HMOX1 and Parkinson disease: The presence of redox imbalance in slices exposed to Rot is revealed by an altered GSH/GSSG ratio at 3 h (Figure 3A), well in agreement with similar models of PD) [31], and supported by the upregulation of Srxn1, belonging to the anti-oxidant response mechanism [24], and a trend toward increasing Hmox1, not only a redox sensor [32] and a transcription factor of the battery of anti-oxidant genes [24], but also the key enzyme in UCB production [10] (Figure 2A,B).