risk score model, and COX analysis identified prognostic biomarkers. ssGSEA assessed immune tumor infiltration, and Autodock performed molecular docking. A total of 217 DERGs were linked to endocrine resistance, estrogen signaling, and the cell cycle. The prognostic risk score and nomogram based on DERGs were highly predictive of cervical cancer prognosis and could serve as independent risk factors. The risk score influenced the tumor immune microenvironment by affecting immune cell presence. SCARA3 and FASN emerged as independent prognostic factors, with molecular docking confirming strong binding between EED and FASN. DERGs can aid in creating a reliable prognostic model and predicting overall survival in cervical cancer patients, offering new insights into the impact of EED on cancer progression and highlighting environmental factors related to cancer risks and development.</p></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011011/pdfft?md5=045f1945fcc0d2e55bcb7a3c52ca7651&pid=1-s2.0-S0147651324011011-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243158","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}
引用次数: 0
Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids 纳米塑料暴露诱发的线粒体功能障碍导致人脑器官组织干细胞分化紊乱
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117063

Nanoplastics are ubiquitous in our daily lives, raising concerns about their potential impact on the human brain. Many studies reported that nanoplastics permeate the blood-brain barrier and influence cellular processes in mouse models. However, the neurotoxic effects of ingesting nanoplastics on human brain remain poorly understood. Here, we treated cerebral organoids with polystyrene nanoplastics to model the effects of nanoplastic exposure on human brain. Importantly, we found that mitochondria might be the significant organelles affected by polystyrene nanoplastics using immunostaing and RNA-seq analysis. Subsequently, we observed the increased cell death and decreased cell differentiation in our cerebral organoids. In conclusion, our findings shed insights on the mechanisms underlying the toxicity of nanoplastics on human brain organoids, providing an evaluation system in detection potential environmental toxicity on human brain.

纳米塑料在我们的日常生活中无处不在,引发了人们对其对人类大脑潜在影响的担忧。许多研究报告称,纳米塑料可渗透血脑屏障并影响小鼠模型的细胞过程。然而,人们对摄入纳米塑料对人脑的神经毒性影响仍然知之甚少。在这里,我们用聚苯乙烯纳米塑料处理脑器质性组织,模拟纳米塑料暴露对人脑的影响。重要的是,通过免疫测定和 RNA-seq 分析,我们发现线粒体可能是受聚苯乙烯纳米塑料影响的主要细胞器。随后,我们观察到大脑有机体中细胞死亡增加,细胞分化减少。总之,我们的研究结果揭示了纳米塑料对人脑器官组织的毒性机制,为检测环境对人脑的潜在毒性提供了一个评估系统。
{"title":"Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids","authors":"","doi":"10.1016/j.ecoenv.2024.117063","DOIUrl":"10.1016/j.ecoenv.2024.117063","url":null,"abstract":"<div><p>Nanoplastics are ubiquitous in our daily lives, raising concerns about their potential impact on the human brain. Many studies reported that nanoplastics permeate the blood-brain barrier and influence cellular processes in mouse models. However, the neurotoxic effects of ingesting nanoplastics on human brain remain poorly understood. Here, we treated cerebral organoids with polystyrene nanoplastics to model the effects of nanoplastic exposure on human brain. Importantly, we found that mitochondria might be the significant organelles affected by polystyrene nanoplastics using immunostaing and RNA-seq analysis. Subsequently, we observed the increased cell death and decreased cell differentiation in our cerebral organoids. In conclusion, our findings shed insights on the mechanisms underlying the toxicity of nanoplastics on human brain organoids, providing an evaluation system in detection potential environmental toxicity on human brain.</p></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011394/pdfft?md5=b76ea6044f363719112395b83b2de105&pid=1-s2.0-S0147651324011394-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243153","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}
引用次数: 0
Integrated transcriptomics and proteomics analyses reveal the ameliorative effect of hepatic damage in tilapia caused by polystyrene microplastics with chlorella addition 转录组学和蛋白质组学综合分析揭示了添加小球藻对聚苯乙烯微塑料造成的罗非鱼肝损伤的改善作用。
