Tiancheng Wang

Peking University Third Hospital, Peping, Beijing, China

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Publications (16)60.71 Total impact

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    ABSTRACT: Graphene oxide (GO) shows great promise in in vivo drug delivery and therapy applications. However, several reports have reported an in vivo toxicity of GO. In this study, we found that the toxicity of GO intravenously injected into mice could be tuned by dose, size and exposure protocols of GO. The exposure to a single dose of 2.1 mg kg−1 (single-high-dose exposure) small size GO or large size GO caused macrophage nodule formation in the lungs of the mice, and the exposure to seven repeated doses of 0.3 mg kg−1 (multiple-low-dose exposure) large size GO also induced small macrophage nodule formation, serious lymphocyte infiltration around the bronchioles in the lungs of the mice, and even death of the mice. Nephritic inflammatory reactions were also observed after the multiple-low-dose exposure to large size GO. However, no obvious lung toxicity but hepatic inflammatory infiltration was observed after the exposure to multiple-low-dose small size GO. GO accumulation in the macrophage nodules was verified by Raman mapping. These findings will benefit the applications of GO in the future, especially in biomedical fields.
    Toxicol. Res. 08/2014;
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    ABSTRACT: To understand the regulation of genetic damage by epigenetics at the early stage of carcinogenesis after hexavalent chromium [Cr(VI)] exposure, we profiled plasma miRNA expression in workers exposed to Cr(VI), and assessed genetic damage to explore their association with DNA repair genes mediated by differently expressed miRNA. Genetic damages were evaluated using cytokinesis-block micronucleus assay (CBMN) and serum 8-hydroxyguanine (8-OHdG) ELISA assay. Blood Cr level showed significant association with plasma miR-3940-5p level (r=-0.33, P=0.001) and non-linear relationship with micronuclei frequency in CBMN and serum 8-OHdG level (βstd=0.29, P=0.039; βstd=0.35, P=0.001), with micronuclei frequency not increasing apparently under high Cr exposure. In contrast, no significant association was found between plasma miR-3940-5p level and the two genetic indicators. However, plasma miR-3940-5p level was linked to micronuclei frequency under high blood Cr level (βstd=0.18, P=0.015). To explore the effect of miR-3940-5p on genetic damage under high Cr exposure, the protein expression levels of miR-3940-5p-mediated DNA repair genes in leukocytes were quantified using enzyme-linked immunosorbent assay for subjects with high blood Cr level. The results showed that XRCC2 and BRCC3 protein levels were statistically associated with miR-3940-5p level respectively (βstd=-0.31, P=0.010; βstd=-0.24, P=0.037). Meanwhile, a weak but statistically negative association between XRCC2 level and micronuclei frequency was found (βstd=-0.15, P=0.027). These data suggests that high Cr(VI) does not always aggravate genetic damage after reaching a high Cr(VI) exposure in real situation, which may be due to the regulation of miRNA on DNA repair genes responsive to high Cr(VI) exposure.
    Toxicology Letters 06/2014; · 3.15 Impact Factor
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    ABSTRACT: The role of chromate exposure in the deregulation of total lymphocyte and other immune factors is largely unclear. We aimed to examine alteration of the Th1/Th2/Th17 cytokine profile and humoral indicators caused by occupational chromate exposure. A cross-sectional study was conducted in two similar workshops (groups 1 and 2) with 106 male occupational workers and 50 matched local controls. Environmental and biological exposures were assessed by measuring chromium concentrations in workplace air, and in whole blood and urine samples of the workers. Cytokines in serum (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17A) were determined by CBA assay, while immunoglobin (IgA, IgM, IgG, IgE) and complement (C3, C4) were evaluated by immunonephelometric and ELISA methods. Micronucleus analysis was also used to explore the relationship between genotoxicity and immunotoxicity. Compared with the control group, environmental chromate exposure in groups 1 and 2 was much higher, and the mean values of IL-6, IL-10, IFN-γ, IL-17A and IFN-γ/IL-4 were significantly decreased in group 1. In group 2, IgA and IgG levels were reduced, while C3 and C4 were increased. Levels of IFN-γ, IgG and IgA were all inversely associated with whole blood chromium, while C3 and C4 were positively associated with whole blood chromium (p<0.05). Both IL-10 and IL-17A were inversely associated with urine chromium. Correlations were also found between IL-10, IL-17A and micronucleus (r=-0.329, r=-0.312, respectively). Occupational exposure to chromate could downregulate the cellular and humoral factors of the immune system.
