Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

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• 作者：Wang Suhua (1)
  Lu Rongzhu (1)
  Yin Changqing (2)
  Xing Guangwei (1)
  Han Fangan (3)
  Jing Junjie (4)
  Xu Wenrong (1)
  Michael Aschner (5)
  
• 关键词：Paradichlorobenzene ; Oxidative stress ; Trace elements ; Liver ; Kidney
• 刊名：Biological Trace Element Research
• 出版年：2010
• 出版时间：September 2010
• 年：2010
• 卷：136
• 期：3
• 页码：320-336
• 全文大小：233KB
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• 作者单位：Wang Suhua (1)
  Lu Rongzhu (1)
  Yin Changqing (2)
  Xing Guangwei (1)
  Han Fangan (3)
  Jing Junjie (4)
  Xu Wenrong (1)
  Michael Aschner (5)
  
  1. Department of Preventive Medicine, School of Medical Science and Laboratory Medicine, Jiangsu University, 301 Xuefu Rd, Zhenjiang, Jiangsu, 212013, China
  2. Zhenjiang Environmental Monitoring Center, Zhenjiang, Jiangsu, 212002, China
  3. Zhenjiang Center for Disease Control and Prevention, Zhenjiang, Jiangsu, 212003, China
  4. Center of Chemical Analysis, School of Chemistry and Chemical Engineering, Jiangsu University, Zhenjiang, Jiangsu, 212013, China
  5. Department of Pediatrics, Pharmacology and Center for Molecular Neuroscience, Vanderbilt University Medical Center, Nashville, TN, 37232, USA
  

文摘

Paradichlorobenzene (pDCB) has been used as a space deodorant and moth repellant, as well as an intermediate in the chemical industry. Given its broad applications and high volatility, considerable concern exists regarding the adverse health effects of pDCB in the home and the workplace. In this study, changes in lipid peroxidation, antioxidants, and trace element levels in the liver and kidney of pDCB-treated mice were investigated to determine their roles in toxicity. Mice were orally gavaged once daily for seven consecutive days with pDCB (0 (corn oil control), 450, and 900?mg/kg). The level of malondialdehyde (MDA), an end product of lipid peroxidation, markedly increased in the high-dose pDCB group in both the liver and kidney compared with the control group. Changes in hepatic levels of reduced glutathione (GSH) in the pDCB groups were indistinguishable from the control group, while renal levels of reduced GSH in the high-dose pDCB group were significantly lowered in comparison to the control and the low-dose groups. Superoxide dismutase (SOD) activity in the liver of mice treated with pDCB showed a downward trend, whereas there was no consistent trend associated with changes in SOD activity in the kidney. Additionally, renal iron levels in the high-dose pDCB group were significantly decreased compared with the low-dose group and the controls, whereas hepatic iron content in the low-dose pDCB group was significantly lower compared with the controls. Selenium and zinc levels in the kidney were both significantly decreased in the high-dose pDCB group vs. the control and low-dose groups. There were no treatment-induced changes in copper levels in either the kidney or liver. However, a significant increase was found in the liver zinc/copper ratio in the high-dose pDCB group vs. the controls. In addition, blood zinc levels showed a downward trend with increased pDCB dosage. These results suggest that pDCB toxicity is mediated by oxidative damage and tissue-specific alterations in trace element levels both in the liver and the kidney of mice.