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117076
Fish exhibit varying responses to polystyrene microplastics (MPs) depending on particle size. Previous studies suggested that microorganisms adhering to the surface of MPs can induce toxic effects. In this study, Tilapia were exposed to MPs of control (group A), 75 nm (B), 7.5 μm (C), 750 μm (D), as well as combinations of all sizes (E) and 75 nm MPs with Chlorella vulgaris addition (F) for 7, 10 and 14 days. Histopathological changes in liver of tilapia were assessed using enzyme activities, transcriptomics and proteomics. The results showed that in groups combined MPs of different particle sizes and those supplemented with chlorella, MPs were localized on the surface of goblet cells, leading to vacuoles, constricted hepatic sinuses and nuclei displacement. Exposure to 7.5 and 750 μm MPs significantly increased the contents of fatty acid synthase (FAS), adenosine triphosphate (ATP), acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL), total cholesterol (TC), total triglyceride (TG) contents at 7 and 10 days. In particular, cytochrome p450 1a1 (EROD), reactive oxygen species (ROS) and superoxide dismutase (SOD) were markedly elevated following exposure to MPs. Apoptotic markers caspase-3, and inflammatory markers, including tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β), had a similar upward trend in comparisons of group C vs A at 7 d, group D vs A at 14 d. The peroxisome proliferator activated receptor (PPAR) signaling pathway, spliceosome, was highly enriched during the 7-day exposure of medium sized MPs, while largest MPs in the comparison of group D vs A at 14 d activated pathways such as phagosome, apoptosis, salmonella infection. Transcriptomic analysis revealed that after 14 days, the kyoto encyclopedia of genes and genomes (KEGG) pathways associated with protein processing in endoplasmic reticulum and the PPAR signaling has been significantly enriched in the Chlorella-supplemented group, which was further confirmed via the proteomic analysis. Overall, the findings highlight the size-dependent effects of MPs on histopathological changes, gene and protein expression in the liver of tilapia, and C. vulgaris effectively attenuated liver damages, likely through modulation of endoplasmic reticulum protein processing and PPAR signaling pathways.
鱼类对聚苯乙烯微塑料(MPs)的反应因颗粒大小而异。以前的研究表明,粘附在微塑料表面的微生物会诱发毒性效应。在这项研究中,罗非鱼分别接触了对照组(A 组)、75 纳米(B 组)、7.5 微米(C 组)、750 微米(D 组)的微塑料,以及所有尺寸的微塑料组合(E 组)和添加了小球藻的 75 纳米微塑料(F 组),时间分别为 7 天、10 天和 14 天。利用酶活性、转录组学和蛋白质组学评估罗非鱼肝脏的组织病理学变化。结果表明,在不同粒径的 MPs 组和添加小球藻的组中,MPs 定位于鹅口疮细胞表面,导致空泡、肝窦收缩和细胞核移位。暴露于 7.5 和 750 μm MPs 7 天和 10 天后,脂肪酸合成酶(FAS)、三磷酸腺苷(ATP)、乙酰-CoA 羧化酶(ACC)、脂蛋白脂肪酶(LPL)、总胆固醇(TC)、总甘油三酯(TG)的含量明显增加。特别是,细胞色素 p450 1a1 (EROD)、活性氧 (ROS) 和超氧化物歧化酶 (SOD) 在接触 MPs 后明显升高。凋亡标志物 caspase-3 和炎症标志物,包括肿瘤坏死因子 α(TNF-α)和白细胞介素-1β(IL-1β),在 7 d 时 C 组与 A 组、14 d 时 D 组与 A 组的比较中也有类似的上升趋势。在中型 MPs 暴露 7 天期间,过氧化物酶体增殖激活受体(PPAR)信号通路--剪接体高度富集,而在 D 组与 A 组 14 天的比较中,最大的 MPs 激活了吞噬体、细胞凋亡、沙门氏菌感染等通路。转录组学分析表明,14 天后,与内质网蛋白质加工和 PPAR 信号转导相关的京都基因和基因组百科全书(KEGG)通路在补充 Chlorella 的组中显著富集,这一点在蛋白质组学分析中得到了进一步证实。总之,研究结果强调了MPs对罗非鱼肝脏组织病理学变化、基因和蛋白质表达的大小依赖性影响,而C. vulgaris可能通过调节内质网蛋白质加工和PPAR信号通路,有效减轻了肝脏损伤。
{"title":"Integrated transcriptomics and proteomics analyses reveal the ameliorative effect of hepatic damage in tilapia caused by polystyrene microplastics with chlorella addition","authors":"","doi":"10.1016/j.ecoenv.2024.117076","DOIUrl":"10.1016/j.ecoenv.2024.117076","url":null,"abstract":"<div><div>Fish exhibit varying responses to polystyrene microplastics (MPs) depending on particle size. Previous studies suggested that microorganisms adhering to the surface of MPs can induce toxic effects. In this study, Tilapia were exposed to MPs of control (group A), 75 nm (B), 7.5 μm (C), 750 μm (D), as well as combinations of all sizes (E) and 75 nm MPs with <em>Chlorella vulgaris</em> addition (F) for 7, 10 and 14 days. Histopathological