The Experts below are selected from a list of 6357 Experts worldwide ranked by ideXlab platform
Xianghong Zhang - One of the best experts on this subject based on the ideXlab platform.
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High mobility group box-1 protects against Aflatoxin G1-induced pulmonary epithelial cell damage in the lung inflammatory environment.
Toxicology letters, 2020Co-Authors: Lifei Kang, Ling-xiao Xing, Chunping Liu, Ningfei Guo, Xiaoyi Liu, Xiuqing Wang, Wenli Guo, Shelly M. Xie, Xianghong ZhangAbstract:Abstract Aflatoxin G1 (AFG1) is a member of the carcinogenic Aflatoxin family. Our previous studies indicated that oral administration of AFG1 caused tumor necrosis factor (TNF)-α-dependent inflammation that enhanced oxidative DNA damage in alveolar epithelial cells, which may be related to AFG1-induced lung carcinogenesis. High mobility group box-1 (HMGB1) is a nuclear DNA-binding protein; the intracellular and extracellular roles of HMGB1 have been shown to contribute to DNA repair and sterile inflammation. The role of HMGB1 in DNA damage in an Aflatoxin-induced lung inflammatory environment was investigated in this study. Upregulation of HMGB1, TLR2, and RAGE was observed in AFG1-induced lung inflamed tissues and adenocarcinoma. Blocking AFG1-induced inflammation by neutralization of TNF-α inhibited the upregulation of HMGB1 in mouse lung tissues, suggesting that AFG1-induced TNF-α-dependent inflammation regulated HMGB1 expression. In the in vitro human pulmonary epithelial cell line model, Beas-2b, AFG1 directly enhanced the cytosolic translocation of HMGB1 and its extracellular secretion. The addition of extracellular soluble HMGB1 protected AFG1-induced DNA damage through the TLR2/NF-κB pathway in Beas-2b cells. In addition, blockade of endogenous HMGB1 by siRNA significantly enhanced AFG1-induced damage. Thus, our findings showed that both extracellularly-released and nuclear and cytosolic HMGB1 could protect the cell from AFG1-induced cell damage in a TNF-α-dependent lung inflammatory environment.
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Oral administration of Aflatoxin G1 induces chronic alveolar inflammation associated with lung tumorigenesis
Toxicology letters, 2014Co-Authors: Chunping Liu, Xia Yan, Ling-xiao Xing, Haitao Shen, Peilu Shao, Athena M. Soulika, Xinxing Meng, Xianghong ZhangAbstract:Abstract Our previous studies showed oral gavage of Aflatoxin G1 (AFG1) induced lung adenocarcinoma in NIH mice. We recently found that a single intratracheal administration of AFG1 caused chronic inflammatory changes in rat alveolar septum. Here, we examine whether oral gavage of AFG1 induces chronic lung inflammation and how it contributes to carcinogenesis. We evaluated chronic lung inflammatory responses in Balb/c mice after oral gavage of AFG1 for 1, 3 and 6 months. Inflammatory responses were heightened in the lung alveolar septum, 3 and 6 months after AFG1 treatment, evidenced by increased macrophages and lymphocytes infiltration, up-regulation of NF-κB and p-STAT3, and cytokines production. High expression levels of superoxide dismutase (SOD-2) and hemoxygenase-1 (HO-1), two established markers of oxidative stress, were detected in alveolar epithelium of AFG1-treated mice. Promoted alveolar type II cell (AT-II) proliferation in alveolar epithelium and angiogenesis, as well as increased COX-2 expression were also observed in lung tissues of AFG1-treated mice. Furthermore, we prolonged survival of the mice in the above model for another 6 months to examine the contribution of AFG1-induced chronic inflammation to lung tumorigenesis. Twelve months later, we observed that AFG1 induced alveolar epithelial hyperplasia and adenocarcinoma in Balb/c mice. Up-regulation of NF-κB, p-STAT3, and COX-2 was also induced in lung adenocarcinoma, thus establishing a link between AFG1-induced chronic inflammation and lung tumorigenesis. This is the first study to show that oral administration of AFG1 could induce chronic lung inflammation, which may provide a pro-tumor microenvironment to contribute to lung tumorigenesis.
