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Astrocytes are more resistant than cerebral endothelial cells toward geno- and cytotoxicity mediated by short-term oxidative stress.
Bresgen, N; Jaksch, H; Bauer, HC; Eckl, P; Krizbai, I; Tempfer, H;
J Neurosci Res. 2006; 84(8):1821-1828
Originalarbeiten (Zeitschrift)


Bauer Hans Christian
Jaksch-Bogensperger Heidi
Tempfer Herbert


Evidence is accumulating that capillary endothelial cells (cEC) and astrocytes play a pivotal role in neuroprotection, in particular with respect to counteract oxidative injury. Furthermore, differences among both cell types in response to oxidative stress have been shown and astrocytes seem to be more tolerant in terms of cytotoxicity, however, no reports exist on oxidative stress mediated genotoxicity in astrocytes. We investigated genotoxic and cytotoxic effects of oxidative stress in astrocytes and cECs induced by hypoxia/reoxygenation or by the redox cycling quinone DMNQ. Additionally, the dependence of these effects on glucose availabilty was also studied. On exposure to Hy/Re or 10 muM DMNQ for 24 hr, the frequency of micronucleated and apoptotic cells was significantly increasing, however, astrocytes proved to be more resistant to apoptosis induction, in particular on use of DMNQ. In astrocytes, the low background rates of necrotic cells were not affected and a significant necrosis induction was only detectable in cECs exposed to DMNQ for 24 hr. Short-term exposure to DMNQ (1 hr) had no effect in astrocytes but exerted significant geno- and cytotoxicity in cECs. Increasing the glucose concentration markedly reduced oxidative stress mediated geno- and cytotoxicity in astrocytes. Surprisingly, glucose deprivation (aglycemia) suppressed DMNQ induced micronucleus formation in astrocytes without affecting the frequency of apoptotic cells. Our results indicate that astrocytes are more resistant to oxidative stress than cECs, in particular regarding the potential to counteract genotoxicity as well as apoptosis induction mediated by a short term oxidative insult.

Useful keywords (using NLM MeSH Indexing)

Analysis of Variance


Animals, Newborn

Apoptosis/drug effects


Astrocytes/drug effects


Cell Death/drug effects

Cell Death/physiology

Cells, Cultured

Cerebral Cortex/cytology*

Endothelial Cells/drug effects

Endothelial Cells/physiology*





Oxidative Stress/drug effects

Oxidative Stress/physiology*

Time Factors

Find related publications in this database (Keywords)

oxidative stress