changes in liver of tilapia were assessed using enzyme activities, transcriptomics and proteomics. The results showed that in groups combined MPs of different particle sizes and those supplemented with chlorella, MPs were localized on the surface of goblet cells, leading to vacuoles, constricted hepatic sinuses and nuclei displacement. Exposure to 7.5 and 750 μm MPs significantly increased the contents of fatty acid synthase (FAS), adenosine triphosphate (ATP), acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL), total cholesterol (TC), total triglyceride (TG) contents at 7 and 10 days. In particular, cytochrome p450 1a1 (EROD), reactive oxygen species (ROS) and superoxide dismutase (SOD) were markedly elevated following exposure to MPs. Apoptotic markers caspase-3, and inflammatory markers, including tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β), had a similar upward trend in comparisons of group C vs A at 7 d, group D vs A at 14 d. The peroxisome proliferator activated receptor (PPAR) signaling pathway, spliceosome, was highly enriched during the 7-day exposure of medium sized MPs, while largest MPs in the comparison of group D vs A at 14 d activated pathways such as phagosome, apoptosis, salmonella infection. Transcriptomic analysis revealed that after 14 days, the kyoto encyclopedia of genes and genomes (KEGG) pathways associated with protein processing in endoplasmic reticulum and the PPAR signaling has been significantly enriched in the <em>Chlorella</em>-supplemented group, which was further confirmed via the proteomic analysis. Overall, the findings highlight the size-dependent effects of MPs on histopathological changes, gene and protein expression in the liver of tilapia, and <em>C. vulgaris</em> effectively attenuated liver damages, likely through modulation of endoplasmic reticulum protein processing and PPAR signaling pathways.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011527/pdfft?md5=dfce350f2e3ccc46b79e4bccdcebbfb6&pid=1-s2.0-S0147651324011527-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277784","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}
引用次数: 0
Silica nanoparticles cause ovarian dysfunction and fertility decrease in mice via oxidative stress-activated autophagy and apoptosis 纳米二氧化硅颗粒通过氧化应激激活的自噬和细胞凋亡导致小鼠卵巢功能障碍和生育能力下降。
IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-09-19 DOI: 10.1016/j.ecoenv.2024.117049
Silica nanoparticles (SiNPs) are widely used in various commercial applications, which inevitably increase the risk of human exposure. It’s reported that SiNPs have toxic effects on fertility, however, the specific mechanism of female reproductive toxicity induced by SiNPs remains confusing. In this study, female C57BL/6 mice at the age of 8 weeks were administrated orally with SiNPs at doses of 0, 3, and 10 mg/kg bw. every day in the presence/absence of NAC for eight weeks. The results showed that SiNPs could cause damage to ovaries and reduce the number of ovarian follicles, which led to disruption of sex hormone, altered estrous cyclicity and decreased female fertility. In addition, SiNPs induced oxidative stress in the ovary, as manifested by increased ROS and MDA levels, decreased SOD activity and inhibition of the Nrf2/HO-1 signaling pathway. Further study revealed that exposure to SiNPs resulted in mitochondrial dysfunction and promoted autophagy mediated by PI3K/AKT/mTOR and PINK1/Parkin signaling pathways. Meanwhile, apoptosis is also involved in SiNPs-induced cell death in a cooperative and synchronized manner, as evidenced by an increase in apoptosis-positive cells and activation of the ATM/p53-mediated apoptotic pathway. The supplementation of NAC restored most of the reproductive characteristics of the mice to its physiological range. These results demonstrated that SiNPs could cause ovarian damage via inducing oxidative stress and mitochondrial dysfunction, which led to autophagy and apoptosis, and ultimately resulting in abnormal folliculogenesis and female subfertility.
