Dietary High Vanadium Causes Oxidative Damage-Induced Renal and Hepatic Toxicity in Broilers
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  • 作者:Juan Liu (1)
    Hengmin Cui (1)
    Xiaodong Liu (1)
    Xi Peng (1)
    Junliang Deng (1)
    Zhicai Zuo (1)
    Wei Cui (1)
    Yuanxin Deng (1)
    Kangping Wang (1)
  • 关键词:Dietary high vanadium ; Oxidative damage ; Vanadium toxicity ; Kidney ; Liver ; Broiler
  • 刊名:Biological Trace Element Research
  • 出版年:2012
  • 出版时间:February 2012
  • 年:2012
  • 卷:145
  • 期:2
  • 页码:189-200
  • 全文大小:3030KB
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  • 作者单位:Juan Liu (1)
    Hengmin Cui (1)
    Xiaodong Liu (1)
    Xi Peng (1)
    Junliang Deng (1)
    Zhicai Zuo (1)
    Wei Cui (1)
    Yuanxin Deng (1)
    Kangping Wang (1)

    1. Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Ya’an, Sichuan, 625014, China
文摘
The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet (vanadium 0.073?mg/kg), and five high vanadium diets (vanadium 5?mg/kg, high vanadium group I; 15?mg/kg, high vanadium group II; 30?mg/kg, high vanadium group III; 45?mg/kg, high vanadium group IV; and 60?mg/kg, high vanadium group V) throughout the experimental period of 42?days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30-0?mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.

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