Environmental Toxicology最新文献_第8页

Berberine Attenuates Cerulein-Induced Acute Pancreatitis by Modulating Nrf2/NOX2 Signaling Pathway via AMPK Activation 小檗碱通过AMPK激活调节Nrf2/NOX2信号通路，减轻蓝蛋白诱导的急性胰腺炎

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-26 DOI: 10.1002/tox.24468

Sapana P. Bansod, Mohd Aslam Saifi, Shrilekha Chilvery, Nandkumar Doijad, Chandraiah Godugu

{"title":"Berberine Attenuates Cerulein-Induced Acute Pancreatitis by Modulating Nrf2/NOX2 Signaling Pathway via AMPK Activation","authors":"Sapana P. Bansod, Mohd Aslam Saifi, Shrilekha Chilvery, Nandkumar Doijad, Chandraiah Godugu","doi":"10.1002/tox.24468","DOIUrl":"10.1002/tox.24468","url":null,"abstract":"<div>\u0000 \u0000 AMP-activated protein kinase (AMPK) is the master regulator of cellular energy which gets activated during energy stress and restores tissue homeostasis. AMPK is widely expressed in the pancreas and is involved in protein synthesis. In cerulein-induced acute pancreatitis (AP), diminished AMPK activity in the pancreatic tissue may be associated with pancreatic inflammation and oxidative stress. Our results demonstrated that berberine (BR) treatment produced significant decrease in plasma amylase and lipase levels and improved histopathological features in AP mice model. Myeloperoxidase (MPO) activity indicated that BR suppressed the infiltration of neutrophils in pancreas. BR treatment markedly decreased the levels of proinflammatory cytokines including interleukins (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) via inhibition of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) expression. In addition, BR activates the nuclear factor erythroid 2–related factor 2 (Nrf2) signaling and inhibits cerulein-induced oxidative-nitrosative stress. Mechanistically, we found inhibition of AMPK activity in cerulein-induced AP, while BR-treated animals showed marked increase in the AMPK expression. Together, our study indicated that BR-mediated AMPK activation in pancreatic tissues demonstrated attenuation of cerulein-induced oxidative stress and inflammation. Based on our observations, further exploration of this promising natural product against AP and associated complications may lead to promising therapeutic options.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 5","pages":"764-773"},"PeriodicalIF":4.4,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142888142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lead Mediated Lipopolysaccharides Exacerbates Fatty Liver Processes in High-Fat Diets-Induced Mice 铅介导的脂多糖加剧了高脂饮食诱导小鼠的脂肪肝过程

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-23 DOI: 10.1002/tox.24463

Penghui Nie, Liehai Hu, Tao You, Tiantian Jia, Hengyi Xu

{"title":"Lead Mediated Lipopolysaccharides Exacerbates Fatty Liver Processes in High-Fat Diets-Induced Mice","authors":"Penghui Nie, Liehai Hu, Tao You, Tiantian Jia, Hengyi Xu","doi":"10.1002/tox.24463","DOIUrl":"10.1002/tox.24463","url":null,"abstract":"<div>\u0000 \u0000 Obesity leads to a variety of health risks, and lead, which is ranked second in Agency for Toxic Substances and Disease Registry's priority list of harmful substances, may be more harmful to individuals that are obese. C57BL/6 mice were fed a normal diet or a high-fat diet with or without exposure to 1 g/L lead exposure in drinking water for 8 consecutive weeks. Serum and hepatic biochemistry analysis, histopathological observation, and RT-qPCR were used to explore the potential mechanism of liver damage in obese individuals after Pb exposure, and fecal microbiota transplantation was performed to investigate the role of the gut microbiota in the progression of fatty liver disease. We found that the progression of fatty liver disease induced by high-fat diets was accelerated by chronic lead intake. In addition, the occurrences of liver injury in recipient mice suggested the role of the gut microbiota. These findings indicated that the combination of lead and a HFD exacerbated hepatic lipotoxicity by activating LPS-mediated inflammation, and that gut microbiota disorders and impaired intestinal barrier function play pivotal roles in the progression of fatty liver disease.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 5","pages":"750-763"},"PeriodicalIF":4.4,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142879848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of Aluminum Oxide Nanoparticles in the Spinal Cord of Male Wistar Rats and the Potential Ameliorative Role of Melatonin 氧化铝纳米颗粒在雄性Wistar大鼠脊髓中的作用及褪黑素的潜在改善作用

