X-ray induced L02 cells damage rescued by new anti-oxidant NADH.
OBJECTIVE
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.


CONCLUSIONS
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.
Liu
Fa-Quan
FQ
Department of Oncology, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, Guangdong Province, China. liufaquan@163.net
Zhang
Ji-Ren
JR
D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D022781:Hepatocytes / Q000187:drug effects* / Q000502:physiology / Q000528:radiation effects*; D006801:Humans; D009243:NAD / Q000494:pharmacology*
D000975:Antioxidants; D009243:NAD