19 results on '"Sheng, Lei"'
Search Results
2. BmNPV Resistance of Silkworm Larvae Resulting from the Ingestion of TiO2 Nanoparticles
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Li, Bing, Xie, Yi, Cheng, Zhe, Cheng, Jie, Hu, Rengping, Gui, Suxin, Sang, Xuezi, Sun, Qingqing, Zhao, Xiaoyang, Sheng, Lei, Shen, Weide, and Hong, Fashui
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- 2012
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3. Titanium dioxide nanoparticles oral exposure induce osteoblast apoptosis, inhibit osteogenic ability and increase lipogenesis in mouse.
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Xu, Jingxi, Ze, Xiao, Zhao, Linchuan, Sheng, Lei, and Ze, Yuguan
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TITANIUM dioxide nanoparticles ,WNT signal transduction ,BONE regeneration ,RUNX proteins ,LIPID synthesis ,BONE morphogenetic proteins ,TITANIUM dioxide - Abstract
Titanium dioxide nanoparticles (TiO 2 -NPs) are widely used in food, paint, coating, cosmetic, and composite orthodontic material. As a common food additive, TiO 2 -NPs can accumulate in various organs of human body, but the effect and underlying mechanism of bone remain unclear. Here mice were exposed to TiO 2 -NPs by oral gavage, and histological staining of femoral sections showed that TiO 2 -NPs reduced bone formation and enhanced osteoclast activity and lipogenesis, contributing to decreased trabecula bone. Transmission electron microscope (TEM) as well as biochemical and flow cytometry analysis of osteoblast exhibited that TiO 2 -NPs accumulated in osteoblast cytoplasm and impaired mitochondria ultrastructure with increased reactive oxygen species (ROS) and lipid hyperoxide, resulting in osteoblast apoptosis. In terms of mechanism, TiO 2 -NPs treatment inhibited expression of AKT and then increased pro-apoptotic protein Bax expression which was failure to form heterodimers with decreased anti-apoptotic Bcl-2, activating downstream Caspase-9 and Caspase-3 and inducing apoptosis. Additionally, TiO 2 -NPs suppressed Wnt3a level and then activated anti-Glycogen synthesis kinase (GSK-3β) phosphorylation, and ultimately resulted in degradation of β-catenin which down-regulated Runt-related transcription factor 2 (Runx2) and Osterix, inhibiting expression of osteogenic related proteins. Together, these results revealed that exposure of TiO 2 -NPs induced apoptosis and inhibited osteoblast differentiation through suppressing PI3K/AKT and Wnt/β-catenin signaling pathways, resulting in reduction of trabecula bone. • TiO 2 -NPs inhibited osteogenesis and enhanced lipogenesis, decreasing trabecula bone. • TiO 2 -NPs activated intrinsic apoptosis via inhibiting PI3K/AKT pathway. • TiO 2 -NPs inhibited osteoblast differentiation through Wnt/β-catenin pathway. [ABSTRACT FROM AUTHOR]
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- 2024
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4. Nanoparticulate TiO2-mediated inhibition of the Wnt signaling pathway causes dendritic development disorder in cultured rat hippocampal neurons.
