Hyperoxia changes the balance of the thioredoxin/peroxiredoxin system in the neonatal rat brain

Reactive oxygen species (ROS) and intrinsic antioxidant defense systems play an important role in both physiological cell signaling processes and many pathological states, including neurodegenerative disorders and oxygen-toxicity.Here we report that short exposures to non-physiologic oxygen levels change the balance of the ROS-dependent thioredoxin/peroxiredoxin system in the developing rat brain. The aim of this study was to evaluate the expression of peroxiredoxins, thioredoxin 1, sulfiredoxin 1, and DJ-1 on gene and protein level under hyperoxic conditions. Six-days old Wistar rats were exposed to 80% oxygen for 6–48 h while sex-matched littermates were kept in room-air and served as controls. Oxygen-toxicity significantly induced upregulation of peroxiredoxins 1 and 2, peroxiredoxin sulfonic form, thioredoxin 1, and sulfiredoxin 1 in the brains of infant rats. Additionally, hyperoxia reduced the level of DJ-1, a hydroperoxide-responsive protein in the developing rat brain.The pathology of hyperoxia-mediated injury to the developing brain is still elusive and oxygen administration to neonates is often inevitable. These findings may provide evidence for the development of targeted therapeutic strategies to enhance the antioxidative defense of the immature brain.

► High oxygen levels change the balance of the Trx/Prx system in the immature rat brain.
► Oxygen-toxicity induces upregulation of peroxiredoxins, thioredoxin and sulfiredoxin.
► Hyperoxia reduces the level of DJ-1 in the developing rat brain.
► Our results might lead to therapeutically alterations of cellular resistance to hyperoxia.