    Occupational and environmental medicine 06/2013; · 3.64 Impact Factor
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    ABSTRACT: Alumina nanoparticles (NPs) are among the most important nanomaterials and are widely used in diverse areas. In this study, we evaluated the bioavailability and toxicity of alumina NPs in mice after oral exposure, compared with traditional alumina powder. Our results indicated that negligible alumina NPs were absorbed post-exposure and alumina NPs did not influence the balance of essential trace elements, including Fe, Cu and Zn. Preliminary toxicological evaluations suggested that alumina NPs were of low toxicity. The body weights were similar among the mice exposed to alumina NPs, alumina powder and 0.9% NaCl aqueous solution. The low toxicity was also indicated by the unchanged serum biochemical parameters. The implications related to the ongoing safety evaluations and applications of alumina NPs are discussed.
    Toxicol. Res. 07/2012; 1(1):69-74.
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    ABSTRACT: One hundred chromate production workers chronically exposed to low-level of hexavalent chromium [Cr(vi)] and eighty healthy individuals free from Cr exposure were recruited to the study. Personal sampling of airborne Cr was conducted and Cr content was quantified by Flame Atomic Absorption Spectrometry (FAAS). At the end of the sampling shift, blood samples were collected and element concentrations were measured by inductively coupled plasma mass spectrometry (ICP-MS) for Cr, Cd, Cu, Mo and Se and inductively coupled plasma atomic emission spectrometry (ICP-AES) for Ca, Fe, Mg and Zn. According to our results, 90% of the chromate production workers were exposed to airborne Cr in a concentration lower than 50 μg m(-3), which is the threshold limit value recommended by the American Conference of Governmental Industrial Hygienists and Chinese Ministry of Health. After Cr(vi) exposure, a significant increase in blood Cr, Cd, Fe, Mg, Mo, Se and Zn concentrations was observed, as well as a significant decrease in Ca concentration. A decrease in blood Cu was only observed among female workers. Blood Cr concentrations of the exposed workers (median = 15.68 ng mL(-1)) was four times higher than that of the controls (median = 3.03 ng mL(-1)), and significantly correlated with airborne Cr (r = 0.568, P<0.001). In addition, the inter-element correlations exhibited significant differences between the two groups. Our findings of the related health effects suggested that the underlying mechanisms of chronic Cr(vi) exposure on blood element homeostasis might be partly explained by oxidative stress in the body, dysfunction of Fe metabolism and renal injury.
    Metallomics 04/2012; 4(5):463-72. · 4.10 Impact Factor
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    ABSTRACT: To determine the nephritic toxicity of chromate after chronic occupational exposure. The environmental contamination was assessed by measuring the chromium (Cr) in 8-h airborne sampler. The integrated level of Cr was determined by Cr concentrations in the whole blood (WB-Cr) and the urine (U-Cr). The renal glomerular and tubule impairment was evaluated by determination of cystatin C (Cys-C) in the serum and microalbumin (mALB), urinary beta(2)-microglobulin (β(2)M), N-acetyl-beta-D-glucosaminidase (NAG) activity in the urine. The mean occupational exposure time to Cr was 12.86 years with average daily air level of 27.13 μg/m(3) comparing to 0.11 μg/m(3) of the background level. The WB-Cr and U-Cr were 23.49 μg/L and 17.41 μg/g creatinine (Cre), respectively in the chromate-exposed workers comparing to 3.32 μg/L and 1.52 μg/g Cre in the controls. The serum Cys-C and urinary mALB were significantly increased in the chromate-exposed workers. Exposure to Cr seems to induce an enhanced level of urinary NAG activity and β(2)M concentration. The increased serum Cys-C concentration was positively correlated with the level of serum Cre. The U-Cr was positively correlated to the concentrations of urinary mALB, β(2)M, and the activity of NAG. Chronic occupational exposure to chromate causes comprehensive renal impairment though more severity could occur in the tubule than in the glomerular.
