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

beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability. Research Abstract Details 

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beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability. Abstract Text:

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

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 beta-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.

beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability. Publishing Authors By Initials

CR Li,Z Zhou,RX Lin,D Zhu,YN Sun,LL Tian,L Li,Y Gao,SQ Wang,CR Li,Z Zhou,RX Lin,D Zhu,YN Sun,LL Tian,L Li,Y Gao,SQ Wang,

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beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of cellular biochemistry

VOLUME: 102

Page Numbers: 748-58

Journal Abbreviation: J. Cell. Biochem.

ISSN: 0730-2312

DAY: 15

MONTH: Oct

YEAR: 2007

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

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LANGUAGE: eng

NlmUniqueID: 8205768

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Grant and Affiliation Information for beta-sitosterol decreases irradiation-induced thymocyte early damage by regulation of the intracellular redox balance and maintenance of mitochondrial membrane stability.

AFFILIATION: Department of Biotechnology, Beijing Institute of Radiation Medicine, Taiping Road 27#, Haidian district, Beijing 100850, People's Republic of China.

Country: United States

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MEDLINETA: J Cell Biochem

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