[Changes of thioredoxin mRNA level in neurons with mitochondrial dysfunction insulted by H2O2]

Oxidative stress and mitochondrial deficiency have been considered to be associated with the mechanisms of many neurodegenerative diseases. Sodium azide (NaN3) is a special inhibitor of mitochondrion cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. In this experiment, the neurotoxic effects of H2O2 on primary cultured neurons and NaN3-induced mitochondrial dysfunctional neurons were detected by means of cell viability measurement (MTT) and analyzed through morphological observation. Furthermore, the changes of thioredoxin mRNA level in both normal and abnormal cultured neurons insulted by H2O2 were analyzed by semiquantitative RT-PCR in order to explore the role of Trx, an important redox regulatory protein, in modulating the process of neuronal injury. It was found that mitochondrial dysfunctional neurons could be damaged by H2O2 in a dose- and time-dependent manner and the expression of Trx decreased during certain dose (0-200 mumol/L) and time (0-4 h) of H2O2 treatment. But in normal neurons the effects of H2O2 treatment seemed to be less evident. It suggests that in neurons with mitochondrial dysfunction, the redox modulation of thioredox seems to be more prominent.