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-20 DOI: 10.1002/tox.24466

Nermeen G. Abdelhameed, Yasmine H. Ahmed, Noha A. E. Yasin, Mohamed Y. Mahmoud, Mohamed A. El-sakhawy

{"title":"Effects of Aluminum Oxide Nanoparticles in the Spinal Cord of Male Wistar Rats and the Potential Ameliorative Role of Melatonin","authors":"Nermeen G. Abdelhameed, Yasmine H. Ahmed, Noha A. E. Yasin, Mohamed Y. Mahmoud, Mohamed A. El-sakhawy","doi":"10.1002/tox.24466","DOIUrl":"10.1002/tox.24466","url":null,"abstract":"<div>\u0000 \u0000 Aluminum oxide nanoparticles (Al2O3 NPs) are widely utilized in vaccine manufacturing and other medical preparations. Melatonin has numerous effects as an antioxidant and anti-apoptotic. The purpose of this study was to examine the beneficial impact of melatonin on Al2O3 NPs toxicity in the spinal cord. Forty male rats were divided into four groups: Group I, the negative controls (received standard diet and distilled water); Group II, Al2O3 NPs (received 30 mg/kg bw Al2O3 NPs); Group III, melatonin and Al2O3 NPs (received 30 mg/kg bw Al2O3 NPs + 10 mg/kg bw melatonin); Group IV, melatonin (received 10 mg/kg bw melatonin). All treatments were administered daily for 28 days by gastric gavage. After that, all rats were sacrificed, then, the samples from different spinal cords were subjected to histopathological, biochemical, and immunohistochemical analyses. Al2O3 NPs markedly elevated malondialdehyde and 8-hydroxydeoxyguanosine while inhibiting superoxide dismutase and catalase. Al2O3 NPs also induced histological alterations in both gray and white matter manifested by neuronal degeneration, vacuolation, axonal degeneration, ballooning, and fusion of myelin sheaths. Furthermore, immunohistochemical results displayed a strong positive expression of caspase-3. Conversely, melatonin significantly mitigated the effects of Al2O3 NPs by increasing the activities of antioxidant enzymes and inhibiting malondialdehyde and 8-hydroxydeoxyguanosine. Moreover, melatonin alleviated most histological alterations induced by Al2O3 NPs and reduced caspase-3 immunoreactivity. Collectively, melatonin could protect the spinal cord and mitigate Al2O3 NPs-induced neurotoxicity.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 5","pages":"737-749"},"PeriodicalIF":4.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142867282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Coleus vettiveroides Root Extract Protects Against Thioacetamide-Induced Chronic Liver Injury by Inhibiting NF-κB Signaling Pathway 鹅掌楸根提取物通过抑制 NF-κB 信号通路保护硫代乙酰胺诱导的慢性肝损伤

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-20 DOI: 10.1002/tox.24465

Kadmad Abdul Hameed Mohamed Azar, Devaraj Ezhilarasan, Munusamy Karthick, Karthik Shree Harini, Venkatesan Kumar

{"title":"Coleus vettiveroides Root Extract Protects Against Thioacetamide-Induced Chronic Liver Injury by Inhibiting NF-κB Signaling Pathway","authors":"Kadmad Abdul Hameed Mohamed Azar, Devaraj Ezhilarasan, Munusamy Karthick, Karthik Shree Harini, Venkatesan Kumar","doi":"10.1002/tox.24465","DOIUrl":"10.1002/tox.24465","url":null,"abstract":"<div>\u0000 \u0000 The roots of Coleus vettiveroides (CV) have been traditionally used in Indian medicinal systems such as Ayurveda and Siddha for its antioxidant, anti-inflammatory, and antidiabetic effects. This study examines the antifibrotic potential of CV ethanolic root extract (CVERE) against thioacetamide (TAA)-induced liver fibrosis in Wistar rats. TAA was administered via i.p., thrice weekly for 11 weeks to induce liver fibrosis in rats. In separate groups, rats were administered with TAA and were concurrently treated with CVERE 125 mg/kg, CVERE 250 mg/kg, and silymarin (SIL) 100 mg/kg. Liver marker enzymes of hepatotoxicity, oxidative stress markers, proinflammatory marker gene expression (TNF-α, NF-κB, COX, and ILs), fibrotic marker gene expression (collagen I and III), immune histochemical expression of fibrosis marker proteins, and histopathologic changes were analyzed. TAA administration led to a significant (p < 0.001) increase in the serum level of hepatotoxic marker enzymes. The TAA-treated group showed higher levels (p < 0.001) of MDA and reduced activities of SOD and CAT in the liver. TAA administration increased CYP2E1 expression, proinflammatory, and fibrotic marker gene expressions in rat liver. The histopathology of the liver confirms TAA-induced architectural distortion and fibrotic changes. CVERE and SIL simultaneous treatments significantly protected against TAA-induced oxidative stress, inflammation, and liver fibrosis. In conclusion, CVERE inhibited TAA-induced liver fibrosis through downregulation of TAA metabolic activation, redox imbalance, and inflammation through repression of the NF-κB pathway.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 5","pages":"723-736"},"PeriodicalIF":4.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142867280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

