RESUMO
Radiation therapy is routinely used in the management of primary central nervous system malignancies. However, the efficacy of this therapeutic modality is limited by the occurrence of resistance. In the present study, we investigated whether modulation of oxidative stress might underlie glioma cell radioresistance. Superoxide dismutase activity in irradiated M059J cells was two-fold higher than that in untreated controls, but did not significantly change in U-87 and U-138 cells. This is accompanied by an increase in reactive oxygen species content and decreases in cells viability. Pharmacological or genetic modulation of oxidative stress could be associated with an enhancement in the susceptibility of tumor cells to radiation therapy.
Assuntos
Neoplasias Encefálicas/enzimologia , Glioma/enzimologia , Estresse Oxidativo , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Animais , Catalase/metabolismo , Sobrevivência Celular , Radicais Livres/metabolismo , Raios gama , Expressão Gênica , Tolerância a Radiação , Ratos , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Transfecção , Células Tumorais Cultivadas/efeitos da radiaçãoRESUMO
According to the free radical theory of aging, biological senescence processes develop from a general failure to maintain organism's homeostasis, probably due to oxidative stress. The brain is particularly susceptible to oxidative damage, and astrocytes are chiefly responsible for its antioxidant defense. Here we evaluated and compared the enzymatic antioxidant activities, mitochondrial superoxide production, and oxidative damage in biomolecule in cortex astrocytes from newborn Wistar rats maintained for 10-13 or 40-47 days in culture. We show that, besides an increase in antioxidant enzyme activities in matured astrocyte cultures, there was an increase in lipoperoxidation and in protein oxidation, probably due to an increase in mitochondrial electron transport chain superoxide production. This could indicate that the increasing in defense mechanisms was not sufficient to avoid oxidative biomolecule damage during maturation.