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β‐sitosterol decreases irradiation‐induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability
Author(s) -
Li Chun Rong,
Zhou Zhe,
Lin Ru Xin,
Zhu Dan,
Sun Yu Ning,
Tian Lin Lin,
Li Lu,
Gao Yue,
Wang Sheng Qi
Publication year - 2007
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21326
Subject(s) - apoptosis , intracellular , reactive oxygen species , superoxide dismutase , cytochrome c , catalase , microbiology and biotechnology , cytosol , mitochondrion , dna damage , programmed cell death , chemistry , cell damage , biochemistry , antioxidant , biology , enzyme , dna
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 breaks 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. J. Cell. Biochem. 102: 748–758, 2007. © 2007 Wiley‐Liss, Inc.