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Hong, Fashui, Ze, Yuguan, Zhou, Yaoming, Hong, Jie, Yu, Xiaohon, Sheng, Lei, and Wang, Ling
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Titanium dioxide nanoparticles (TiO
2 NPs) are increasingly used in daily life, in industry, and in environmental clearing, but their potential neurodevelopmental toxicity has been highly debated. In this study, we explored whether TiO2 NPs inhibited development of dendritic morphology and identified possible molecular mechanisms associated with this inhibition in primary cultured rat hippocampal neurons. Results showed that TiO2 NPs decreased neurite length, the number of branches and the spine density, and impaired mitochondrial function in the developing neurons. Furthermore, TiO2 NPs significantly reduced the expression of several proteins involved in canonical Wnt3a/β-catenin signaling including Wnt3a, β-catenin, p-GSK-3β, and CyclinD1 and conversely, elevated GSK-3β expression. In addition to altering expression of proteins involved in canonical Wnt3a/β-catenin signaling, TiO2 NPs decreased expression of proteins invovled in non-canonical Wnt signaling, including, MKLP1, CRMP3, ErbB4, and KIF17. Taken together, these results indicate that suppression of dendritic development caused by TiO2 NPs is associated with inhibition of activation of the Wnt/β-catenin pathway or non-canonical Wnt pathway-induced expression of microtubule cytoskeletal components in the developing neurons. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2139-2149, 2017. [ABSTRACT FROM AUTHOR]- Published
- 2017
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5. Mechanisms of nanosized titanium dioxide-induced testicular oxidative stress and apoptosis in male mice
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Zhao, Xiaoyang, Sheng, Lei, Wang, Ling, Hong, Jie, Yu, Xiaohong, Sang, Xuezi, Sun, Qingqing, Ze, Yuguan, and Hong, Fashui
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endocrine system ,Oxidative stress ,Research ,Testis ,Titanium dioxide nanoparticles ,Gene expression ,Sertoli cell apoptosis - Abstract
Background Due to the increased application of titanium dioxide nanoparticles (TiO2 NPs) in the food industry and daily life, their potential toxic effects in humans and animals have been investigated. However, very few studies have focused on testicular oxidative stress and/or apoptosis. Methods In order to understand the possible molecular mechanisms of testicular lesions following exposure to TiO2 NPs, male mice were exposed to 2.5, 5, or 10 mg/kg body weight TiO2 NPs for 90 consecutive days. Testicular oxidative stress and apoptosis were then evaluated, and the testicular mRNA expression of several genes and their proteins involved in oxidative stress and/or apoptosis was investigated. Results TiO2 NPs entered Sertoli cells and caused severe testicular oxidative damage and/or apoptosis, accompanied by excessive production of reactive oxygen species and peroxidation of lipids, proteins and DNA as well as a significant reduction in antioxidant capacity. Furthermore, exposure to TiO2 NPs resulted in the up-regulation of caspase-3, Nrbp2, and cytochrome c expression, and caused down-regulation of SOD, CAT, GPx, GST, GR, Cyp1b1, Car3, Bcl-2, Acaa2, and Axud1 expression in mouse testis. Conclusions TiO2 NPs entered Sertoli cells via the blood-testis barrier and were deposited in mouse seminiferous cord and/or Sertoli cells, causing oxidative damage and apoptosis.
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- 2014
6. Ti O2 nanoparticle-induced neurotoxicity may be involved in dysfunction of glutamate metabolism and its receptor expression in mice.
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Ze, Xiao, Su, Mingyu, Zhao, Xiaoyang, Jiang, Hao, Hong, Jie, Yu, Xiaohong, Liu, Dong, Xu, Bingqing, Sheng, Lei, Zhou, Qiuping, Zhou, Junling, Cui, Jingwen, Li, Kai, Wang, Ling, Ze, Yuguan, and Hong, Fashui
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TITANIUM dioxide nanoparticles ,NANOPARTICLES ,NEUROTOXICOLOGY ,GLUTAMIC acid metabolism ,GLUTAMATE receptors ,LABORATORY mice - Abstract
ABSTRACT Titanium dioxide nanoparticles (TiO
2 NPs) have been used in environmental management, food, medicine, and industry. But TiO2 NPs have been demonstrated to cross the blood-brain barrier and store up in the brain organization, leading to glutamate-mediated neurotoxicity. However, the neurotoxicity in the brain is not well understood. In this study, mice were exposed to 1.25, 2.5, or 5 mg/kg body weight TiO2 NPs for 9 months, and the glutamate-glutamine cyclic pathway and expressions of glutamate receptors associated with the hippocampal neurotoxicity were investigated. Our findings showed elevations of glutamate release and phosphate-activated glutaminase activity, and reductions in glutamine and glutamine synthetase in the hippocampus following exposure to TiO2 NPs. Furthermore, TiO2 NPs significantly inhibited the expression of N-methyl- d-aspartate receptor subunits (including NR1, NR2A, and NR2B) and metabotropic glutamate receptor 2 in mouse hippocampus. These findings suggest that the imbalance of glutamate metabolism triggered inhibitions of glutamate receptor expression in the TiO2 NP-exposed hippocampus. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 655-662, 2016. [ABSTRACT FROM AUTHOR]- Published
- 2016
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7. Suppression of neurite outgrowth of primary cultured hippocampal neurons is involved in impairment of glutamate metabolism and NMDA receptor function caused by nanoparticulate TiO2.
