Retraction: C. Yue, W. Lian, M. Duan, D. Xia, X. Cao, and J. Peng, "The Predictive Efficacy of Programmed Cell Death in Immunotherapy of Melanoma: A Comprehensive Analysis of Gene Expression Data for Programmed Cell Death Biomarker and Therapeutic Target Discovery," Environmental Toxicology 39, no. 3 (2024): 1858-1873, https://doi.org/10.1002/tox.24051. The above article, published online on 22 December 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the authors; the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC.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.
引用本文：岳晨，李伟，段明，夏东，曹晓霞，彭军，“程序性细胞死亡在黑色素瘤免疫治疗中的预测作用：程序性细胞死亡生物标志物基因表达数据的综合分析和治疗靶点的发现”，环境毒理学杂志，39,no。3 (2024): 1858-1873, https://doi.org/10.1002/tox.24051。上述文章于2023年12月22日在线发表在Wiley在线图书馆（http://onlinelibrary.wiley.com/）上，经作者同意撤回；杂志主编Paul B. Tchounwou；和Wiley期刊有限责任公司。经过出版商的调查，双方得出结论，这篇文章完全是在妥协的同行评议过程的基础上被接受的。因此，这篇文章必须撤回。
{"title":"RETRACTION: The Predictive Efficacy of Programmed Cell Death in Immunotherapy of Melanoma: A Comprehensive Analysis of Gene Expression Data for Programmed Cell Death Biomarker and Therapeutic Target Discovery.","authors":"","doi":"10.1002/tox.24477","DOIUrl":"https://doi.org/10.1002/tox.24477","url":null,"abstract":"<p><strong>Retraction: </strong>C. Yue, W. Lian, M. Duan, D. Xia, X. Cao, and J. Peng, \"The Predictive Efficacy of Programmed Cell Death in Immunotherapy of Melanoma: A Comprehensive Analysis of Gene Expression Data for Programmed Cell Death Biomarker and Therapeutic Target Discovery,\" Environmental Toxicology 39, no. 3 (2024): 1858-1873, https://doi.org/10.1002/tox.24051. The above article, published online on 22 December 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the authors; the journal Editor-in-Chief, Paul B. Tchounwou; and Wiley Periodicals LLC.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.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002457","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}
Metal–organic frameworks (MOFs) have been gaining significant attention due to their potential application in medicine. Here, we investigated the effect of zeolite imidazole framework‐8 (ZIF‐8) on neuro‐behavioral parameters, histopathology, inflammation, and oxidative stress levels of rats' brain samples. Forty‐eight male Wistar rats were injected by four injections of saline or ZIF‐8 at different doses of 5, 10, or 20 mg/kg via the caudal vein. Y‐Maze, Morris‐Water Maze (MWM), and three chamber tests were conducted to explore working memory, spatial learning and memory, and social interactions, respectively. Histological staining and immunohistochemistry were used to evaluate pathological changes and astrocyte activation levels. The inflammation levels were measured using quantitative real‐time reverse‐transcription polymerase chain reaction (qRT‐PCR). The total antioxidant capacity (TAC) and oxidative stress production were assessed by biochemical assays. The results showed that ZIF‐8 induces neuromotor impairment dose‐dependently. Although histopathological studies indicated increased neuronal loss, inflammatory changes, and elevated active astrocytes in the hippocampus, the expression levels of IL‐1β and TNF‐α were not significantly increased in ZIF‐8‐treated rats. The TAC level significantly reduced and the malondialdehyde (MDA) level remarkably increased in the brain tissues. Our findings suggest that administration of ZIF‐8 induce neuromotor impairment, probably through amplified inflammation and oxidative stress.
{"title":"Zeolite Imidazole Framework‐8 Exacerbates Astrocyte Activation and Oxidative Stress in the Brain of Rats","authors":"Sadaf Abdi, Moein Shirzad, Maryam Ghasemi‐Kasman, Leyla Nadalinezhad, Shahram Ghasemi, Ebrahim Zabihi, Aliakbar Rajabzadeh","doi":"10.1002/tox.24467","DOIUrl":"https://doi.org/10.1002/tox.24467","url":null,"abstract":"Metal–organic frameworks (MOFs) have been gaining significant attention due to their potential application in medicine. Here, we investigated the effect of zeolite imidazole framework‐8 (ZIF‐8) on neuro‐behavioral parameters, histopathology, inflammation, and oxidative stress levels of rats' brain samples. Forty‐eight male Wistar rats were injected by four injections of saline or ZIF‐8 at different doses of 5, 10, or 20 mg/kg via the caudal vein. Y‐Maze, Morris‐Water Maze (MWM), and three chamber tests were conducted to explore working memory, spatial learning and memory, and social interactions, respectively. Histological staining and immunohistochemistry were used to evaluate pathological changes and astrocyte activation levels. The inflammation levels were measured using quantitative real‐time reverse‐transcription polymerase chain reaction (qRT‐PCR). The total antioxidant capacity (TAC) and oxidative stress production were assessed by biochemical assays. The results showed that ZIF‐8 induces neuromotor impairment dose‐dependently. Although histopathological studies indicated increased neuronal loss, inflammatory changes, and elevated active astrocytes in the hippocampus, the expression levels of <jats:italic>IL‐1β</jats:italic> and <jats:italic>TNF‐α</jats:italic> were not significantly increased in ZIF‐8‐treated rats. The TAC level significantly reduced and the malondialdehyde (MDA) level remarkably increased in the brain tissues. Our findings suggest that administration of ZIF‐8 induce neuromotor impairment, probably through amplified inflammation and oxidative stress.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"20 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142935510","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}
The current study aimed to investigate the sub‐acute effects of oxamyl on male Albino rats following oral administration of either 0.031 or 0.31 mg/kg/day for 14 consecutive days. The findings demonstrated that oxamyl produced a significant impact on most of the examined blood profile and biomarkers, along with a significant progressive and discernible alterations in the histology of organs. According to the results obtained, the potential mechanisms by which oxamyl causes its toxic effects on rats are identified as the inflammation indices, the inhibition of transaminases, alkaline phosphatase, and antioxidant enzymes, as well as the production of thiobarbituric acid reactive substances (TBARs) in organs following oxamyl treatment based on histopathological examinations. Due to the substantial genetic similarities between rats and humans, it is therefore anticipated that oxamyl will have comparable detrimental effects on humans.
