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Huang P.,Capital Medical University | Li J.,Chinese Academy of Sciences | Zhang S.,Capital Medical University | Chen C.,Capital Medical University | And 9 more authors.
Environmental Toxicology and Pharmacology

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. © 2010 Elsevier B.V. Source

Huang P.,Capital Medical University | Chen C.,Capital Medical University | Chen C.,Niujie Community Health Service Center | Wang H.,Capital Medical University | And 12 more authors.
Ecotoxicology and Environmental Safety

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 (MnCl2) for 30 days, 90 days, or for 90 days followed by a 30-day post-exposure recovery period. Results showed that MnCl2 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. © 2010 Elsevier Inc. Source

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