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Hong, Fashui, Sheng, Lei, Ze, Yuguan, Hong, Jie, Zhou, Yingjun, Wang, Ling, Liu, Dong, Yu, Xiaohong, Xu, Bingqing, Zhao, Xiaoyang, and Ze, Xiao
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NEUROTOXICOLOGY , *HIPPOCAMPUS (Brain) , *METHYL aspartate , *GLUTAMINE synthetase , *PROTEIN expression , *GLUTAMIC acid metabolism - Abstract
Numerous studies have indicated that nano-titanium dioxide (TiO 2 ) can induce neurotoxicity in vitro and in vivo , however, it is unclear whether nano-TiO 2 affects neurite outgrowth of hippocampal neurons. In order to investigate the mechanism of neurotoxicity, rat primary cultured hippocampal neurons on the fourth day of culture were exposed to 5, 15, and 30 μg/mL nano-TiO 2 for 24 h, and nano-TiO 2 internalization, dendritic growth, glutamate metabolism, expression of N-methyl- d -aspartate (NMDA) receptor subunits (NR1, NR2A and NR2B), calcium homeostasis, sodium current (I Na ) and potassium current (I K ) were examined. Our findings demonstrated that nano-TiO 2 crossed the membrane into the cytoplasm or nucleus, and significantly suppressed dendritic growth of primary cultured hippocampal neurons in a concentration-dependent manner. Furthermore, nano-TiO 2 induced a marked release of glutamate to the extracellular region, decreased glutamine synthetase activity and increased phosphate-activated glutaminase activity, elevated intracellular calcium ([Ca 2+ ]i), down-regulated protein expression of NR1, NR2A and NR2B, and increased the amplitudes of the I Na and I K . In addition, nano-TiO 2 increased nitric oxide and nitrice synthase, attenuated the activities of Ca 2+ -ATPase and Na + /K + -ATPase, and increased the ADP/ATP ratio in the primary neurons. Taken together, these findings indicate that nano-TiO 2 inhibits neurite outgrowth of hippocampal neurons by interfering with glutamate metabolism and impairing NMDA receptor function. [ABSTRACT FROM AUTHOR]
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- 2015
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8. Mechanisms of TiO2 nanoparticle-induced neuronal apoptosis in rat primary cultured hippocampal neurons.
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Sheng, Lei, Ze, Yuguan, Wang, Ling, Yu, Xiaohong, Hong, Jie, Zhao, Xiaoyang, Ze, Xiao, Liu, Dong, Xu, Bingqing, Zhu, Yunting, Long, Yi, Lin, Anan, Zhang, Chi, Zhao, Yue, and Hong, Fashui
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Exposure to titanium dioxide nanoparticles (TiO
2 NPs) has been demonstrated to decrease learning and memory of animals. However, whether the impacts of these NPs on the recognition function are involved in hippocamal neuron damages is poorly understood. In this study, primary cultured hippocampal neurons from one-day-old fetal Sprague-Dawley rats were exposed to 5, 15, or 30 µg/mL TiO2 NPs for 24 h, we investigated cell viability, ultrastructure, and mitochondrial membrane potential (MMP), calcium homeostasis, oxidative stress, antioxidant capacity, apoptotic signaling pathway associated with the primary cultured hippocamal neuron apoptosis. Our findings showed that TiO2 NP treatment resulted in reduction of cell viability, promoted lactate dehydrogenase release, apoptosis, and increased neuron apoptotic rate in a dose-dependent manner. Furthermore, TiO2 NPs led to [Ca2+ ]i elevation, and MMP reduction, up-regulated protein expression of cytochrome c, Bax, caspase-3, glucose-regulated protein 78, C/EBP homologous protein and caspase-12, and down-regulated bcl-2 expression in the primary cultured hippocampal neurons. These findings suggested that hippocampal neuron apoptosis caused by TiO2 NPs may be associated with mitochondria-mediated signal pathway and endoplasmic reticulum-mediated signal pathway. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 103A: 1141-1149, 2015. [ABSTRACT FROM AUTHOR]- Published
- 2015
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9. Immunomodulatory effects in the spleen-injured mice following exposure to titanium dioxide nanoparticles.