{"title":"The Sub‐Acute Potential Risk of Oxamyl in Male Albino Rats","authors":"Maher S. Salama, Khaled A. Osman, Rania Elbanna","doi":"10.1002/tox.24462","DOIUrl":"https://doi.org/10.1002/tox.24462","url":null,"abstract":"The current study aimed to investigate the sub‐acute effects of oxamyl on male Albino rats following oral administration of either 0.031 or 0.31 mg/kg/day for 14 consecutive days. The findings demonstrated that oxamyl produced a significant impact on most of the examined blood profile and biomarkers, along with a significant progressive and discernible alterations in the histology of organs. According to the results obtained, the potential mechanisms by which oxamyl causes its toxic effects on rats are identified as the inflammation indices, the inhibition of transaminases, alkaline phosphatase, and antioxidant enzymes, as well as the production of thiobarbituric acid reactive substances (TBARs) in organs following oxamyl treatment based on histopathological examinations. Due to the substantial genetic similarities between rats and humans, it is therefore anticipated that oxamyl will have comparable detrimental effects on humans.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"43 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142888092","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}
Sapana P. Bansod, Mohd Aslam Saifi, Shrilekha Chilvery, Nandkumar Doijad, Chandraiah Godugu
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.
{"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":"https://doi.org/10.1002/tox.24468","url":null,"abstract":"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.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"19 1","pages":""},"PeriodicalIF":4.5,"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}
Penghui Nie, Liehai Hu, Tao You, Tiantian Jia, Hengyi Xu
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.
{"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":"https://doi.org/10.1002/tox.24463","url":null,"abstract":"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.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"25 1","pages":""},"PeriodicalIF":4.5,"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}
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.
{"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":"https://doi.org/10.1002/tox.24465","url":null,"abstract":"The roots of <jats:italic>Coleus vettiveroides</jats:italic> (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 (<jats:italic>p</jats:italic> < 0.001) increase in the serum level of hepatotoxic marker enzymes. The TAA‐treated group showed higher levels (<jats:italic>p</jats:italic> < 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.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"24 1","pages":""},"PeriodicalIF":4.5,"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}
Nermeen G. Abdelhameed, Yasmine H. Ahmed, Noha A. E. Yasin, Mohamed Y. Mahmoud, Mohamed A. El‐sakhawy
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.
{"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":"https://doi.org/10.1002/tox.24466","url":null,"abstract":"Aluminum oxide nanoparticles (Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> 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 Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> 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, Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs (received 30 mg/kg bw Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs); Group III, melatonin and Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs (received 30 mg/kg bw Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> 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. Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs markedly elevated malondialdehyde and 8‐hydroxydeoxyguanosine while inhibiting superoxide dismutase and catalase. Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> 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 Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs by increasing the activities of antioxidant enzymes and inhibiting malondialdehyde and 8‐hydroxydeoxyguanosine. Moreover, melatonin alleviated most histological alterations induced by Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs and reduced caspase‐3 immunoreactivity. Collectively, melatonin could protect the spinal cord and mitigate Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs‐induced neurotoxicity.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"14 1","pages":""},"PeriodicalIF":4.5,"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}
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.
{"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":"https://doi.org/10.1002/tox.24459","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"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}
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.
{"title":"PM<sub>2.5</sub> 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":"https://doi.org/10.1002/tox.24461","url":null,"abstract":"<p><p>Fine particulate matter (PM<sub>2.5</sub>) 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 PM<sub>2.5</sub> (0, 1.5, 7.5, and 37.5 mg/kg) for 4 weeks. To investigate the mechanism, foam cells were exposed to PM<sub>2.5</sub> (0, 25, 50, and 100 μg/mL) for 24 h. The results showed that PM<sub>2.5</sub> exposure caused collagen fibers thinner and muscle fibers were disorganized. PM<sub>2.5</sub> exposure significantly affected the expression of MMP2, MMP9, TIMP2, and vimentin in aortas of atherosclerotic rats. Moreover, PM<sub>2.5</sub> exposure increased the expression of the Notch signaling pathways which was correlated with the expression of atherosclerotic plaque stability-related genes. PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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 PM<sub>2.5</sub> exposure can cause atherosclerotic plaques to become unstable, aggravating the progression of atherosclerosis, a process in which the Notch signaling pathway is crucial.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"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}
Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4-144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC50) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1-Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.
{"title":"Effects of Flurochloridone on the Developmental Toxicity in Zebrafish (Danio rerio) Embryo.","authors":"Mingjun Yang, Jingying Hu, Fang Tian, Minjie Xia, Zhijun Zhou, Weihua Li","doi":"10.1002/tox.24460","DOIUrl":"https://doi.org/10.1002/tox.24460","url":null,"abstract":"<p><p>Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4-144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC<sub>50</sub>) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1-Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799952","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}
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