αCypermethrin-Induced Biochemical and Molecular Cascades Underlying Ovine Ovarian Granulosa Cell Dysfunctions α氯菊酯诱导的雌性卵巢颗粒细胞功能障碍的生化和分子级联。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-15 DOI: 10.1002/tox.24459

Poonam Kumari Singh, Bogapathi Sampath Kumar, Sumanta Nandi, Paluru Subramniyam Parameswara Gupta, Sukanta Mondal

{"title":"αCypermethrin-Induced Biochemical and Molecular Cascades Underlying Ovine Ovarian Granulosa Cell Dysfunctions","authors":"Poonam Kumari Singh, Bogapathi Sampath Kumar, Sumanta Nandi, Paluru Subramniyam Parameswara Gupta, Sukanta Mondal","doi":"10.1002/tox.24459","DOIUrl":"10.1002/tox.24459","url":null,"abstract":"<div>\u0000 \u0000 The present study was conducted to evaluate the impact of α-Cypermethrin (αCYP), the second most commonly used pesticide in India, on the ovine ovarian granulosa cells (GCs) viability, growth, apoptosis, and steroidogenesis. GCs collected from abattoir-derived ovine ovaries were cultured for 3/6 days in the presence of various concentrations of αCYP (0, 1, 10, 25, 50, and 100 μM). The results revealed a binary effect on GCs, where metabolic activity and viability rates were significantly (p < 0.05) lower from 25 μM onwards. Estrogen concentration was significantly low from the 1 μM dose, whereas progesterone concentration showed a significant increase (10 μM) in the spent media of cultured GCs. The cytotoxicity in the GCs exposed to αCYP revealed significant changes in LDH, ROS, CUPRAC, and GST activity (all at 25 μM) and MDA (at 10 μM) compared to those observed in the control group. The gene expression profiles of cultured GCs showed a significant up-regulation of CYP11A1, FSHR (all at 1 μM), StAR, BAX, and CASP3 (all at 10 μM), 3βHSD1 (at 25 μM), and significant down-regulation of CYP17A1 and ERS2 (all at 25 μM), CYP19A1 and 17βHSD (all at 1 μM), ESR1 and BCL2 (all at 10 μM) in comparison to those observed in control groups. The results of the present experiment demonstrated that αCYP affected the growth and functional parameters of GCs, the expression of steroid hormone-associated genes, and hormone secretion.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 4","pages":"694-706"},"PeriodicalIF":4.4,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PM2.5 Induces the Instability of Atherosclerotic Plaques by Activating the Notch Signaling Pathway In Vivo and In Vitro PM2.5通过激活Notch信号通路在体内和体外诱导动脉粥样硬化斑块的不稳定性

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-13 DOI: 10.1002/tox.24461

Tianyang Zhao, Yuezhu Zhang, Xu Li, Zhili Ge, Jingjing Shi, Tianyou Wang, Jiaxin Zhang, Xinyu Zhang, Huibin Jiang, Liting Zhou, Lin Ye