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Sang, Xuezi, Fei, Min, Sheng, Lei, Zhao, Xiaoyang, Yu, Xiaohong, Hong, Jie, Ze, Yuguan, Gui, Suxin, Sun, Qingqing, Ze, Xiao, Wang, Ling, and Hong, Fashui
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Immune injuries following the exposure of titanium dioxide nanoparticles (TiO
2 NPs) have been greatly concerned along with the TiO2 NPs are widely used in pharmacology and daily life. However, very little is known about the immunomodulatory mechanisms in the spleen-injured mice due to TiO2 NPs exposure. In this study, mice were continuously exposed to 2.5, 5, or 10 TiO2 NPs mg kg−1 body weight for 90 days with intragastric administration to investigate the immunomodulatory mechanisms in the spleen. The findings showed that TiO2 NPs exposure resulted in significant increases in spleen and thymus indices, and titanium accumulation, in turn led to histopathological changes and splenocyte apoptosis. Furthermore, the exposure of TiO2 NPs could significantly increase the levels of macrophage inflammatory protein (MIP)−1α, MIP-2, Eotaxin, monocyte chemotactic protein-1, interferon-γ, vascular cell adhesion molecule-1, interleukin-13, interferon-γ-inducible protein-10, migration inhibitory factor, CD69, major histocompatibility complex, protein tyrosine phosphatase, protein tyrosine kinase 1, basic fibroblast growth factor, Fasl, and GzmB expression, whereas markedly decrease the levels of NKG2D, NKp46, 2B4 expression involved in immune responses, lymphocyte healing and apoptosis. These findings would better understand toxicological effects induced by TiO2 NPs exposure. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 3562-3572, 2014. [ABSTRACT FROM AUTHOR]- Published
- 2014
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10. TiO2 Nanoparticles Induced Hippocampal Neuroinflammation in Mice.
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Ze, Yuguan, Sheng, Lei, Zhao, Xiaoyang, Hong, Jie, Ze, Xiao, Yu, Xiaohong, Pan, Xiaoyu, Lin, Anan, Zhao, Yue, Zhang, Chi, Zhou, Qiuping, Wang, Ling, and Hong, Fashui
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TITANIUM dioxide nanoparticles , *HIPPOCAMPUS diseases , *INFLAMMATION , *NANOMEDICINE , *TUMOR necrosis factors , *LABORATORY mice - Abstract
Titanium dioxide nanoparticles (TiO2 NPs) have been used in various medical and industrial areas. However, the impacts of these nanoparticles on neuroinflammation in the brain are poorly understood. In this study, mice were exposed to 2.5, 5, or 10 mg/kg body weight TiO2 NPs for 90 consecutive days, and the TLRs/TNF-α/NF-κB signaling pathway associated with the hippocampal neuroinflammation was investigated. Our findings showed titanium accumulation in the hippocampus, neuroinflammation and impairment of spatial memory in mice following exposure to TiO2 NPs. Furthermore, TiO2 NPs significantly activated the expression of Toll-like receptors (TLR2, TLR4), tumor necrosis factor-α, nucleic IκB kinase, NF-κB-inducible kinase, nucleic factor–κB, NF-κB2(p52), RelA(p65), and significantly suppressed the expression of IκB and interleukin-2. These findings suggest that neuroinflammation may be involved in TiO2 NP-induced alterations of cytokine expression in mouse hippocampus. Therefore, more attention should be focused on the application of TiO2 NPs in the food industry and their long-term exposure effects, especially in the human central nervous system. [ABSTRACT FROM AUTHOR]
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- 2014
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11. Neurotoxic characteristics of spatial recognition damage of the hippocampus in mice following subchronic peroral exposure to TiO2 nanoparticles.