    International Archives of Occupational and Environmental Health 04/2011; 84(4):393-401. · 2.10 Impact Factor
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    ABSTRACT: Because of the possible health threat of nanodiamonds (NDs) to organisms, the pulmonary toxicity and translocation of NDs in different sizes in mice were investigated after intratracheal instillation administration. Biochemical assays, ultrastructural and histopathological evaluations of the lungs of the control and the ND exposed mice were carried out at 1, 7, 14 or 28 days post-exposure. Exposure to 1.0 mg/kg NDs with an average diameter of 4 nm produced a temporary lung index increase at 1 day post-exposure. NDs did not have evident adverse effects in the lungs within the studied period according to histopathological and ultrastructural investigations. Furthermore, no lipid peroxidation of the lung was observed. On the whole, intratracheally instilled NDs are of low pulmonary toxicity. In addition, the amount of NDs in alveolar decreased with time elapsed and the macrophages burdened with NDs were clearly observed in the bronchia from 1 day to 28 days post-exposure. Thus we affirm the critical role of alveolar macrophages in the main excretion pathway of NDs from the lungs, i.e. they engulf the NDs, migrate upward to the trachea by escalator/mucociliary system and finally enter the pharynx.
    Diamond and Related Materials 01/2010; · 1.71 Impact Factor
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    ABSTRACT: The purpose of this study is to evaluate the overall toxicity of nasal instilled nanoscale copper particles (23.5 nm) in mice. Pathological examination, target organs identification, and blood biochemical assay of experimental mice were carried out in comparison with micro-sized copper particles (17 microm). However, only in the high-dose group of copper nanoparticles (40 mg/kg body weight instilled for three times in one week), the body weight of mice were retarded and significant pathological changes were observed. There were hydropic degeneration around the central vein and the spotty necrosis of hepatocytes in the liver and swelling in the renal glomerulus, while, severe lesion associated with the decreased number of olfactory cells and the dilapidated laminated structure were also observed in the olfactory bulb. The serum biochemical assay also indicated the sign of renal and hepatic lesion. However, there were no obvious pathological and physiological damages in the mice after instilling different-sized copper nanoparticles with low dose of 1 mg/kg body weight. The retention and distribution of copper in various tissues show that the liver, kidneys and olfactory bulb are the main accumulated tissues for copper particles, which were determined by high sensitive element-specific technique of ICP-MS. The copper contents of the liver, kidneys and the olfactory bulb increase significantly at the group of 40 mg/kg compared to the control group, which is in agreement with the histological changes. Therefore, the data indicate that nasal inhaled copper particles at very high dosage can translocate to other organs and tissues and further induce certain lesions. The present results are helpful to get better understanding of the risk assessment and evaluation for copper nanoparticles.
    Journal of Nanoscience and Nanotechnology 11/2009; 9(11):6335-43. · 1.15 Impact Factor
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    ABSTRACT: Epidemiologic studies have revealed that pollution by ambient particulates is associated with respiratory and cardiovascular diseases, particularly in older people. Toxicologic sensitivity of nanoparticles in different ages was investigated for the first time to demonstrate and explain an age-related difference in response to manufactured nanoparticles. Young, adult, and old rats physiologically inhaled air containing aerosol of manufactured SiO2 nanoparticles (24.1 mg/m3; 40 min/day) for four weeks. Changes in serum biomarkers, hemorheologic, pulmonary inflammation, heart injury, and pathology in rats of different ages and their corresponding controls were compared. Inhalation of SiO2 nanoparticles under identical conditions caused pulmonary and cardiovascular alterations in old rats, yet less change in young and adult rats, including pulmonary inflammation, myocardial ischemic damage, atrio-ventricular blockage, and increase in fibrinogen concentration and blood viscosity. Old individuals were more sensitive to nanoparticle exposure than the young and adult rats. The risk of causing pulmonary damages was: old > young > adult The risk of cardiovascular disorder was observed only in old age. Our results suggest that different ages may require different biomarkers for identifying pulmonary toxicity during inhalation of nanoparticles.
