β-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability

Rong Li Chun, Zhe Zhou, Xin Lin Ru, Dan Zhu, Ning Sun Yu, Lin Tian Lin, Lu Li, Yue Gao, Qi Wang Sheng

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

Both radiation injury and oxidation toxicity occur when cells are exposed to ion irradiation (IR), ultimately leading to apoptosis. This study was designed to determine the effect of β-sitosterol (BSS) on early cellular damage in irradiated thymocytes and a possible mechanism of effect on irradiation-mediated activation of the apoptotic pathways. Thymocytes were irradiated (6 Gy) with or without BSS. Cell apoptosis and apoptosis-related proteins were evaluated. BSS decreased irradiation-induced cell death and nuclear DNA strand break while attenuating intracellular reactive oxygen species (ROS) and increasing the activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). BSS decreased the release of cytochrome c from mitochondria to the cytosol and the mitochondrio-nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, BSS partially inhibited the radiation-induced increase of cleaved caspase 3 and cleaved PARP, and attenuated the activation of JNK and AP-1. In addition, evidence suggests that ROS generated by irradiation are involved in this course of cell damage. The results indicate that BSS confers a radioprotective effect on thymocytes by regulation of the intracellular redox balance which is carried out via the scavenging of ROS and maintenance of mitochondrial membrane stability.

Original languageEnglish
Pages (from-to)748-758
Number of pages11
JournalJournal of cellular biochemistry
Volume102
Issue number3
DOIs
StatePublished - Oct 15 2007

Keywords

  • Apoptosis
  • Irradiation
  • Radioprotection
  • Reactive oxygen species
  • Signal pathway
  • β-sitosterol

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