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Ze, Yuguan, Sheng, Lei, Zhao, Xiaoyang, Ze, Xiao, Wang, Xuecen, Zhou, Qiuping, Liu, Jialiang, Yuan, Yifei, Gui, Suxin, Sang, Xuezi, Sun, Qingqing, Hong, Jie, Yu, Xiaohong, Wang, Ling, Li, Bingyan, and Hong, Fashui
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NEUROTOXICOLOGY , *HIPPOCAMPUS physiology , *TITANIUM dioxide , *METAL nanoparticles , *GENE expression , *LABORATORY mice - Abstract
Highlights: [•] TiO2 NPs exposure resulted in hippocampus injury and decreased spatial recognition of mice. [•] TiO2 NPs exposure resulted in decreased long-term potentiation. [•] TiO2 NPs exposure caused down-regulation of NR2A and NR2B expression in hippocampus. [•] TiO2 NPs decreased expression of CaMKIV, CREB-1 and FosB/DFosB. [Copyright &y& Elsevier]
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- 2014
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12. BmNPV Resistance of Silkworm Larvae Resulting from the Ingestion of TiO Nanoparticles.
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Li, Bing, Xie, Yi, Cheng, Zhe, Cheng, Jie, Hu, Rengping, Gui, Suxin, Sang, Xuezi, Sun, Qingqing, Zhao, Xiaoyang, Sheng, Lei, Shen, Weide, and Hong, Fashui
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Bombyx mori nucleopolyhedrovirus (BmNPV) causes infection in the silkworm that is often lethal. The infection is hard to prevent, partly because of the nature of the virus particles and partly because of the different strains of B. mori. Titanium dioxide nanoparticles (TiO NPs) have been demonstrated to have antimicrobial properties. The present study investigated whether TiO NPs added to an artificial diet can increase the resistance of B. mori larvae to BmNPV and examined the molecular mechanism behind any resistance shown. The results indicated that ingested TiO NPs decreased reactive oxygen species and NO accumulation in B. mori larvae under BmNPV infection, which in turn led to a decrease in their growth inhibition and mortality. In addition, the TiO NPs significantly promoted the expression of resistance-related genes, including those encoding superoxide dismutase, catalase, glutathione peroxidase, acetylcholine esterase, carboxylesterase, heat shock protein 21, glutathione S transferase o1, P53, and transferring and of genes encoding cytochrome p302 and nitric oxide synthase. These findings are a useful addition to the understanding of the mechanism of BmNPV resistance of B. mori larvae in response to TiO NPs addition. Such information also provides a theoretical basis for the use of TiO NPs in sericulture. [ABSTRACT FROM AUTHOR]
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- 2013
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13. Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications
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Gui, Suxin, Sang, Xuezi, Zheng, Lei, Ze, Yuguan, Zhao, Xiaoyang, Sheng, Lei, Sun, Qingqing, Cheng, Zhe, Cheng, Jie, Hu, Renping, Wang, Ling, Hong, Fashui, and Tang, Meng
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Male ,Titanium ,Dose-Response Relationship, Drug ,Surface Properties ,Research ,Gene Expression Profiling ,Health, Toxicology and Mutagenesis ,Body Weight ,Administration, Oral ,Gene Expression ,Titanium dioxide nanoparticles ,Apoptosis ,Mice, Inbred Strains ,Kidney ,Toxicology ,Gene-expressed profile ,Mice ,Oxidative Stress ,Retraction Note ,Animals ,Nanoparticles ,Kidney Diseases ,Lipid Peroxidation ,Particle Size ,Nephrotoxicity - Abstract