    Environmental Science and Technology 12/2008; 42(23):8985-92. · 5.26 Impact Factor
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    ABSTRACT: The biomedical application of single-walled carbon nanotubes (SWCNTs), such as drug delivery and cancer treatment, requires a clear understanding of their fate and toxicological profile after intravenous administration. In this study, the long-term accumulation and toxicity of intravenously injected SWCNTs in the main organs (such as liver, lung and spleen) in mice were carefully studied. Although SWCNTs stayed in mice over 3 months, they showed low toxicity to mice. The long-term accumulation of SWCNTs in the main organs was evidenced by using Raman spectroscopy and TEM technique. Statistically significant changes in organ indices and serum biochemical parameters (LDH, ALT and AST) were observed. The histological observations demonstrate that slight inflammation and inflammatory cell infiltration occurred in lung, but the serum immunological indicators (CH 50 level and TNF-alpha level) remained unchanged. No apoptosis was induced in the main organs. The decreasing glutathione (GSH) level and increasing malondialdehyde (MDA) level suggest that the toxicity of SWCNTs might be due to the oxidative stress.
    Toxicology Letters 09/2008; 181(3):182-9. · 3.15 Impact Factor
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    ABSTRACT: The tumor-inhibitory effect of C60(OH)x was tested on the murine H22 hepatocarcinoma model. Doses of 0.2 and 1.0 mg kg(-1) body weight both showed significant antitumor activity with tumor inhibition rates of 31.9 and 38.4%, respectively, when mice were treated for 17 consecutive days. The damnification of liver was prominently reduced. Furthermore, histological examination indicated that an envelope of fibroblasts and lymphocytes was formed surrounding tumor tissues in the C60(OH)x-treated group, which inhibited the infiltration of tumor to the neighboring normal skeleton muscle tissues. To understand the antitumor mechanism, the immunomodulatory activity of C60(OH)x was investigated. The results indicate that C60(OH)x enhances the phagocytosis of peritoneal macrophages and elevates the activity of arginase and acid phosphatase in vivo. The tumor necrosis factor alpha production of C60(OH)x-treated macrophages also increases in vitro. These results suggest that C60(OH)x can enhance the innate immunity of tumor-bearing mice, and therefore inhibits growth of the tumor.
    Small 07/2008; 4(8):1168-75. · 7.82 Impact Factor
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    ABSTRACT: In order to evaluate the toxicity of TiO(2) particles, the acute toxicity of nano-sized TiO(2) particles (25 and 80nm) on adult mice was investigated compared with fine TiO(2) particles (155nm). Due to the low toxicity, a fixed large dose of 5g/kg body weight of TiO(2) suspensions was administrated by a single oral gavage according to the OECD procedure. In 2 weeks, TiO(2) particles showed no obvious acute toxicity. However, the female mice showed high coefficients of liver in the nano-sized (25 and 80nm) groups. The changes of serum biochemical parameters (ALT/AST, LDH) and pathology (hydropic degeneration around the central vein and the spotty necrosis of hepatocytes) of liver indicated that the hepatic injury was induced after exposure to mass different-sized TiO(2) particles. In addition, the nephrotoxicity like increased BUN level and pathology change of kidneys was also observed in the experimental groups. The significant change of serum LDH and alpha-HBDH in 25 and 80nm groups showed the myocardial damage compared with the control group. However, there are no abnormal pathology changes in the heart, lung, testicle (ovary), and spleen tissues. Biodistribution experiment showed that TiO(2) mainly retained in the liver, spleen, kidneys, and lung tissues, which indicated that TiO(2) particles could be transported to other tissues and organs after uptake by gastrointestinal tract.
    Toxicology Letters 02/2007; 168(2):176-85. · 3.15 Impact Factor
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    ABSTRACT: To assess the toxicity of copper nanoparticles (23.5 nm) in vivo, LD(50), morphological changes, pathological examinations and blood biochemical indexes of experimental mice are studied comparatively with micro-copper particles (17 microm) and cupric ions (CuCl(2).2H(2)O). The LD(50) for the nano-, micro-copper particles and cupric ions exposed to mice via oral gavage are 413, >5000 and 110 mg/kg body weight, respectively. The toxicity classes of nano and ionic copper particles both are class 3 (moderately toxic), and micro-copper is class 5 (practically non-toxic) of Hodge and Sterner Scale. Kidney, liver and spleen are found to be target organs of nano-copper particles. Nanoparticles induce gravely toxicological effects and heavy injuries on kidney, liver and spleen of experimental mice, but micro-copper particles do not, on mass basis. Results indicate a gender dependent feature of nanotoxicity. Several factors such as huge specific surface area, ultrahigh reactivity, exceeding consumption of H(+), etc. that likely cause the grave nanotoxicity observed in vivo are discussed.