纳米二氧化硅(SiNPs)被广泛应用于各种商业领域,这不可避免地增加了人类接触的风险。据报道,SiNPs 对生育能力有毒害作用,但 SiNPs 诱导雌性生殖毒性的具体机制仍然扑朔迷离。本研究以 8 周大的雌性 C57BL/6 小鼠为研究对象,在 NAC 存在/不存在的情况下,每天分别口服 0、3 和 10 mg/kg 体重剂量的 SiNPs,连续八周。结果表明,SiNPs 会对卵巢造成损伤,减少卵泡数量,从而导致性激素紊乱、发情周期改变和雌性生育能力下降。此外,SiNPs 还会诱发卵巢氧化应激,表现为 ROS 和 MDA 水平升高、SOD 活性降低以及 Nrf2/HO-1 信号通路受抑制。进一步研究发现,暴露于 SiNPs 会导致线粒体功能障碍,并在 PI3K/AKT/mTOR 和 PINK1/Parkin 信号通路的介导下促进自噬。同时,细胞凋亡也以合作和同步的方式参与了 SiNPs 诱导的细胞死亡,表现为凋亡阳性细胞的增加和 ATM/p53 介导的细胞凋亡途径的激活。补充 NAC 后,小鼠的大部分生殖特征恢复到生理范围。这些结果表明,SiNPs 可通过诱导氧化应激和线粒体功能障碍造成卵巢损伤,从而导致自噬和细胞凋亡,最终导致卵泡生成异常和雌性不孕。
{"title":"Silica nanoparticles cause ovarian dysfunction and fertility decrease in mice via oxidative stress-activated autophagy and apoptosis","authors":"","doi":"10.1016/j.ecoenv.2024.117049","DOIUrl":"10.1016/j.ecoenv.2024.117049","url":null,"abstract":"<div><div>Silica nanoparticles (SiNPs) are widely used in various commercial applications, which inevitably increase the risk of human exposure. It’s reported that SiNPs have toxic effects on fertility, however, the specific mechanism of female reproductive toxicity induced by SiNPs remains confusing. In this study, female C57BL/6 mice at the age of 8 weeks were administrated orally with SiNPs at doses of 0, 3, and 10 mg/kg bw. every day in the presence/absence of NAC for eight weeks. The results showed that SiNPs could cause damage to ovaries and reduce the number of ovarian follicles, which led to disruption of sex hormone, altered estrous cyclicity and decreased female fertility. In addition, SiNPs induced oxidative stress in the ovary, as manifested by increased ROS and MDA levels, decreased SOD activity and inhibition of the Nrf2/HO-1 signaling pathway. Further study revealed that exposure to SiNPs resulted in mitochondrial dysfunction and promoted autophagy mediated by PI3K/AKT/mTOR and PINK1/Parkin signaling pathways. Meanwhile, apoptosis is also involved in SiNPs-induced cell death in a cooperative and synchronized manner, as evidenced by an increase in apoptosis-positive cells and activation of the ATM/p53-mediated apoptotic pathway. The supplementation of NAC restored most of the reproductive characteristics of the mice to its physiological range. These results demonstrated that SiNPs could cause ovarian damage via inducing oxidative stress and mitochondrial dysfunction, which led to autophagy and apoptosis, and ultimately resulting in abnormal folliculogenesis and female subfertility.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0147651324011254/pdfft?md5=07fadece97b877518c7c690375bba167&pid=1-s2.0-S0147651324011254-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277788","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}
引用次数: 0
期刊
Ecotoxicology and Environmental Safety
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1