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Aflatoxin G1-induced oxidative stress causes DNA damage and triggers apoptosis through MAPK signaling pathway in A549 cells.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Jing Liu, Yuan Wang, Hongguang Lian, Juan Wang, Xianghong ZhangAbstract:Our previous studies showed that Aflatoxin G1 (AFG1) could induce lung adenocarcinoma, and that the cancer cells originated from alveolar type II cells (AT-II cells). Recently, we found AFG1 induced structural impairment in rat AT-II cells, which may account for an early event in lung tumorigenesis. However, the mechanism of AFG1-induced AT-II cell damage remains unclear. DNA damage and apoptosis induced by oxidative stress are well accepted causes of cell damage. Thus, we explore whether AFG1 activates the reactive oxygen species (ROS)/MAPK/apoptosis pathway to cause cell damage in human AT-II cells like the cell line (A549). We found AFG1 induced oxidative stress by increasing ROS generation and caused DNA double-strand breaks (DSBs) by up-regulating γH2AX expression. AFG1 also triggered apoptosis in A549 cells by regulating Fas/FasL, caspase-8, Bax, Bcl-2, and activating caspase-3. Pre-treatment with antioxidant n-acetyl-l-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells. Furthermore, we found AFG1 activated ROS-mediated JNK and p38 pathways to induce cell apoptosis in A549 cells. In conclusion, our results indicate that AFG1 induces oxidative DNA damage and triggers apoptosis through ROS-mediated JNK and p38 signaling pathways in A549 cells, which may contribute to AFG1-induced AT-II cell damage.
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Impairment of alveolar type-II cells involved in the toxicity of Aflatoxin G1 in rat lung
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2012Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Xin Xing, Xianghong ZhangAbstract:Abstract Our previous studies showed intragastric administration of Aflatoxin G 1 (AFG 1 ) could induce lung adenocarcinoma, which derived from alveolar type II cells (AT-II cells). AT-II cells contribute to Aflatoxin B 1 (AFB 1 ) metabolism and also serve as the potential progenitor cells for AFB 1 -induced tumorigenesis. Thus, AT-II cells may constitute a target for AFG 1 exposure and serve as progenitor cells for tumorigenesis induced by AFG 1 . The current experiment was designed to identify the acute toxicity of AFG 1 in AT-II cells following a single intratracheal administration of AFG 1 . We observed inflammatory changes in the alveolar septum at days 3 and 7 after AFG 1 treatment, which resolved by 14 days. We also found AFG 1 caused lamellar bodies damage in AT-II cells at days 3 and 7 post-treatment. Surfactant protein C (SP-C) expression, an AT-II cell-specific marker, was reduced at day 7 post-treatment. The structural and functional impairment in AT-II cells returned to normal by day 14. Moreover, we found that AFG 1 induced a elevation of intracellular calcium concentration [Ca 2+ ]i in AT-II cells in vitro , which may contribute to the decreased SP-C expression. In conclusion, our results show AFG 1 induces structural and functional impairment in AT-II cells involved in the acute toxicity of AFG 1 in lung.
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Effect of Aflatoxin G1 on the expression of HLA- I molecule in human esophageal epithelial cells
Wei sheng yan jiu = Journal of hygiene research, 2011Co-Authors: Jinfeng Cui, Xianghong Zhang, Jun-ling WangAbstract:OBJECTIVE To explore the effect of AFG1 on the expression of human leukocyte antigen (HLA-I) molecule in human esophageal epithelial cells. METHOD Western Blot and RT-PCT analysis was used to explore the effect of AFG1 on the antigen presenting function of primary cultured esophageal epithelial cells. RESULTS The protein expression of HLA-ABC was significantly decreased in the groups treated with 100, 1000 and 2000 microg/L AFG1 as compared with the solvent control group (P < 0.05). Within the range of 100 - 2000 microg/L AFG1, the protein expression level of HLA-ABC of esophageal epithelial cells decreased gradually, and showed significant negative correlation (r = -0.921, n = 3, P < 0.01). The effect of AFG1 on the expression of HLA-ABC mRNA was further confirmed by RT-PCR analysis. The results showed that after treated with 100 microg/L, 1000 microg/L and 2000 microg/L AFG1, the expression of HLA-A mRNA was decreased significantly as compared with the solvent control (P < 0.05), and the expression of HLA-B mRNA was decreased in the 2000 microg/L AFG1 treated group (P < 0.05), while there was no effect on the expression of HLA-C mRNA. CONCLUSION The expression of HLA- I molecule in human esophageal epithelial cells could be inhibited by AFG1 treatment.
