14 results on '"Sang, Xuezi"'
Search Results
2. 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
3. Phoxim-induced damages of Bombyx mori larval midgut and titanium dioxide nanoparticles protective role under phoxim-induced toxicity.
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Su, Junju, Li, Bing, Cheng, Shen, Zhu, Zhou, Sang, Xuezi, Gui, Suxin, Xie, Yi, Sun, Qingqing, Cheng, Zhe, Cheng, Jie, Hu, Rengping, Shen, Weide, Xia, Qingyou, Zhao, Ping, and Hong, Fashui
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BAYTHION ,CHOLINESTERASE inhibitors ,SUPEROXIDE dismutase ,TITANIUM dioxide ,ACETYLCHOLINESTERASE ,THIOLS - Abstract
ABSTRACT Phoxim ( O, O-diethyl O-(alpha-cyanobenzylideneamino) phosphorothioate) is a powerful organophosphorus pesticide with high potential for Bombyx mori larvae of silkworm exposure. However, it is possible that during the phoxim metabolism, there is generation of reactive oxygen species (ROS) and phoxim may produce oxidative stress and neurotoxicity in an intoxicated silkworm. Titanium dioxide nanoparticles (TiO
2 NPs) pretreatment has been demonstrated to increase antioxidant capacity and acetylcholinesterase (AChE) activity in organisms. This study was, therefore, undertaken to determine phoxim-induced oxidative stress and neurotoxicity to determine whether phoxim intoxication alters the antioxidant system and AChE activity in the B. mori larval midgut, and to determine whether TiO2 NPs pretreatment attenuates phoxim-induced toxicity. The findings suggested that phoxim exposure decreased survival of B. mori larvae, increased malondialdehyde (MDA), carbonyl and 8-OHdG levels, and ROS accumulation in the midgut. Furthermore, phoxim significantly decreased the activities of AChE, superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), glutathione- S-transferase (GST), and levels of ascorbic acid (AsA), reduced glutathione (GSH), and thiol in the midgut. TiO2 pretreatment, however, could increase AChE activity, and remove ROS via activating SOD, CAT, APX, GR, and GST, and accelerating AsA-GSH cycle, thus attenuated lipid, protein, and DNA peroxidation and improve B. mori larval survival under phoxim-induced toxicity. Moreover, this experimental system would help nanomaterials to be applied in the sericulture. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1355-1366, 2014. [ABSTRACT FROM AUTHOR]- Published
- 2014
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4. 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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5. 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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6. Oxidative damage of lung and its protective mechanism in mice caused by long-term exposure to titanium dioxide nanoparticles.
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Sun, Qingqing, Tan, Danlin, Zhou, Qiuping, Liu, Xiaorun, Cheng, Zhe, Liu, Gan, Zhu, Min, Sang, Xuezi, Gui, Suxin, Cheng, Jie, Hu, Renping, Tang, Meng, and Hong, Fashui
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Exposure to titanium dioxide nanoparticles (TiO
2 NPs) elicits an adverse response such as oxidative damage. The molecular targets of TiO2 NPs remain largely unidentified. In the present study, the function and signal pathway of nuclear factor erythroid 2 related factor 2 (Nrf2) in protection against TiO2 NPs-induced oxidative stress in the mouse lung were investigated. Mice were exposed to 10 mg/kg body weight by an intratracheal administration for 15-90 days. With increasing exposed terms, TiO2 NPs were significantly accumulated and increased the reactive oxygen species (ROS) production in lung, which resulted in severe pulmonary edema, inflammatory response and pneumonocyte apoptosis for 90 days. Furthermore, TiO2 NPs exposure could greatly induce expression of Nrf2, heme oxygenase 1 (HO-1), and glutamate-cysteine ligase catalytic subunit (GCLC) from 15-day to 75-day exposure, whereas 90-day exposure caused significant decreases of three factors expression levels in lung. Our findings imply that the induction of Nrf2 expression is an adaptive intracellular response to TiO2 NPs-induced oxidative stress in the mouse lung, and that Nrf2 is protective against TiO2 NPs-induced pulmonary damages during certain exposure terms. © 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A 100A:2554-2562, 2012. [ABSTRACT FROM AUTHOR]- Published
- 2012
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7. 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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8. 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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9. 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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10. 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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11. 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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12. 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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13. 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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14. Titanium dioxide nanoparticles relieve biochemical dysfunctions of fifth-instar larvae of silkworms following exposure to phoxim insecticide
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Li, Bing, Hu, Rengping, Cheng, Zhe, Cheng, Jie, Xie, Yi, Gui, Suxin, Sun, Qingqing, Sang, Xuezi, Gong, Xiaolan, Cui, Yaling, Shen, Weide, and Hong, Fashui
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TITANIUM dioxide , *NANOPARTICLES , *INSECTICIDES , *SILKWORMS , *INSECT pests , *ASPARTATE aminotransferase , *MALATE dehydrogenase - Abstract
Abstract: Phoxim insecticide is widely used in agriculture, which is toxic to insect pests and nontarget organisms. The phoxim poisoning is hard to prevent for silkworms. TiO2 NPs have been widely applied in whitening, brightening foods, toothpaste or sunscreens, and orally-administered drugs. However, whether TiO2 NPs can increase resistance of silkworm to phoxim poisoning has not been reported. The results demonstrated that added TiO2 NPs significantly decreased reduction of protein, glucose and pyruvate contents, lactate dehydrogenase, succinate dehydrogenase and malate dehydrogenase activities, and attenuated increases of free amino acids, urea, uric acid and lactate levels, activities of protease, alanine aminotransferase and aspartate aminotransferase in the hemolymph of silkworms caused by phoxim exposure. From the present study, it is clearly evident that added TiO2 NPs may relieve toxic impacts of phoxim insecticide on silkworm metabolism, which in turn may result in an increase in silk yield. [Copyright &y& Elsevier]
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- 2012
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