Basic Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 15, 2003; 9(8): 1781-1785
Published online Aug 15, 2003. doi: 10.3748/wjg.v9.i8.1781
X-ray induced L02 cells damage rescued by new anti-oxidant NADH
Fa-Quan Liu, Ji-Ren Zhang
Fa-Quan Liu, Ji-Ren Zhang, Department of Oncology, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, Guangdong Province, China
Author contributions: All authors contributed equally to the work.
Supported by Healthcare Research Fundation of the Tenth Five-Year Plan of PLA, No, 01MA138
Correspondence to: Fa-Quan Liu, Department of Oncology, Zhujiang Hospital,First Military Medical University, Guangzhou, 510282, China.
Telephone: +86-20-85143202 Fax: +86-20-85143200
Received: August 6, 2002
Revised: August 15, 2002
Accepted: October 18, 2002
Published online: August 15, 2003

AIM: To explore molecular mechanism of nicotinamide adenine dinucleotide (NADH) antagonization against X-ray induced L02 cells damage.

METHODS: L02 liver cells were cultured in RPMI 1640, exposed to X-ray irradiation and continued to culture in the presence or absence of NADH. Cellular viability was analyzed by routine MTT methods. The percent age of apoptotic cells and positive expressions of p53, bax and bcl-2, fas, fasL proteins were determined by FCM. Level of intracellular ROS was determined by confocal microscope scanning. Morphological change was detected by scanning electron micrograph.

RESULTS: The viability of L02 cells was decreased with increasing dose of X-ray irradiation. NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P < 0.05). At the same time, NADH could reduce level of intracellular ROS in radiated L02 cells.

CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS. However, further investigation of its mechanism is worthwhile.

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