Ling-xiao Xing - One of the best experts on this subject based on the ideXlab platform.
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High mobility group box-1 protects against Aflatoxin G1-induced pulmonary epithelial cell damage in the lung inflammatory environment.
Toxicology letters, 2020Co-Authors: Lifei Kang, Ling-xiao Xing, Chunping Liu, Ningfei Guo, Xiaoyi Liu, Xiuqing Wang, Wenli Guo, Shelly M. Xie, Xianghong ZhangAbstract:Abstract Aflatoxin G1 (AFG1) is a member of the carcinogenic Aflatoxin family. Our previous studies indicated that oral administration of AFG1 caused tumor necrosis factor (TNF)-α-dependent inflammation that enhanced oxidative DNA damage in alveolar epithelial cells, which may be related to AFG1-induced lung carcinogenesis. High mobility group box-1 (HMGB1) is a nuclear DNA-binding protein; the intracellular and extracellular roles of HMGB1 have been shown to contribute to DNA repair and sterile inflammation. The role of HMGB1 in DNA damage in an Aflatoxin-induced lung inflammatory environment was investigated in this study. Upregulation of HMGB1, TLR2, and RAGE was observed in AFG1-induced lung inflamed tissues and adenocarcinoma. Blocking AFG1-induced inflammation by neutralization of TNF-α inhibited the upregulation of HMGB1 in mouse lung tissues, suggesting that AFG1-induced TNF-α-dependent inflammation regulated HMGB1 expression. In the in vitro human pulmonary epithelial cell line model, Beas-2b, AFG1 directly enhanced the cytosolic translocation of HMGB1 and its extracellular secretion. The addition of extracellular soluble HMGB1 protected AFG1-induced DNA damage through the TLR2/NF-κB pathway in Beas-2b cells. In addition, blockade of endogenous HMGB1 by siRNA significantly enhanced AFG1-induced damage. Thus, our findings showed that both extracellularly-released and nuclear and cytosolic HMGB1 could protect the cell from AFG1-induced cell damage in a TNF-α-dependent lung inflammatory environment.
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Enhanced Phenotypic Alterations of Alveolar Type II Cells in Response to Aflatoxin G1-Induced Lung Inflammation
Journal of cellular physiology, 2015Co-Authors: Haitao Shen, Chunping Liu, Peilu Shao, Yuan Wang, Juan Wang, Ziqiang Tian, Xin Zhao, Ling-xiao XingAbstract:Recently, we discovered that Aflatoxin G1 (AFG1) induces chronic lung inflammatory responses, which may contribute to lung tumorigenesis in Balb/C mice. The cancer cells originate from alveolar type II cells (AT-II cells). The activated AT-II cells express high levels of MHC-II and COX-2, may exhibit altered phenotypes, and likely inhibit antitumor immunity by triggering regulatory T cells (Tregs). However, the mechanism underlying phenotypic alterations of AT-II cells caused by AFG1-induced inflammation remains unknown. In this study, increased MHC-II expression in alveolar epithelium was observed and associated with enhanced Treg infiltration in mouse lung tissues with AFG1-induced inflammation. This provides a link between phenotypically altered AT-II cells and Treg activity in the AFG1-induced inflammatory microenvironment. AFG1-activated AT-II cells underwent phenotypic maturation since AFG1 upregulated MHC-II expression on A549 cells and primary human AT-II cells in vitro. However, mature AT-II cells may exhibit insufficient antigen presentation, which is necessary to activate effector T cells, due to the absence of CD80 and CD86. Furthermore, we treated A549 cells with AFG1 and TNF-α together to mimic an AFG1-induced inflammatory response in vitro, and we found that TNF-α and AFG1 coordinately enhanced MHC-II, CD54, COX-2, IL-10, and TGF-β expression levels in A549 cells compared to AFG1 alone. The phenotypic alterations of A549 cells in response to the combination of TNF-α and AFG1 were mainly regulated by TNF-α-mediated induction of the NF-κB pathway. Thus, enhanced phenotypic alterations of AT-II cells were induced in response to AFG1-induced inflammation. Thus, AT-II cells are likely to suppress anti-tumor immunity by triggering Treg activity. J. Cell. Physiol. 230: 1199–1211, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company
