Ecotoxicology and Environmental Safety最新文献

Retraction notice to “Improving wheat physio-biochemical attributes in ciprofloxacin-polluted saline soil using nZVI-modified biochar” [Ecotoxicol. Environ. Saf., 286 C, (2024) 117202] 《利用nzvi改性生物炭改善环丙沙星污染盐渍土壤中小麦生理生化特性》的撤稿通知[生态毒理学杂志]。环绕。Saf。， 286 c,(2024) 117202]。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-05-01 Epub Date: 2026-04-11 DOI: 10.1016/j.ecoenv.2026.120033

Ghulam Murtaza , Muhammad Usman , Zeeshan Ahmed , Sajjad Hyder , Mona S. Alwahibi , Humaira Rizwana , Javed Iqbal , Basharat Ali , Rashid Iqbal , Shabir Ahmad , Gang Deng , Hafiz Ghulam Muhu Din Ahmed , Yawen Zeng

引用次数: 0

Corrigendum to “CISD2-mediated mitochondrial dysfunction and iron redistribution contributes to ferroptosis in arsenic-induced nonalcoholic steatohepatitis” [Ecotoxicol. Environ. Saf. 289:117694/EES-23-4255] “cisd2介导的线粒体功能障碍和铁再分配有助于砷诱导的非酒精性脂肪性肝炎中的铁中毒”[Ecotoxicol]的更正。环绕。Saf 289:117694 / ee - 23 - 4255]。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-05-01 Epub Date: 2026-04-14 DOI: 10.1016/j.ecoenv.2026.120102

Jingyuan Zhang, Lu Wang, Yang Lu, Fei Zheng, Xiaoqian Ding, Xiaofeng Yao, Jie Bai, Ningning Wang, Guang Yang, Tianming Qiu, Xiance Sun

引用次数: 0

Intrauterine exposure to glyphosate-based herbicide during pregnancy induces testicular impairment via activating ferroptosis in offspring. 妊娠期间宫内暴露于草甘膦除草剂通过激活后代铁下垂诱导睾丸损伤。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-05-01 Epub Date: 2026-04-13 DOI: 10.1016/j.ecoenv.2026.120123

Guangdong Bai, Ruiqi Wang, Yihao Tong, Yilin Bai, Hua Yuan, Baoming Shi, Teng Teng, Wei He

{"title":"Intrauterine exposure to glyphosate-based herbicide during pregnancy induces testicular impairment via activating ferroptosis in offspring.","authors":"Guangdong Bai, Ruiqi Wang, Yihao Tong, Yilin Bai, Hua Yuan, Baoming Shi, Teng Teng, Wei He","doi":"10.1016/j.ecoenv.2026.120123","DOIUrl":"10.1016/j.ecoenv.2026.120123","url":null,"abstract":"<p><p>Glyphosate-based herbicide (GBH) is a broad-spectrum herbicide extensively used in agriculture, which poses increased residual risks in grains and food products, thereby endangering human health. However, the impact of maternal GBH exposure on fetal testicular development, as well as the protective effects of dietary betaine supplementation, remains inadequately understood. Hereby, pregnant sow models were established to elucidate the effects of GBH exposure at concentrations of 20 and 100 mg/kg and to investigate the protective mechanisms of betaine. The results showed that GBH and betaine had no significant differences on blood biochemical, colostrum composition and immunoglobulin. However, 100 mg/kg GBH treatment damaged the testicular morphology and barrier function, and disturbed testosterone synthesis in fetal testis. Subsequently, we found that high concentration GBH exposure triggered oxidative stress and inflammatory responses of testis, and inhibited the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant signaling pathway, which further restrained mitochondrial fusion. Moreover, the accumulation of lipid peroxides and Fe<sup>2+</sup> indicated that at a 100 mg/kg GBH treatment caused testicular ferroptosis. Conversely, dietary supplementation with betaine appears to inhibit ferroptosis by modulating the expression of ferritin light chain (FTL), acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL4), and ferritin, thereby promoting testosterone synthesis and enhancing testicular development to some extent. In conclusion, these findings enhance our understanding of the risks associated with fetal testicular exposure to GBH in pregnant women and elucidate the protective mechanisms of betaine against GBH poisoning.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"316 ","pages":"120123"},"PeriodicalIF":6.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147661987","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

