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Mechanism of hepatocellular damage in rat caused by low serum selenium

  • Yi Lu
  • , Bo Qu
  • , Chang Liu
  • , Liang Yu
  • , Xuemin Liu
  • , Haohua Wang
  • , An Jiang
  • , Xiaogang Zhang
  • Xi'an Jiaotong University

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

The aim of this paper is to investigate the mechanism of hepatocellular damage in rats caused by low serum selenium. Thirty six rats were randomly divided into 2 groups: group A (fed with low-selenium diet from the Keshan Disease area with the content of selenium being 0.017 mg/kg); group B [fed with selenium-supplemented diet and 0.3 mg/L selenium (Na2SeO3) was added to the drinking water]. Both were respectively fed for 12 weeks. At the end of the 12th week, the levels of serum selenium, glutathione peroxidase (GPX) and malondialdehyde (MDA) in hepatic tissue were measured; the hepatocellular ultrastructure and apoptosis were observed as well. The levels of serum selenium and GPX in group A were markedly lower than those in group B. MDA level in group A was significantly higher than that in group B. Under the electron microscope (EM), the mitochondria were remarkably changed in group A. The rate of liver cell apoptosis appeared much higher in group A as well. It indicated that the damage caused by selenium deficiency was through the process of oxidation. Selenium deficiency led to apoptosis of hepatocytes where oxidative damage to mitochondria might be the cause.

Original languageEnglish
Pages (from-to)255-258
Number of pages4
JournalFrontiers of Medicine in China
Volume2
Issue number3
DOIs
StatePublished - 2008

Keywords

  • Apoptosis
  • Hepatocyte
  • Low-selenium
  • Mitochondria
  • Oxidative damage

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