Literature DB >> 23786587

Molecular hydrogen protects human lymphocyte AHH-1 cells against 12C6+ heavy ion radiation.

Yanyong Yang1, Fu Gao, Hong Zhang, Yijuan Hunag, Pei Zhang, Cong Liu, Bailong Li, Jianming Cai.   

Abstract

PURPOSE: To investigate the potential protective role of molecular hydrogen (H(2)) against (12)C(6+) heavy ion radiation, which is a major hazard for space travel and has been also widely used in heavy ion radiotherapy.
MATERIALS AND METHODS: H(2) was dissolved in Roswell Park Memorial Institute (RPMI) 1640 medium under high pressure (0.4 Mpa) to a saturated level by using an apparatus produced by our department. A 2-[6-(4'-hydroxy) phenoxy-3H-xanthen-3-on-9-yl] benzoate (HPF) probe and a 2',7'-Dichlorodihydrofluorescein diacetate (H2DCFH-DA) fluorescent dye were used to measure the intracellular reactive oxygen species (ROS) level. Cell apoptosis were determined by double-staining with Annexin V-fluorescein isothiocyanate (Annexin V-FITC) and propidium iodide (PI) as well as a Hoechst 33342 staining method alternatively. Subsequently, cell cycle analysis was performed using a PI staining method and the expression of apoptotic protein was examined by Western blot.
RESULTS: In this study, we demonstrated H(2) reduced ROS level in Human lymphocyte AHH-1 cells as well as in the radiolysis of water. Our data also showed H(2) attenuated (12)C(6+) radiation- induced cell apoptosis and also alleviated radiation-induced G2/M cell cycle arrest. Heavy ion radiation-induced Caspase 3 activation was also inhibited by H(2) treatment.
CONCLUSION: In conclusion, these data showed that H(2) attenuated (12)C(6+) radiation-induced cell apoptosis through reducing the ROS level and modulating apoptotic molecules, thus indicating the potential of H(2) as a safe and effective radioprotectant.

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Year:  2013        PMID: 23786587     DOI: 10.3109/09553002.2013.817704

Source DB:  PubMed          Journal:  Int J Radiat Biol        ISSN: 0955-3002            Impact factor:   2.694


  11 in total

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10.  Monophosphoryl lipid a attenuates radiation injury through TLR4 activation.

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