Ying Han

Capital Medical University, Peping, Beijing, China

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Publications (6)10.07 Total impact

  • Toxicology Letters 08/2013; 221:S244. DOI:10.1016/j.toxlet.2013.05.602 · 3.26 Impact Factor
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    ABSTRACT: Toxicity due to overexposure to manganese (Mn) is becoming increasingly prevalent. Mn-induced neurodegenerative toxicity has been demonstrated, but little is known concerning the adverse effects of the element on the liver. Under physiological conditions, manganese primarily exists as divalent manganese (Mn(2+)) and trivalent manganese (Mn(3+)). The present study was designed to evaluate and compare the effects of Mn(2+) and Mn(3+) on oxidative hepatic damage, membrane fluidity and histopathological changes in rats. Rats exposed to Mn(2+) or Mn(3+) (2.0mg Mn/kg body weight) showed significant inhibition of superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity, as well as decreased levels of glutathione (GSH) and increased levels of malondialdehyde (MDA) in liver tissues. We also showed a significant inhibition of SOD activity and increased MDA levels in hepatocyte nuclei. We also observed reduced Na(+),K(+)-ATPase activity, increased MDA levels and decreased plasma membrane fluidity, which was accompanied by an increase of fluorescence anisotropy (r) values, in hepatic plasma membranes. In addition, Mn(2+) and Mn(3+) both caused histopathological changes, such as mononuclear cell infiltration, congestion, enlargement of the veins and sinusoids, hepatocellular damage, necrotic changes, mitochondrial hyperplasia, swelling and vacuolization, as determined by light and electron microscopy. Taken together, these data suggest that both Mn(2+) and Mn(3+) inhibit the normal physiological functioning of the liver. Under the experimental conditions used, the adverse effects of Mn(2+) were more severe than those of Mn(3+).
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 03/2012; 64(3):197-203. DOI:10.1016/j.etp.2010.08.006 · 1.86 Impact Factor
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    ABSTRACT: To investigate the effects of CdTe QDs (cadmium telluride quantum dots) on oxidative stress and DNA damage of liver cells in mice. Thirty ICR male mice were randomly divided into 5 groups: one negative control (normal saline) group. Three CdTe QDs groups (exposed by intravenous injection of 0.2 ml of CdTe QDs at the concentration of 3.75, 37.5 and 375 nmol/ml respectively) for electron paramagnetic resonance (EPR) test, and another positive control group (exposed by intravenous injection of 0.2 ml of cyclophosphamide 20 mg/ml) for single cell gel electrophoresis (SCGE) test. All mice were decapitated 24h after the injection, free radicals and DNA damage of liver cells were detected by EPR and SCGE. The levels of oxygen free radicals detected by EPR were increased with the increase of CdTe QDs. The tail length, olive tail moment, tail DNA (%) and the ratio of tail/head examined by SCGE were also increased with the increase of the dosage of CdTe QDs (P < 0.01). CdTe QDs could induce oxidative stress and DNA damage of liver cells in mice with a dose-effect relationship.
    Wei sheng yan jiu = Journal of hygiene research 01/2012; 41(1):31-4, 39.
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    ABSTRACT: Water-soluble quantum dots (QDs) have shown potential as tumor diagnostic agents. However, little is known about their biological behaviors in vivo. Male ICR mice were intravenously given a single dose (2.5μmolkg−1 body weight) of water-soluble cadmium–telluride (CdTe) QDs (the QDs are approximately 4nm in diameter and have maximal emission at 630nm). Inductively coupled plasma mass spectrometry (ICP-MS) was used for measuring the kinetic action of 111Cd and 125Te for 7days. The plasma kinetics of Cd and Te followed a two-compartment model, in which Cd exhibited greater apparent volume of distribution, greater clearance, faster distribution half-life, and significantly slower elimination half-life compared to Te. Contrary to its relatively transient fate in the plasma, high levels of Cd persisted in the liver and kidneys. Te accumulated primarily in the spleen. The different plasma kinetics and distribution patterns of Cd and Te imply that CdTe QDs have been part of the degradation or aggregation in vivo. KeywordsQuantum dot–Kinetics–Biodistribution–ICP-MS–Mice–Health effects–Nanomedicine
    Journal of Nanoparticle Research 10/2011; 13(10):5373-5380. DOI:10.1007/s11051-011-0523-8 · 2.18 Impact Factor
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    ABSTRACT: Manganese (Mn) toxicity is most often found in mining and welding industry workers. Accumulation of manganese in the brain can result in a syndrome similar to that of Parkinson's disease. Observations on former Mn-alloy workers suggested that residual effects could last for years after exposure. The objective of this study was to assess effects of Mn in the liver of rats following subacute or subchronic exposure and after recovery. Male Sprague-Dawley rats were exposed to manganese chloride (MnCl(2)) for 30 days, 90 days, or for 90 days followed by a 30-day post-exposure recovery period. Results showed that MnCl(2) exposure resulted in liver injury in rats and the extent of injury correlated positively with exposure time. The effect in mitochondria was stronger than in the membrane or nucleus. Most of the changes in these biomarkers recovered when manganese exposure ceased.
    Ecotoxicology and Environmental Safety 05/2011; 74(4):615-22. DOI:10.1016/j.ecoenv.2010.08.011 · 2.76 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the contents of lanthanum (La), cerium (Ce), and neodymium (Nd) that accumulate in nuclei and mitochondria isolated from the liver and their corresponding potential oxidative damage effects on nuclei and mitochondria. Five-week-old male imprinting control region (ICR) mice were exposed to chlorides of La, Ce, or Nd by oral gavage with one of three doses: 10, 20, or 40 mg/kgBW/day for 6 weeks. The concentrations of administered elements in hepatocyte nuclei and mitochondria were determined with inductively coupled plasma-mass (ICP-MS) spectrometry. The accumulation of La, Ce, and Nd in hepatocyte nuclei and mitochondria gradually increased in a dose-dependent manner with exposure to the elements, although the concentrations of La, Ce, and Nd in hepatocyte mitochondria were lower than those in their counterpart nuclei. In hepatocyte nuclei, superoxide dismutase (SOD) and catalase (CAT) activities decreased, whereas glutathione peroxidase (GPx) activity, glutathione (GSH) and malondialdehyde (MDA) levels increased. In hepatocyte mitochondria, SOD, CAT, and GPx activities and GSH levels were significantly decreased, and MDA levels were significantly increased. These results suggest that La, Ce, and Nd presumably enter hepatocytes and mainly accumulate in the nuclei and induce oxidative damage in hepatic nuclei and mitochondria.
    01/2011; 31(1):25-32. DOI:10.1016/j.etap.2010.09.001