Reactive oxygen species are continuously generated during oxidative metabolism and have to be efficiently detoxified in order to prevent oxidative damage. This process is especially important for the brain, since this organ consumes about 20% of the oxygen utilized by the human body. Brain astrocytes contribute to the antioxidative potential of the brain in multiple ways and provide antioxidative support to neurons. A key molecule for these processes is the antioxidative tripeptide glutathione (GSH). Astrocytes contain around 8 mM of GSH which enables these cells to efficiently detoxify peroxides and drugs via GSH peroxidase and GSH S-transferase reactions, respectively, thereby protecting neighboring neurons against oxidants and toxins (Hirrlinger & Dringen 2010). In addition, astrocytes provide precursors for neuronal GSH synthesis. This metabolic cooperation involves the release of GSH from astrocytes via multidrug resistance proteins and the extracellular cleavage of GSH by astroglial gamma-glutamyl transpeptidase and neuronal aminopeptidase (Hirrlinger & Dringen 2010). Drugs and toxins can modulate this astrocytic supply of GSH precursors, for example by lowering or accelerating GSH export from astrocytes (Tulpule & Dringen 2011; Brandmann et al 2012). Furthermore, astrocytes are considered as important regulators in the metabolism of the redox active metals iron and copper in brain and to protect neurons against the toxic potential of metal ions and metal-containing nanoparticles. Astrocytes efficiently accumulate large amounts of iron, copper and of metal-containing nanoparticles (Tulpule et al 2010; Geppert et al 2011; Scheiber et al 2012) and store metal ions in proteins such as ferritin and metallothioneins, thereby protecting other brain cells against metal toxicity. In addition, astrocytes are considered to supply neurons with trace elements such as iron and copper which are essential for neuronal metabolism. For example, copper export from primary astrocytes is mediated by the Menkes protein ATP7A and the cellular localization of this protein depends on the copper availability (Scheiber et al 2012). The contribution of astrocytes in multiple antioxidative and supportive pathways in brain suggests that compromised astrocytic functions will severely affect normal brain metabolism.