Blue light exposure exacerbates obesity in high-fat diet-fed mice by inducing mitochondrial dysfunction in the white adipose tissue. 蓝光照射通过诱导白色脂肪组织中的线粒体功能障碍，加剧了高脂肪饮食小鼠的肥胖。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-05-01 Epub Date: 2026-04-13 DOI: 10.1016/j.ecoenv.2026.120111

Bo Yang, Guiyun Shi, Lin Zhao, Lina Tuerxunaili, Weinila Asihaer, Miaomiao Song, Yao Zhu, Chang Liu, Yi Jiao

{"title":"Blue light exposure exacerbates obesity in high-fat diet-fed mice by inducing mitochondrial dysfunction in the white adipose tissue.","authors":"Bo Yang, Guiyun Shi, Lin Zhao, Lina Tuerxunaili, Weinila Asihaer, Miaomiao Song, Yao Zhu, Chang Liu, Yi Jiao","doi":"10.1016/j.ecoenv.2026.120111","DOIUrl":"10.1016/j.ecoenv.2026.120111","url":null,"abstract":"<p><p>The increasing prevalence of artificial light sources has rendered blue light (BL) a novel environmental metabolic disruptor. This study aimed to investigate the potential effects of BL exposure on mitochondrial function in the adipose tissue of high-fat diet (HFD) mice. A total of 36 mice were divided into the normal diet (ND) and HFD groups and subsequently exposed to white light (WL) and BL. Body weight was monitored regularly, and glucose tolerance and insulin sensitivity were assessed using intraperitoneal glucose tolerance tests (IPGTT) and intraperitoneal insulin tolerance tests (IPITT). Body fat was measured using nuclear magnetic resonance, and overall energy metabolism was evaluated using a metabolic energy monitoring system. After the mice were humanely sacrificed, inguinal white adipose tissue (iWAT), epididymal white adipose tissue (eWAT), and brown adipose tissue (BAT) were collected for weighing, histological analysis, and serum biochemical analysis. Oxidative stress indicators were detected by flow cytometry and other methods. We found that, in HFD-fed mice, BL exposure significantly increased body weight and body fat, exacerbated insulin resistance, and reduced oxygen consumption and thermogenesis. Transcriptomic analysis revealed that BL exposure induced oxidative stress in the white adipose tissue and suppressed the oxidative phosphorylation pathway. RT-qPCR and western blotting of the iWAT confirmed the downregulation of key genes in this pathway. Collectively, our results suggest that BL may target the adipose tissue, trigger oxidative stress, suppress oxidative phosphorylation, impair mitochondrial function, and exacerbate obesity.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"316 ","pages":"120111"},"PeriodicalIF":6.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147661985","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

ATF3 links endoplasmic reticulum stress to ferroptosis via transcriptional activation of ALOX12 in benzene-induced hematotoxicity. 在苯诱导的血液毒性中，ATF3通过ALOX12的转录激活将内质网应激与铁死亡联系起来。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-05-01 Epub Date: 2026-04-13 DOI: 10.1016/j.ecoenv.2026.120130

HuaFeng Zeng, YuXi Li, HongTing Zhao, Lin Chen, Lin Xu, ShaoYing Wang, YuFan Zhang, HaoChen Wang, ShuYun Huang, Yunqiang Xu, Chunnian You, Lei Sun, FengZhen Cui, Huanwen Tang

