Brain protein oxidation: what does it reflect?

Abstract

Antioxidant neuroprotection: Since the elaboration of the concept of oxidative stress in the 1980s, the idea that this phenomenon may be particularly involved in diseases of the brain has become widely accepted (Halliwell, 2006). Embedded in the framework of neuroprotection, the investigation of antioxidant strategies was fuelled by the repeated observation of redox dysregulation and outright oxidative damage on the molecular scale in many chronic and acute conditions involving neuronal dysfunction (Moosmann and Behl, 2002). In fact, different approaches of pharmacological antioxidant neuroprotection worked surprisingly well in animal studies; however, they have so far refused to work, almost without exception, in the clinic. The failure of NXY-059 in 2007, which was the latest candidate in a series of substances tested for ischemic stroke, was a disturbing setback in this respect (Shuaib et al., 2007). The very obvious discrepancy between success rates in mice, rats and humans had not been anticipated, as many drugs based neuronal receptor pharmacology had found their ready translation from animal studies into the clinic. What might have been the specific causes of failure when it comes to antioxidant neuroprotection?