{"title":"PM2.5 Induces the Instability of Atherosclerotic Plaques by Activating the Notch Signaling Pathway In Vivo and In Vitro","authors":"Tianyang Zhao, Yuezhu Zhang, Xu Li, Zhili Ge, Jingjing Shi, Tianyou Wang, Jiaxin Zhang, Xinyu Zhang, Huibin Jiang, Liting Zhou, Lin Ye","doi":"10.1002/tox.24461","DOIUrl":"10.1002/tox.24461","url":null,"abstract":"<div>\u0000 \u0000 Fine particulate matter (PM2.5) can exacerbate the instability of atherosclerotic plaques although the exact chemical process driving atherosclerosis remains unknown. In order to create atherosclerotic models, a high-fat diet and vitamin D3 injections were given to 56 Wistar rats in this investigation. The atherosclerotic rats were split into four groups at random and given different doses of PM2.5 (0, 1.5, 7.5, and 37.5 mg/kg) for 4 weeks. To investigate the mechanism, foam cells were exposed to PM2.5 (0, 25, 50, and 100 μg/mL) for 24 h. The results showed that PM2.5 exposure caused collagen fibers thinner and muscle fibers were disorganized. PM2.5 exposure significantly affected the expression of MMP2, MMP9, TIMP2, and vimentin in aortas of atherosclerotic rats. Moreover, PM2.5 exposure increased the expression of the Notch signaling pathways which was correlated with the expression of atherosclerotic plaque stability-related genes. PM2.5 exposure also increased the apoptosis rate of foam cells. The expression of MMP2, MMP9, and vimentin was increased and TIMP2 was decreased with the increasing PM2.5 dose in foam cells. The inhibition of the Notch signaling pathway can alleviate the alteration of atherosclerotic plaque stability-related genes. The findings demonstrated that PM2.5 exposure can cause atherosclerotic plaques to become unstable, aggravating the progression of atherosclerosis, a process in which the Notch signaling pathway is crucial.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 4","pages":"683-693"},"PeriodicalIF":4.4,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

3-Chloro-1,2-Propanediol Exposure Induces Cardiotoxicity and Behavioural Abnormalities in Zebrafish Embryos 3-氯-1,2-丙二醇暴露诱导斑马鱼胚胎心脏毒性和行为异常。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-08 DOI: 10.1002/tox.24440

Jing Wang, Qiang Yuan, Weitao Hu, Zhijun Ye, Li Zhang, Zhipeng Wang, Jiejun Liu, Ling Huang, Fasheng Liu, Xinjun Liao, Juhua Xiao, Shouhua Zhang, Zigang Cao

{"title":"3-Chloro-1,2-Propanediol Exposure Induces Cardiotoxicity and Behavioural Abnormalities in Zebrafish Embryos","authors":"Jing Wang, Qiang Yuan, Weitao Hu, Zhijun Ye, Li Zhang, Zhipeng Wang, Jiejun Liu, Ling Huang, Fasheng Liu, Xinjun Liao, Juhua Xiao, Shouhua Zhang, Zigang Cao","doi":"10.1002/tox.24440","DOIUrl":"10.1002/tox.24440","url":null,"abstract":"<div>\u0000 \u0000 Numerous contemporary diseases are linked to food contamination. Pathogenic agents might stem from certain food ingredients or result from pollution stemming from food processing or packaging. One such contaminant is 3-Chloro-1,2-propanediol (3-MCPD), it has been previously reported to be produced during the preparation of chemical sauces, as well as during the heating of baked goods. Yet, uncertainty surrounds its potential to induce embryonic developmental toxicity. In this study, zebrafish were employed as the focal point to assess the impact of 3-MCPD on initial embryonic development, heart functionality, and behavior. The research unveiled that exposure of zebrafish embryos to 18, 36, and 54 mM 3-MCPD led to cardiac anomalies, including pericardial edema, reduced heart rate, and elongated SV-BA distance. Additionally, 3-MCPD exposure triggered aberrations in cardiac-related gene expression and an elevation in oxidative stress. Notably, behavioral changes were observed in 3-MCPD-exposed zebrafish embryos, while vascular development appeared unaffected. This study introduces a novel basis for comprehensive exploration of 3-MCPD toxicity.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 4","pages":"664-673"},"PeriodicalIF":4.4,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to “Biochemical Study on the Protective Effect of Curcumin on Acetaminophen and Gamma-Irradiation Induced Hepatic Toxicity in Rats” M. M. T. Eassawy, A. A. M. Salem, and A. F. M. Ismail, “ Biochemical Study on the Protective Effect of Curcumin on Acetaminophen and Gamma-Irradiation Induced Hepatic Toxicity in Rats,” Environmental Toxicology 36 (2021): 748–763, https://doi.org/10.1002/tox.23077. 修正《姜黄素对对乙酰氨基酚和γ辐照致大鼠肝毒性保护作用的生化研究》M. T. Eassawy， A. A. M. Salem， A. F. M. Ismail，“姜黄素对对乙酰氨基酚和γ辐射诱导的大鼠肝毒性的保护作用的生化研究”，环境毒理学36 (2021):748-763,https://doi.org/10.1002/tox.23077。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-12-04 DOI: 10.1002/tox.24458