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Oral administration of Aflatoxin G1 induces chronic alveolar inflammation associated with lung tumorigenesis
Toxicology letters, 2014Co-Authors: Chunping Liu, Xia Yan, Ling-xiao Xing, Haitao Shen, Peilu Shao, Athena M. Soulika, Xinxing Meng, Xianghong ZhangAbstract:Abstract Our previous studies showed oral gavage of Aflatoxin G1 (AFG1) induced lung adenocarcinoma in NIH mice. We recently found that a single intratracheal administration of AFG1 caused chronic inflammatory changes in rat alveolar septum. Here, we examine whether oral gavage of AFG1 induces chronic lung inflammation and how it contributes to carcinogenesis. We evaluated chronic lung inflammatory responses in Balb/c mice after oral gavage of AFG1 for 1, 3 and 6 months. Inflammatory responses were heightened in the lung alveolar septum, 3 and 6 months after AFG1 treatment, evidenced by increased macrophages and lymphocytes infiltration, up-regulation of NF-κB and p-STAT3, and cytokines production. High expression levels of superoxide dismutase (SOD-2) and hemoxygenase-1 (HO-1), two established markers of oxidative stress, were detected in alveolar epithelium of AFG1-treated mice. Promoted alveolar type II cell (AT-II) proliferation in alveolar epithelium and angiogenesis, as well as increased COX-2 expression were also observed in lung tissues of AFG1-treated mice. Furthermore, we prolonged survival of the mice in the above model for another 6 months to examine the contribution of AFG1-induced chronic inflammation to lung tumorigenesis. Twelve months later, we observed that AFG1 induced alveolar epithelial hyperplasia and adenocarcinoma in Balb/c mice. Up-regulation of NF-κB, p-STAT3, and COX-2 was also induced in lung adenocarcinoma, thus establishing a link between AFG1-induced chronic inflammation and lung tumorigenesis. This is the first study to show that oral administration of AFG1 could induce chronic lung inflammation, which may provide a pro-tumor microenvironment to contribute to lung tumorigenesis.
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Aflatoxin G1-induced oxidative stress causes DNA damage and triggers apoptosis through MAPK signaling pathway in A549 cells.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Jing Liu, Yuan Wang, Hongguang Lian, Juan Wang, Xianghong ZhangAbstract:Our previous studies showed that Aflatoxin G1 (AFG1) could induce lung adenocarcinoma, and that the cancer cells originated from alveolar type II cells (AT-II cells). Recently, we found AFG1 induced structural impairment in rat AT-II cells, which may account for an early event in lung tumorigenesis. However, the mechanism of AFG1-induced AT-II cell damage remains unclear. DNA damage and apoptosis induced by oxidative stress are well accepted causes of cell damage. Thus, we explore whether AFG1 activates the reactive oxygen species (ROS)/MAPK/apoptosis pathway to cause cell damage in human AT-II cells like the cell line (A549). We found AFG1 induced oxidative stress by increasing ROS generation and caused DNA double-strand breaks (DSBs) by up-regulating γH2AX expression. AFG1 also triggered apoptosis in A549 cells by regulating Fas/FasL, caspase-8, Bax, Bcl-2, and activating caspase-3. Pre-treatment with antioxidant n-acetyl-l-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells. Furthermore, we found AFG1 activated ROS-mediated JNK and p38 pathways to induce cell apoptosis in A549 cells. In conclusion, our results indicate that AFG1 induces oxidative DNA damage and triggers apoptosis through ROS-mediated JNK and p38 signaling pathways in A549 cells, which may contribute to AFG1-induced AT-II cell damage.