Background Numerous studies have demonstrated that titanium dioxide nanoparticles (TiO2 NPs) induced nephrotoxicity in animals. However, the nephrotoxic multiple molecular mechanisms are not clearly understood. Methods Mice were exposed to 2.5, 5 and 10 mg/kg TiO2 NPs by intragastric administration for 90 consecutive days, and their growth, element distribution, and oxidative stress in kidney as well as kidney gene expression profile were investigated using whole-genome microarray analysis technique. Results Our findings suggest that TiO2 NPs resulted in significant reduction of renal glomerulus number, apoptosis, infiltration of inflammatory cells, tissue necrosis or disorganization of renal tubules, coupled with decreased body weight, increased kidney indices, unbalance of element distribution, production of reactive oxygen species and peroxidation of lipid, protein and DNA in mouse kidney tissue. Furthermore, microarray analysis showed significant alterations in the expression of 1, 246 genes in the 10 mg/kg TiO2 NPs-exposed kidney. Of the genes altered, 1006 genes were associated with immune/inflammatory responses, apoptosis, biological processes, oxidative stress, ion transport, metabolic processes, the cell cycle, signal transduction, cell component, transcription, translation and cell differentiation, respectively. Specifically, the vital up-regulation of Bcl6, Cfi and Cfd caused immune/ inflammatory responses, the significant alterations of Axud1, Cyp4a12a, Cyp4a12b, Cyp4a14, and Cyp2d9 expression resulted in severe oxidative stress, and great suppression of Birc5, Crap2, and Tfrc expression led to renal cell apoptosis. Conclusions Axud1, Bcl6, Cf1, Cfd, Cyp4a12a, Cyp4a12b, Cyp2d9, Birc5, Crap2, and Tfrc may be potential biomarkers of kidney toxicity caused by TiO2 NPs exposure.
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14. Decreased spermatogenesis led to alterations of testis-specific gene expression in male mice following nano-TiO2 exposure.
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Hong, Fashui, Zhao, Xiaoyang, Si, Wenhui, Ze, Yuguan, Wang, Ling, Zhou, Yingjun, Hong, Jie, Yu, Xiaohong, Sheng, Lei, Liu, Dong, Xu, Bingqing, and Zhang, Jianhao
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SPERMATOGENESIS , *TESTIS , *TITANIUM dioxide nanoparticles , *GENE expression , *LABORATORY mice , *MESSENGER RNA - Abstract
Although TiO 2 nanoparticles (NPs) exposure has been demonstrated to cross blood–testis barrier and accumulate in the testis resulting in the reduction of sperm numbers, limited data with respect to the molecular mechanism of decreased spermatogenesis caused by TiO 2 NP exposure. In this research, testicular damage, sperm number and alterations in testis-specific gene expressions in male mice induced by intragastric administration with TiO 2 NPs for six months were investigated. It was found out that TiO 2 NPs could migrate to cells, deposit in the testis and epididymis and thus cause damages to relevant organs, which are, to be more specific, the reductions of total sperm concentrations and sperm motility and an enhancement in the number of abnormal sperms in the cauda epididymis. Furthermore, the individual expression regarding to the mRNAs and proteins of testis-specific genes, including Cdc2, Cyclin B1, Dmcl, TERT, Tesmin, TESP-1, XPD and XRCCI, were significantly declined, whereas Gsk3-β and PGAM4 expressions were greatly elevated in mouse testis due to the exposures, which in fact implied that the reduced spermatogenesis may be involved in the alternated testis-specific gene expressions in those exposed male mice. [ABSTRACT FROM AUTHOR]
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- 2015
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15. Molecular mechanisms of phoxim-induced silk gland damage and TiO2 nanoparticle-attenuated damage in Bombyx mori.
