FIG. 5.

The mitochondrial H₂O₂ and GSH systems experience larger changes in OxD in CA3 than in CA1 when the Trx system is inhibited by AF. The tissue is pretreated with or without 1 μM AF 1 h before imaging. Tissue is superfused with ASCF in basal condition for ∼8 min, then with 10 μM MD +20 μM MnSOD_m for 15 min. (A) H₂O₂ is consumed by the GSH and Trx systems via several redox enzymes, Gpx, Prx, and Orp. roGFP2-Orp1, the H₂O₂ probe used here, has the subunit Orp (underlined in A), which is reduced by Trx. AF inhibits the Trx system by irreversibly inhibiting TrxR. (B) AF causes an increase in OxD_P in CA1 (left) and in CA3 (right). The change in OxD_P is greater in CA3 than in CA1. (C) AF affects OxD_G slightly in CA1, whereas in CA3, the effect is noticeable. In (B, C), each trace is represented as mean ± SEM (n = 6 OHSCs). ΔOxD is the difference between the steady-state (the last 5 min of MD+MnSOD_m) values of OxD (AF) and OxD (no AF). See Figure 1 legend for indicators of statistical significance. AF, auranofin; Gpx, glutathione peroxidase; Orp, oxidant receptor protein; TrxR, thioredoxin reductase; Prx, peroxiredoxin.