    Toxicology Letters 05/2006; 163(2):109-20. · 3.15 Impact Factor
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    ABSTRACT: [Gd@C82(OH)22]n particles (22 nm in a saline solution) of a dose level as low as 10(-7) mol/kg exhibit a very high antineoplastic efficiency ( approximately 60%) in mice. A dose increment of 1 x 10(-7) mol/kg increases the tumor inhibition rate 26%. [Gd@C82(OH)22]n particles have a strong capacity to improve immunity and interfere with tumor invasion in normal muscle cells, nearly without toxicity in vivo and in vitro. Unlike conventional antineoplastic chemicals, the high antitumor efficiency of nanoparticles is not due to toxic effects to cells because they do not kill the tumor cells directly and only about 0.05% of the used dose is found in the tumor tissues. Results suggest that fullerene derivatives with proper surface modifications and sizes may help realize the dream of tumor chemotherapeutics of high-efficacy and low-toxicity.
    Nano Letters 11/2005; 5(10):2050-7. · 13.03 Impact Factor
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    ABSTRACT: Mercury is a ubiquitous and highly toxic environmental pollutant. In this study, we evaluated the relationship between mercury exposure and oxidative stress, serum and urinary mercury concentrations, oxidative DNA damage, and serum redox status in chronically mercury-exposed persons compared with healthy controls. We measured urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), which we used as a biomarker of oxidative DNA damage in the mercury-exposed persons, by HPLC with electrochemical detection (ECD). We evaluated antioxidant status by measuring the activities of superoxide dismutase and glutathione peroxidase and the concentrations of total reduced glutathione and protein-bound thiols in serum. The significant increase in 8-OHdG concentrations in urine indicated that mercury-induced oxidative damage to DNA occurred in vivo. Differences in body mercury burden and antioxidant enzyme activities were statistically significant between the mercury-exposed persons and controls. Serum and urinary mercury concentrations in the mercury-exposed persons were more than 40-fold higher than in controls. Mercury exposure can induce oxidative DNA damage, whereas the antioxidative repair systems can be expected to minimize DNA lesions caused by mercury. Measurement of urinary 8-OHdG could be useful for evaluating in vivo oxidative DNA damage in mercury-exposed populations.
    Clinical Chemistry 05/2005; 51(4):759-67. · 7.15 Impact Factor
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    ABSTRACT: In this work, the acute oral toxicity of 20- and 120-nm ZnO powder at doses of 1-, 2-, 3-, 4-, 5-g/kg body weight was evaluated referred to the OECD guidelines for testing of chemicals. As the results, both 20- and 120-nm ZnO belong to non-toxic chemicals according to the Globally Harmonized Classification System (GHS) for the classification of chemicals. The distribution determination showed that Zn was mainly retained in the bone, kidney and pancreas after 20- and 120-nm ZnO administration. However, the results of blood measurement suggest that the increase in blood viscosity could be induced by low and median dose of 20-nm ZnO but high dose of 120-nm ZnO. The pathological examination showed that the 120-nm ZnO treated mice had dose–effect pathological damages in stomach, liver, heart and spleen, whereas, 20-nm ZnO displayed negative dose–effect damages in liver, spleen and pancreas. Therefore, we conclude that the liver, spleen, heart, pancreas and bone are the target organs for 20- and 120-nm ZnO oral exposure. More attention should be paid on the potential toxicity induced by low dose of 20-nm ZnO oral exposure.
    Journal of Nanoparticle Research 10(2):263-276. · 2.18 Impact Factor

Publication Stats

723 Citations
60.71 Total Impact Points

Institutions

  • 2006–2014
    • Peking University Third Hospital
      Peping, Beijing, China
  • 2012–2013
    • Peking University
      • • Department of Occupational and Environmental Health Sciences
      • • School of Public Health
      Beijing, Beijing Shi, China