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Li, Bing, Yu, Xiaohong, Gui, Suxin, Xie, Yi, Zhao, Xiaoyang, Hong, Jie, Sun, Qingqing, Sang, Xuezi, Sheng, Lei, Cheng, Zhe, Cheng, Jie, Hu, Rengping, Wang, Ling, Shen, Weide, and Hong, Fashui
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MOLECULAR biology , *BAYTHION , *SILKWORMS , *INSECT development , *INSECT anatomy , *TITANIUM dioxide nanoparticles , *PHYSIOLOGICAL effects of insecticides - Abstract
Highlights: [•] Phoxim exposure resulted in decrease of the cocooning rate of B. mori. [•] TiO2 NPs could increase the cocooning rate of B. mori under phoxim toxicity. [•] Phoxim exposure damaged silk gland and decreased Fib-L, Ser2, Ser3, and P25 expressions. [•] TiO2 NPs could relieve silk gland damage and increase Fib-L, Ser2, Ser3, and P25 expressions. [Copyright &y& Elsevier]
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- 2014
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16. Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice.
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Ze, Yuguan, Zheng, Lei, Zhao, Xiaoyang, Gui, Suxin, Sang, Xuezi, Su, Junju, Guan, Ning, Zhu, Liyuan, Sheng, Lei, Hu, Renping, Cheng, Jie, Cheng, Zhe, Sun, Qingqing, Wang, Ling, and Hong, Fashui
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BRAIN injuries , *NANOMEDICINE , *TITANIUM dioxide , *OXIDATIVE stress , *LABORATORY mice , *GENETIC regulation , *CELL proliferation , *REACTIVE oxygen species , *PHYSIOLOGY - Abstract
Abstract: Numerous studies have demonstrated that the brain is one of the target organs in acute or chronic titanium dioxide (TiO2) nanoparticles (NPs) toxicity, and oxidative stress plays an important role in this process. However, whether brain oxidative injury responds to TiO2 NPs by activating the P38-nuclear factor-E2-related factor-2 (Nrf-2) pathway is not fully understood. The present study aimed to examine activation of the P38-Nrf-2 signaling pathway associated with oxidative stress in the mouse brain induced by intranasal administration of TiO2 NPs for 90 consecutive days. Our findings indicate that TiO2 NPs caused overproliferation of spongiocytes and hemorrhage in the mouse brain. Furthermore, TiO2 NPs significantly activated p38, c-Jun N-terminal kinase, nuclear factor kappa B, Nrf-2 and heme oxygenase-1 expression in the brain, which in turn, led to increased production of reactive oxygen species, as well as lipid, protein and DNA peroxidation. These findings suggest that TiO2 NPs-induced oxidative damage in the mouse brain may occur via the p38-Nrf-2 signaling pathway. Therefore, application of TiO2 NPs in the environment should be performed with caution. [Copyright &y& Elsevier]
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- 2013
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17. Titanium dioxide nanoparticle-induced testicular damage, spermatogenesis suppression, and gene expression alterations in male mice.
