SENSITIVITY OF CEREBELLAR GLUTATHIONE SYSTEM TO NEONATAL IONIZING RADIATION EXPOSURE

C.G. DI TORO; P.A. DI TORO; L.M. ZIEHER; L.R. GUELMAN

NEUROTOXICOLOGY

Elsevier

Año: 2007 vol. 28 p. 555 - 561

0161-813X

Reactive oxygen species (ROS) are relevant components of living organisms that, besides their role in the regulation of different importantphysiological functions, when present in excess are capable to affect cell oxidative status, leading to damage of cellular molecules and disturbanceof normal cell function.ROS accumulation has been associated with a variety of conditions such as neurodegenerative diseases and ionizing radiation exposure. Cellability to counteract ROS overproduction depends on the capacity of the endogenous antioxidant defenses – which includes the glutathione (GSH)system – to cope with.Since developing central nervous system (CNS) is especially sensitive to ROS-induced damage, the aim of the present work was to evaluateROS, reduced GSH and oxidized glutathione (GSSG) levels in the cerebellum at different developmental ages after irradiation, in order to test ifany changes were induced on these key oxidative stress-related cellular markers that might explain the high cerebellar vulnerability to radiationinducedinjury. Since intracellular levels of GSH are maintained by glutathione reductase (GSHr), this enzymatic activity was also evaluated.Newborn Wistar rats were irradiated in their cephalic ends and the different parameters were measured, from 1 h to 90 days post-irradiation.Results showed that an early transient increase in ROS levels followed by a decrease in cerebellar weight at 3–5 days post-irradiation wereinduced. An increase in cerebellar GSH levels was induced at 30 days after irradiation, together with a decrease in GSHr activity.These results support the hypothesis that ROS may represent a marker of damage prior to radiation-induced cell death. In contrast, it would besuggested that GSH system might play a role in the compensatory mechanisms triggered to counteract radiation-induced cerebellar damage.