Global transcriptomic profiling of ischemic/reperfusion injury in an in vivo Gpx1 -/- transgenic mouse model.

Glutathione peroxidase (Gpx) is a selenium-containing enzyme that catalyses the reduction of a variety of biological peroxides at the expense of reduced glutathione (GSH). Gpx1 is the most abundant isoform and its role has been implicated in neurodegenerative disorders such as Parkinsons disease (PD), dementia with Lewy bodies tissue (DLB) (Power and Blumbergs, 2009) and traumatic brain injury (Tsuru-Aoyagi et al., 2009). Due to its high abundance, mutation of the Gpx1 allele would lower overall Gpx activity in the brain significantly. Gpx1 knockout (Gpx1-/-) mice do not show overt phenotypic differences, but all indications suggest that these mice are in a chronic pro-oxidant state (Cheng et al. 1999; de Haan et al. 2004). Indeed, a recent study from our laboratory illustrated that the absence of Gpx1 exacerbated stroke injury via increased ROS production and vascular permeability (Wong et al. 2008). Furthermore, Gpx1-/- mice demonstrated an increase in caspase-3 activation and greater infarct volume (Crack et al. 2001)

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