Astrocytosis is a sequential morphological change of astrocytic reaction to tissue damage, and is associated with regulation of
antioxidant defense mechanisms to reduce oxidative damage. The repair
enzymes to oxidative DNA damage, oxidized
purine-nucleoside triphosphatase (hMTH1) and a mitochondrial type of
8-oxoguanine DNA glycosylase (hOGG1-2a) in
brain tumors and neurons of
Alzheimer's disease, were previously reported. In the present study, glial expression of these repair
enzymes under such pathological conditions as
cerebrovascular diseases and metastatic
brain tumors, were investigated. Furthermore, an in-vitro experiment using a
glioma cell-line under oxidative stress was performed to verify the immunohistochemical results of post-mortem materials. As a result, hOGG1-2a immunoreactivities in reactive astrocytes were more intense than those to hMTH1. Oligodendrocytes of acute or subacute stage of
brain infarction were strongly immunoreactive to both repair
enzymes. In-vitro study revealed that, hOGG1-2a is constitutively expressed in both untreated
glioma cells and the
glioma cells under oxidative stress. However, although no immunoreactivity to hMTH1 was found in the control cells, accumulation of hMTH1 was rapidly induced by oxidative stress. These results indicate that the two repair
enzymes to oxidative DNA damage are differentially regulated in glial cells, and that there is a difference in the expression of the repair
enzymes between reactive astrocytes and oligodendrocytes.