引用次数: 0

The Ameliorative Effect of Betulinic Acid on Oxidative Stress in Mice of Cyclophosphamide-Induced Liver Damage 白桦脂酸对环磷酰胺诱发肝损伤小鼠氧化应激的改善作用

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-27 DOI: 10.1002/tox.24444

You Huang, Chaoyang Ma, Lijuan Zhu, Li Kong, Chunlin Huang, Wenjiang Yang, Jiayu He, Mingqi Yang, Lin Huang, Liyun Yuan, Jine Yi

{"title":"The Ameliorative Effect of Betulinic Acid on Oxidative Stress in Mice of Cyclophosphamide-Induced Liver Damage","authors":"You Huang, Chaoyang Ma, Lijuan Zhu, Li Kong, Chunlin Huang, Wenjiang Yang, Jiayu He, Mingqi Yang, Lin Huang, Liyun Yuan, Jine Yi","doi":"10.1002/tox.24444","DOIUrl":"10.1002/tox.24444","url":null,"abstract":"<div>\u0000 \u0000 As a conventional immunosuppressive drug, cyclophosphamide (CYP) exhibits strong hepatotoxicity in clinical applications. Betulinic acid (BA) is a natural triterpenoid that protects against liver damage. However, the underlying mechanism has not yet been elucidated. The purpose of this study was to evaluate the ameliorative effects of BA on CYP-induced hepatotoxicity and further clarify the underlying mechanism. BA pretreatment mitigated CYP-induced liver oxidative damage by alleviating histopathological lesions, reducing reactive oxygen species (ROS) accumulation, and restoring the mRNA expression of antioxidant enzymes (Cu-Sod, Mn-Sod, Cat, and Gsh-Px). BA treatment also suppressed CYP-induced oxidative stress by activating the NRF2 pathway and inhibiting the MAPK signaling pathway. Moreover, BA attenuated CYP-triggered hepatic apoptosis by suppressing excessive mitochondrial fission, boosting mitochondrial fusion, and ameliorating pro-apoptotic protein expression (CASP9 and the ratio of BCL-2/BAX) by blocking the oxidative stress-activated mitochondrial apoptotic pathway. Furthermore, PD98059 (an inhibitor of ERK) and/or BA abated CYP-provoked hepatotoxicity by inhibiting the ERK–MAPK and mitochondrial apoptotic pathways, implying that deactivation of the ERK-mediated mitochondrial apoptotic pathway contributed to the hepatoprotective efficacy of BA against CYP-induced oxidative stress. Therefore, BA could be used as a complementary medicine in patients undergoing CYP treatment owing to its hepatoprotective effects.\u0000 </div>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 4","pages":"608-623"},"PeriodicalIF":4.4,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Efficacy of Three-Dimensional Arterial Spin Labeling and How it Compares Against That of Contrast Enhanced Magnetic Resonance Imaging in Preoperative Grading of Brain Gliomas 回放：三维动脉自旋标记的疗效及其与对比增强磁共振成像在脑胶质瘤术前分级中的比较

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-25 DOI: 10.1002/tox.24452

{"title":"RETRACTION: Efficacy of Three-Dimensional Arterial Spin Labeling and How it Compares Against That of Contrast Enhanced Magnetic Resonance Imaging in Preoperative Grading of Brain Gliomas","authors":"","doi":"10.1002/tox.24452","DOIUrl":"10.1002/tox.24452","url":null,"abstract":"\u0000 \u0000 RETRACTION: K. Wang, H. Guo, X. Tian, Y. Miao, P. Han, and F. Jin, “ Efficacy of Three-Dimensional Arterial Spin Labeling and How it Compares Against That of Contrast Enhanced Magnetic Resonance Imaging in Preoperative Grading of Brain Gliomas,” Environmental Toxicology 38, no. 7 (2023): 1723–1731, https://doi.org/10.1002/tox.23800.\u0000 The above article, published online on 11 April 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The author Feng Jin disagrees with this decision. The other authors did not respond.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 3","pages":"497"},"PeriodicalIF":4.4,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24452","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142697032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0