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Impairment of alveolar type-II cells involved in the toxicity of Aflatoxin G1 in rat lung
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2012Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Xin Xing, Xianghong ZhangAbstract:Abstract Our previous studies showed intragastric administration of Aflatoxin G 1 (AFG 1 ) could induce lung adenocarcinoma, which derived from alveolar type II cells (AT-II cells). AT-II cells contribute to Aflatoxin B 1 (AFB 1 ) metabolism and also serve as the potential progenitor cells for AFB 1 -induced tumorigenesis. Thus, AT-II cells may constitute a target for AFG 1 exposure and serve as progenitor cells for tumorigenesis induced by AFG 1 . The current experiment was designed to identify the acute toxicity of AFG 1 in AT-II cells following a single intratracheal administration of AFG 1 . We observed inflammatory changes in the alveolar septum at days 3 and 7 after AFG 1 treatment, which resolved by 14 days. We also found AFG 1 caused lamellar bodies damage in AT-II cells at days 3 and 7 post-treatment. Surfactant protein C (SP-C) expression, an AT-II cell-specific marker, was reduced at day 7 post-treatment. The structural and functional impairment in AT-II cells returned to normal by day 14. Moreover, we found that AFG 1 induced a elevation of intracellular calcium concentration [Ca 2+ ]i in AT-II cells in vitro , which may contribute to the decreased SP-C expression. In conclusion, our results show AFG 1 induces structural and functional impairment in AT-II cells involved in the acute toxicity of AFG 1 in lung.
Haitao Shen - One of the best experts on this subject based on the ideXlab platform.
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Enhanced Phenotypic Alterations of Alveolar Type II Cells in Response to Aflatoxin G1-Induced Lung Inflammation
Journal of cellular physiology, 2015Co-Authors: Haitao Shen, Chunping Liu, Peilu Shao, Yuan Wang, Juan Wang, Ziqiang Tian, Xin Zhao, Ling-xiao XingAbstract:Recently, we discovered that Aflatoxin G1 (AFG1) induces chronic lung inflammatory responses, which may contribute to lung tumorigenesis in Balb/C mice. The cancer cells originate from alveolar type II cells (AT-II cells). The activated AT-II cells express high levels of MHC-II and COX-2, may exhibit altered phenotypes, and likely inhibit antitumor immunity by triggering regulatory T cells (Tregs). However, the mechanism underlying phenotypic alterations of AT-II cells caused by AFG1-induced inflammation remains unknown. In this study, increased MHC-II expression in alveolar epithelium was observed and associated with enhanced Treg infiltration in mouse lung tissues with AFG1-induced inflammation. This provides a link between phenotypically altered AT-II cells and Treg activity in the AFG1-induced inflammatory microenvironment. AFG1-activated AT-II cells underwent phenotypic maturation since AFG1 upregulated MHC-II expression on A549 cells and primary human AT-II cells in vitro. However, mature AT-II cells may exhibit insufficient antigen presentation, which is necessary to activate effector T cells, due to the absence of CD80 and CD86. Furthermore, we treated A549 cells with AFG1 and TNF-α together to mimic an AFG1-induced inflammatory response in vitro, and we found that TNF-α and AFG1 coordinately enhanced MHC-II, CD54, COX-2, IL-10, and TGF-β expression levels in A549 cells compared to AFG1 alone. The phenotypic alterations of A549 cells in response to the combination of TNF-α and AFG1 were mainly regulated by TNF-α-mediated induction of the NF-κB pathway. Thus, enhanced phenotypic alterations of AT-II cells were induced in response to AFG1-induced inflammation. Thus, AT-II cells are likely to suppress anti-tumor immunity by triggering Treg activity. J. Cell. Physiol. 230: 1199–1211, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company
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Oral administration of Aflatoxin G1 induces chronic alveolar inflammation associated with lung tumorigenesis
Toxicology letters, 2014Co-Authors: Chunping Liu, Xia Yan, Ling-xiao Xing, Haitao Shen, Peilu Shao, Athena M. Soulika, Xinxing Meng, Xianghong ZhangAbstract:Abstract Our previous studies showed oral gavage of Aflatoxin G1 (AFG1) induced lung adenocarcinoma in NIH mice. We recently found that a single intratracheal administration of AFG1 caused chronic inflammatory changes in rat alveolar septum. Here, we examine whether oral gavage of AFG1 induces chronic lung inflammation and how it contributes to carcinogenesis. We evaluated chronic lung inflammatory responses in Balb/c mice after oral gavage of AFG1 for 1, 3 and 6 months. Inflammatory responses were heightened in the lung alveolar septum, 3 and 6 months after AFG1 treatment, evidenced by increased macrophages and lymphocytes infiltration, up-regulation of NF-κB and p-STAT3, and cytokines production. High expression levels of superoxide dismutase (SOD-2) and hemoxygenase-1 (HO-1), two established markers of oxidative stress, were detected in alveolar epithelium of AFG1-treated mice. Promoted alveolar type II cell (AT-II) proliferation in alveolar epithelium and angiogenesis, as well as increased COX-2 expression were also observed in lung tissues of AFG1-treated mice. Furthermore, we prolonged survival of the mice in the above model for another 6 months to examine the contribution of AFG1-induced chronic inflammation to lung tumorigenesis. Twelve months later, we observed that AFG1 induced alveolar epithelial hyperplasia and adenocarcinoma in Balb/c mice. Up-regulation of NF-κB, p-STAT3, and COX-2 was also induced in lung adenocarcinoma, thus establishing a link between AFG1-induced chronic inflammation and lung tumorigenesis. This is the first study to show that oral administration of AFG1 could induce chronic lung inflammation, which may provide a pro-tumor microenvironment to contribute to lung tumorigenesis.
