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2. Retraction Note: Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications

Author

Gui, Suxin, primary, Sang, Xuezi, additional, Zheng, Lei, additional, Ze, Yuguan, additional, Zhao, Xiaoyang, additional, Sheng, Lei, additional, Sun, Qingqing, additional, Cheng, Zhe, additional, Cheng, Jie, additional, Hu, Renping, additional, Wang, Ling, additional, Hong, Fashui, additional, and Tang, Meng, additional

Published
2015
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4. Molecular mechanisms of phoxim-induced silk gland damage and TiO2 nanoparticle-attenuated damage in Bombyx mori

Author

Li, Bing, primary, Yu, Xiaohong, additional, Gui, Suxin, additional, Xie, Yi, additional, Zhao, Xiaoyang, additional, Hong, Jie, additional, Sun, Qingqing, additional, Sang, Xuezi, additional, Sheng, Lei, additional, Cheng, Zhe, additional, Cheng, Jie, additional, Hu, Rengping, additional, Wang, Ling, additional, Shen, Weide, additional, and Hong, Fashui, additional

Published
2014
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5. Mechanisms of nanosized titanium dioxide-induced testicular oxidative stress and apoptosis in male mice

Author

Zhao, Xiaoyang, Sheng, Lei, Wang, Ling, Hong, Jie, Yu, Xiaohong, Sang, Xuezi, Sun, Qingqing, Ze, Yuguan, and Hong, Fashui

Subjects
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.

Published
2014

6. Erratum to: Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications

Author

Gui, Suxin, primary, Sang, Xuezi, additional, Zheng, Lei, additional, Ze, Yuguan, additional, Zhao, Xiaoyang, additional, Sheng, Lei, additional, Sun, Qingqing, additional, Cheng, Zhe, additional, Cheng, Jie, additional, Hu, Renping, additional, Wang, Ling, additional, Hong, Fashui, additional, and Tang, Meng, additional

Published
2013
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8. Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice

Author

Ze, Yuguan, primary, Zheng, Lei, additional, Zhao, Xiaoyang, additional, Gui, Suxin, additional, Sang, Xuezi, additional, Su, Junju, additional, Guan, Ning, additional, Zhu, Liyuan, additional, Sheng, Lei, additional, Hu, Renping, additional, Cheng, Jie, additional, Cheng, Zhe, additional, Sun, Qingqing, additional, Wang, Ling, additional, and Hong, Fashui, additional

Published
2013
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9. Gene-Expression Changes in Cerium Chloride-Induced Injury of Mouse Hippocampus

Author

Cheng, Zhe, primary, Zhao, Haiquan, additional, Ze, Yuguan, additional, Su, Junju, additional, Li, Bing, additional, Sheng, Lei, additional, Zhu, Liyuan, additional, Guan, Ning, additional, Gui, Suxin, additional, Sang, Xuezi, additional, Zhao, Xiaoyang, additional, Sun, Qingqing, additional, Wang, Ling, additional, Cheng, Jie, additional, Hu, Renping, additional, and Hong, Fashui, additional

Published
2013
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11. RETRACTED ARTICLE: Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications

Author

Gui, Suxin, primary, Sang, Xuezi, additional, Zheng, Lei, additional, Ze, Yuguan, additional, Zhao, Xiaoyang, additional, Sheng, Lei, additional, Sun, Qingqing, additional, Cheng, Zhe, additional, Cheng, Jie, additional, Hu, Renping, additional, Wang, Ling, additional, Hong, Fashui, additional, and Tang, Meng, additional

Published
2013
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12. Molecular Mechanisms of Nanosized Titanium Dioxide–Induced Pulmonary Injury in Mice

Author

Li, Bing, primary, Ze, Yuguan, additional, Sun, Qingqing, additional, Zhang, Ting, additional, Sang, Xuezi, additional, Cui, Yaling, additional, Wang, Xiaochun, additional, Gui, Suxin, additional, Tan, Danlin, additional, Zhu, Min, additional, Zhao, Xiaoyang, additional, Sheng, Lei, additional, Wang, Ling, additional, Hong, Fashui, additional, and Tang, Meng, additional

Published
2013
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14. Nanosized TiO2-Induced Reproductive System Dysfunction and Its Mechanism in Female Mice.

Author

Zhao, Xiaoyang, Ze, Yuguan, Gao, Guodong, Sang, Xuezi, Li, Bing, Gui, Suxin, Sheng, Lei, Sun, Qingqing, Cheng, Jie, Cheng, Zhe, Hu, Renping, Wang, Ling, and Hong, Fashui

Subjects
FEMALE reproductive organs, OVARIES, TITANIUM dioxide, CYTOKINES, GENE expression, SERUM, SEX hormones, LABORATORY mice, WOUNDS & injuries
Abstract

Recent studies have demonstrated nanosized titanium dioxide (nano-TiO2)-induced fertility reduction and ovary injury in animals. To better understand how nano-TiO2 act in mice, female mice were exposed to 2.5, 5, and 10 mg/kg nano-TiO2 by intragastric administration for 90 consecutive days; the ovary injuries, fertility, hormone levels, and inflammation-related or follicular atresia-related cytokine expression were investigated. The results showed that nano-TiO2 was deposited in the ovary, resulting in significant reduction of body weight, relative weight of ovary and fertility, alterations of hematological and serum parameters and sex hormone levels, atretic follicle increases, inflammation, and necrosis. Furthermore, nano-TiO2 exposure resulted in marked increases of insulin-like growth factor-binding protein 2, epidermal growth factor, tumor necrosis factor-α, tissue plasminogen activator, interleukin-1β, interleukin -6, Fas, and FasL expression, and significant decreases of insulin-like growth factor-1, luteinizing hormone receptor, inhibin α, and growth differentiation factor 9 expression in mouse ovary. These findings implied that fertility reduction and ovary injury of mice following exposure to nano-TiO2 may be associated with alteration of inflammation-related or follicular atresia-related cytokine expressions, and humans should take great caution when handling nano-TiO2. [ABSTRACT FROM AUTHOR]

Published
2013
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15. Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications

Author

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

Subjects
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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16. Molecular mechanisms of phoxim-induced silk gland damage and TiO2 nanoparticle-attenuated damage in Bombyx mori.

Author

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

Subjects
*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]

Published
2014
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17. Intragastric exposure to titanium dioxide nanoparticles induced nephrotoxicity in mice, assessed by physiological and gene expression modifications.

Author

Gui S, Sang X, Zheng L, Ze Y, Zhao X, Sheng L, Sun Q, Cheng Z, Cheng J, Hu R, Wang L, Hong F, and Tang M

Subjects
Administration, Oral, Animals, Apoptosis drug effects, Body Weight drug effects, Dose-Response Relationship, Drug, Gene Expression Profiling, Kidney metabolism, Kidney ultrastructure, Kidney Diseases genetics, Kidney Diseases pathology, Lipid Peroxidation drug effects, Male, Mice, Mice, Inbred Strains, Nanoparticles administration & dosage, Nanoparticles chemistry, Oxidative Stress drug effects, Particle Size, Surface Properties, Titanium administration & dosage, Titanium chemistry, Gene Expression drug effects, Kidney drug effects, Kidney Diseases chemically induced, Nanoparticles toxicity, Titanium toxicity
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.

Published
2013
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