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Gao, Guodong, Ze, Yuguan, Zhao, Xiaoyang, Sang, Xuezi, Zheng, Lei, Ze, Xiao, Gui, Suxin, Sheng, Lei, Sun, Qingqing, Hong, Jie, Yu, Xiaohong, Wang, Ling, Hong, Fashui, and Zhang, Xueguang
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TITANIUM dioxide nanoparticles , *TESTICULAR diseases , *SPERMATOGENESIS , *GENE expression , *LABORATORY mice , *SEX hormones , *SPERM motility - Abstract
Highlights: [•] Exposure to TiO2 NPs could cross blood–testis barrier and be accumulated in testis. [•] Exposure to TiO2 NPs caused testis and sperm lesions in male mice. [•] Exposure to TiO2 NP decreased sperm numbers and sperm motility in male mice. [•] Exposure to TiO2 NP resulted in imbalance of sex hormones in male mice. [•] Exposure to TiO2 NP caused alteration of 142 genes expression of known function in testis. [ABSTRACT FROM AUTHOR]
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- 2013
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18. Ovarian dysfunction and gene-expressed characteristics of female mice caused by long-term exposure to titanium dioxide nanoparticles
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Gao, Guodong, Ze, Yuguan, Li, Bing, Zhao, Xiaoyang, Zhang, Ting, Sheng, Lei, Hu, Ringhu, Gui, Suxin, Sang, Xuezi, Sun, Qingqing, Cheng, Jie, Cheng, Zhe, Wang, Ling, Tang, Meng, and Hong, Fashui
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GENE expression , *TITANIUM dioxide nanoparticles , *OVARIAN physiology , *SEX hormones , *OXIDATIVE stress , *GENETIC regulation , *PROGESTERONE , *LABORATORY mice - Abstract
Abstract: Although numerous studies have described the accumulation of titanium dioxide nanoparticles (TiO2 NPs) in the liver, kidneys, lung, spleen, and brain, and the corresponding damage, it is unclear whether or not TiO2 NPs can be translocated to the ovary and cause ovarian injury, thus impairing fertility. In the current study, ovarian injury and gene-expressed characteristics in female mice induced by intragastric administration of TiO2 NPs (10mg/kg) for 90 consecutive days were investigated. Our findings indicated that TiO2 NPs can accumulate in the ovary and result in ovarian damage, cause an imbalance of mineral element distribution and sex hormones, decrease fertility or the pregnancy rate and oxidative stress in mice. Microarray analysis showed that in ovaries from mice treated with TiO2 NPs compared to controls, 223 genes of known function were up-regulated, while 65 ovarian genes were down-regulated. The increased expression of Cyp17a1 following TiO2 NPs treatment suggested that the increase in estradiol biosynthesis may be a consequence of increased TiO2 NPs. In addition, the elevated expression of Akr1c18 implied that progesterone metabolism was accelerated, thus causing a decrease in the progesterone concentration. Taken together, the apparent regulation of key ovarian genes supports the hypothesis that TiO2 NPs directly affects ovarian function. [Copyright &y& Elsevier]
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- 2012
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19. Pulmotoxicological effects caused by long-term titanium dioxide nanoparticles exposure in mice
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Sun, Qingqing, Tan, Danning, Ze, Yuguan, Sang, Xuezi, Liu, Xiaorun, Gui, Suxin, Cheng, Zhe, Cheng, Jie, Hu, Renping, Gao, Guodong, Liu, Gan, Zhu, Min, Zhao, Xiaoyang, Sheng, Lei, Wang, Ling, Tang, Meng, and Hong, Fashui
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INFLAMMATION , *TITANIUM dioxide nanoparticles , *LABORATORY mice , *PULMONARY artery , *LIPID peroxidation (Biology) , *CYCLOOXYGENASE 2 , *CYTOKINES , *WOUNDS & injuries - Abstract
Abstract: Exposure to titanium dioxide nanoparticles (TiO2 NPs) has been demonstrated to result in pulmonary inflammation in animals; however, very little is known about the molecular mechanisms of pulmonary injury due to TiO2 NPs exposure. The aim of this study was to evaluate the oxidative stress and molecular mechanism associated with pulmonary inflammation in chronic lung toxicity caused by the intratracheal instillation of TiO2 NPs for 90 consecutive days in mice. Our findings suggest that TiO2 NPs are significantly accumulated in the lung, leading to an obvious increase in lung indices, inflammation and bleeding in the lung. Exposure to TiO2 NPs significantly increased the accumulation of reactive oxygen species and the level of lipid peroxidation, and decreased antioxidant capacity in the lung. Furthermore, TiO2 NPs exposure activated nuclear factor-κB, increased the levels of tumor necrosis factor-α, cyclooxygenase-2, heme oxygenase-1, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-18, interleukin-1β, and CYP1A1 expression. However, TiO2 NPs exposure decreased NF-κB-inhibiting factor and heat shock protein 70 expression. Our results suggest that the generation of pulmonary inflammation caused by TiO2 NPs in mice is closely related to oxidative stress and the expression of inflammatory cytokines. [Copyright &y& Elsevier]
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- 2012
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