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Aflatoxin G1-induced oxidative stress causes DNA damage and triggers apoptosis through MAPK signaling pathway in A549 cells.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Jing Liu, Yuan Wang, Hongguang Lian, Juan Wang, Xianghong ZhangAbstract:Our previous studies showed that Aflatoxin G1 (AFG1) could induce lung adenocarcinoma, and that the cancer cells originated from alveolar type II cells (AT-II cells). Recently, we found AFG1 induced structural impairment in rat AT-II cells, which may account for an early event in lung tumorigenesis. However, the mechanism of AFG1-induced AT-II cell damage remains unclear. DNA damage and apoptosis induced by oxidative stress are well accepted causes of cell damage. Thus, we explore whether AFG1 activates the reactive oxygen species (ROS)/MAPK/apoptosis pathway to cause cell damage in human AT-II cells like the cell line (A549). We found AFG1 induced oxidative stress by increasing ROS generation and caused DNA double-strand breaks (DSBs) by up-regulating γH2AX expression. AFG1 also triggered apoptosis in A549 cells by regulating Fas/FasL, caspase-8, Bax, Bcl-2, and activating caspase-3. Pre-treatment with antioxidant n-acetyl-l-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells. Furthermore, we found AFG1 activated ROS-mediated JNK and p38 pathways to induce cell apoptosis in A549 cells. In conclusion, our results indicate that AFG1 induces oxidative DNA damage and triggers apoptosis through ROS-mediated JNK and p38 signaling pathways in A549 cells, which may contribute to AFG1-induced AT-II cell damage.
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Impairment of alveolar type-II cells involved in the toxicity of Aflatoxin G1 in rat lung
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2012Co-Authors: Haitao Shen, Jun-ling Wang, Xia Yan, Ling-xiao Xing, Xin Xing, Xianghong ZhangAbstract:Abstract Our previous studies showed intragastric administration of Aflatoxin G 1 (AFG 1 ) could induce lung adenocarcinoma, which derived from alveolar type II cells (AT-II cells). AT-II cells contribute to Aflatoxin B 1 (AFB 1 ) metabolism and also serve as the potential progenitor cells for AFB 1 -induced tumorigenesis. Thus, AT-II cells may constitute a target for AFG 1 exposure and serve as progenitor cells for tumorigenesis induced by AFG 1 . The current experiment was designed to identify the acute toxicity of AFG 1 in AT-II cells following a single intratracheal administration of AFG 1 . We observed inflammatory changes in the alveolar septum at days 3 and 7 after AFG 1 treatment, which resolved by 14 days. We also found AFG 1 caused lamellar bodies damage in AT-II cells at days 3 and 7 post-treatment. Surfactant protein C (SP-C) expression, an AT-II cell-specific marker, was reduced at day 7 post-treatment. The structural and functional impairment in AT-II cells returned to normal by day 14. Moreover, we found that AFG 1 induced a elevation of intracellular calcium concentration [Ca 2+ ]i in AT-II cells in vitro , which may contribute to the decreased SP-C expression. In conclusion, our results show AFG 1 induces structural and functional impairment in AT-II cells involved in the acute toxicity of AFG 1 in lung.
Azarmidokht Sheini - One of the best experts on this subject based on the ideXlab platform.