{"title":"ATF3 links endoplasmic reticulum stress to ferroptosis via transcriptional activation of ALOX12 in benzene-induced hematotoxicity.","authors":"HuaFeng Zeng, YuXi Li, HongTing Zhao, Lin Chen, Lin Xu, ShaoYing Wang, YuFan Zhang, HaoChen Wang, ShuYun Huang, Yunqiang Xu, Chunnian You, Lei Sun, FengZhen Cui, Huanwen Tang","doi":"10.1016/j.ecoenv.2026.120130","DOIUrl":"10.1016/j.ecoenv.2026.120130","url":null,"abstract":"<p><p>As a Class I human carcinogen ubiquitous in both industrial and household environments, benzene can cause hematopoietic damage even at low concentrations. However, its precise hematological toxicological molecular mechanism remains incompletely understood. Here, we demonstrate that hydroquinone (HQ), a benzene metabolite, induces ferroptosis and endoplasmic reticulum stress (ERs) in TK6 cells. Mechanistically, through a combination of RNA-Seq and database analyses, we identified ATF3 as a central molecular switch linking ERs to ferroptosis following HQ treatment, with its activation mediated by the PERK pathway. Using oxidative lipidomics, we further identified ALOX12 as a key lipid peroxidase involved in promoting ferroptosis. Moreover, chromatin immunoprecipitation sequencing (ChIP-Seq) and dual-luciferase reporter assays revealed that ATF3 directly binds to the ALOX12 promoter, triggering its transcriptional activation, which in turn accelerates lipid peroxidation and ultimately leads to ferroptosis. In a mouse model of benzene-induced hematotoxicity, knockdown of ATF3 effectively inhibits bone marrow ferroptosis and markedly ameliorates hematopoietic impairment. Importantly, our cohort study revealed that the higher of ATF3, ALOX12, MDA, and lower GSH/GSSG was significantly associated with hematotoxicity in workers exposed to benzene. Collectively, these findings suggest the ATF3-ALOX12 signal axis may represent promising biomarkers for monitoring early hematopoietic damage resulting from low-dose benzene exposure in environmentally exposed populations.</p>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"316 ","pages":"120130"},"PeriodicalIF":6.1,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662005","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

Corrigendum to “Combined transcriptomics and metabolomics to reveal the effects of copper exposure on the liver of rainbow trout (Oncorhynchus mykiss)” [Ecotoxicol. Environ. Saf. 2024, 284, 116996] “联合转录组学和代谢组学揭示铜暴露对虹鳟鱼肝脏的影响”[Ecotoxicol]的勘误表。环绕。中国生物医学工程学报，2017,28(1):449 - 449。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-04-15 Epub Date: 2026-04-03 DOI: 10.1016/j.ecoenv.2026.120097

Junhao Lu , Jinqiang Quan , Jing Zhou , Zhe Liu , Jieping Ding , Tingting Shang , Guiyan Zhao , Lanlan Li , Yingcan Zhao , Xiangru Li , Jiajun Wu

引用次数: 0

Retraction notice to “Carbon-based amendments for sustainable remediation of arsenic-contaminated paddy soils: An insight to greenhouse gases” [Ecotoxicol. Environ. Saf., 300 (2025) 118382] 对“碳基修正法对砷污染水稻土的可持续修复：对温室气体的洞察”的撤回通知[生态毒物]。环绕。Saf。农业科学，300(2025)118382]。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-04-01 Epub Date: 2026-03-19 DOI: 10.1016/j.ecoenv.2026.119997

Muhammad Mahroz Hussain , Muhammad Junaid Nazir , Qasim ali , Nabeel Khan Niazi , Hamna Bashir , Shengsen Wang , Jörg Rinklebe , Ghulam Abbas , Sarmad Frogh Arshad , Muhammad Anwar