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Colorimetric aggregation assay based on array of gold and silver nanoparticles for simultaneous analysis of Aflatoxins, ochratoxin and zearalenone by using chemometric analysis and paper based analytical devices.
Mikrochimica acta, 2020Co-Authors: Azarmidokht SheiniAbstract:A paper based sensor array is presented to discriminate and determine five mycotoxins classified into three categories, namely Aflatoxins, ochratoxins and zearalenone. The gold and silver nanoparticles, synthesized by three different reducing or capping agents, were employed as sensing elements of the fabricated device. These nanoparticles were poured onto hydrophilic circular zones embedded on the hydrophobic substrate. The response of the assay is dependent on the aggregation of nanoparticles for interaction with mycotoxins. Due to aggregation, the gold and silver nanoparticles changed to purple and brown, respectively. Color changes provide unique colorimetric signatures conducive to recognizing the type of mycotoxin, identifying its chemical structure, and finding the fungi that produce it. The discrimination ability of the assay was investigated by both supervised (linear discriminate analysis) and unsupervised (principle component analysis and hierarchical cluster analysis) pattern recognition methods. The assay was applied to the point of need determination of Aflatoxin B1, Aflatoxin G1, Aflatoxin M1, ochratoxin A and zearalenone with a detection limit of 2.7, 7.3, 2.1, 3.3 and 7.0 ng.mL−1, respectively. The fabricated device has high potential of simultaneously determining the mycotoxins in pistachio, wheat, coffee and milk with the help of partial least square method. The root mean square errors for prediction of PLS model were 5.7, 5.2, 1.5, 7.2 and 2.9 for Aflatoxin B1, Aflatoxin G1, Aflatoxin M1, ochratoxin A and zearalenone, respectively.
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Colorimetric aggregation assay based on array of gold and silver nanoparticles for simultaneous analysis of Aflatoxins, ochratoxin and zearalenone by using chemometric analysis and paper based analytical devices
Microchimica Acta, 2020Co-Authors: Azarmidokht SheiniAbstract:A paper based sensor array is presented to discriminate and determine five mycotoxins classified into three categories, namely Aflatoxins, ochratoxins and zearalenone. The gold and silver nanoparticles, synthesized by three different reducing or capping agents, were employed as sensing elements of the fabricated device. These nanoparticles were poured onto hydrophilic circular zones embedded on the hydrophobic substrate. The response of the assay is dependent on the aggregation of nanoparticles for interaction with mycotoxins. Due to aggregation, the gold and silver nanoparticles changed to purple and brown, respectively. Color changes provide unique colorimetric signatures conducive to recognizing the type of mycotoxin, identifying its chemical structure, and finding the fungi that produce it. The discrimination ability of the assay was investigated by both supervised (linear discriminate analysis) and unsupervised (principle component analysis and hierarchical cluster analysis) pattern recognition methods. The assay was applied to the point of need determination of Aflatoxin B1, Aflatoxin G1, Aflatoxin M1, ochratoxin A and zearalenone with a detection limit of 2.7, 7.3, 2.1, 3.3 and 7.0 ng.mL^−1, respectively. The fabricated device has high potential of simultaneously determining the mycotoxins in pistachio, wheat, coffee and milk with the help of partial least square method. The root mean square errors for prediction of PLS model were 5.7, 5.2, 1.5, 7.2 and 2.9 for Aflatoxin B1, Aflatoxin G1, Aflatoxin M1, ochratoxin A and zearalenone, respectively. Graphical abstract Schematic representation of paper based colorimetric sensor array based on gold and silver nanoparticles for both qualitative and quantitative analysis of Aflatoxins, ochratoxin and zearalenone.
K. F. Cardwell - One of the best experts on this subject based on the ideXlab platform.
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Divergence of West African and North American communities of Aspergillus section Flavi.
Applied and environmental microbiology, 1999Co-Authors: Peter J. Cotty, K. F. CardwellAbstract:West African Aspergillus flavus S isolates differed from North American isolates. Both produced Aflatoxin B1. However, 40 and 100% of West African isolates also produced Aflatoxin G1 in NH4 medium and urea medium, respectively. No North American S strain isolate produced Aflatoxin G1. This geographical and physiological divergence may influence Aflatoxin management.