引用次数: 0

Retraction notice to “Sub chronic exposure to crude oil, dispersed oil and dispersant induces histopathological alterations in the gills of the juvenile rabbit fish (Siganus canaliculatus)” [Ecotoxicol. Environ. Saf. 93 (2023) 180–190] 对“亚慢性暴露于原油、分散油和分散剂会引起幼年兔鱼（Siganus canaliculatus）鳃的组织病理学改变”的撤回通知[生态毒物]。环绕。林业科学，93(2023):180-190。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-04-01 Epub Date: 2026-03-20 DOI: 10.1016/j.ecoenv.2026.119995

Esam Agamy

引用次数: 0

Retraction notice to “Histopathological liver alterations in juvenile rabbit fish (Siganus canaliculatus) exposed to light Arabian crude oil, dispersed oil and dispersant” [Ecotoxicol. Environ. Saf., 75 (2012) 171 – 179] 关于“暴露于阿拉伯轻质原油、分散油和分散剂的幼年兔鱼（Siganus canaliculatus）肝脏的组织病理学改变”的撤回通知[Ecotoxicol]。环绕。Saf。生态学报，75(2012)171 - 179。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-04-01 Epub Date: 2026-03-20 DOI: 10.1016/j.ecoenv.2026.119996

Esam Agamy

引用次数: 0

PFOS-mediated suppression of SOX30 impairs DNA double-strand break repair leading to male reproductive dysfunction pfos介导的SOX30抑制损害DNA双链断裂修复，导致男性生殖功能障碍。

IF 6.1 2区环境科学与生态学

Ecotoxicology and Environmental Safety Pub Date : 2026-04-01 Epub Date: 2026-03-28 DOI: 10.1016/j.ecoenv.2026.120081

Kangle Liu , Shijun He , Yuhan Hu , Yaxin Liu , Lei Zhu , Wenfeng Zhang , Xiao Jiang , Jing Gu , Lulu Guo , Zhonghao Zhang , Qing Chen , Lei Sun , Jia Cao , Lin Ao , Jinyi Liu

{"title":"PFOS-mediated suppression of SOX30 impairs DNA double-strand break repair leading to male reproductive dysfunction","authors":"Kangle Liu , Shijun He , Yuhan Hu , Yaxin Liu , Lei Zhu , Wenfeng Zhang , Xiao Jiang , Jing Gu , Lulu Guo , Zhonghao Zhang , Qing Chen , Lei Sun , Jia Cao , Lin Ao , Jinyi Liu","doi":"10.1016/j.ecoenv.2026.120081","DOIUrl":"10.1016/j.ecoenv.2026.120081","url":null,"abstract":"<div><div>Perfluorooctanesulfonic acid (PFOS), a persistent organic pollutant and representative per- and polyfluoroalkyl substance (PFAS), is ubiquitously detected in the environment and human tissues, and mounting evidence has implicated it in male reproductive dysfunction. However, the direct impact of PFOS on meiosis in spermatocytes and the underlying molecular mechanisms remain poorly understood. In this study, by combining chromosome spreading with high-resolution microscopy analysis of spermatocyte subtypes and morphology, we revealed that PFOS exposure decreased the proportion of pachytene spermatocytes and induced abnormal DNA double-strand break (DSB) repair, ultimately leading to a reduction in sperm density. Mechanistically, PFOS exposure suppressed the expression of SOX30, a germ-specific transcription factor, leading to downregulation of its downstream targets RPA2 and RAD51—key proteins of homologous recombination repair (HRR). This suppression resulted in unrepaired DSBs, triggering the pachytene checkpoint and leading to spermatocyte apoptosis. Critically, overexpression of SOX30 in PFOS-exposed GC2 spermatocyte cells restored RPA2/RAD51 expression and rescued DSB repair capacity. These findings identify SOX30 as a critical mediator of PFOS-induced meiotic DSB repair defects and establish it as a potential therapeutic target for mitigating PFAS-associated male infertility. This study provides novel insights into the molecular link between environmental pollutant exposure and impaired meiosis, offering a foundation for developing preventive and therapeutic strategies against PFOS-induced reproductive toxicity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"314 ","pages":"Article 120081"},"PeriodicalIF":6.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571666","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