Figure 2.

Rates of H₂O₂ production by isolated muscle mitochondria of NMRs and mice. The two respiration‐dependent pathways for the matrix consumption of H₂O₂ (see Figure 1) were inhibited by CDNB pre‐treatment and auranofin. (a, c, and e) assays for both species at the normal body temperature of the naked mole‐rat (NMR; 30°C) and the mouse (37°C). (b, d, and f), results are limited to assaying each mitochondrial preparation at each species’ normal body temperature. Data are normalized to mg of mitochondrial protein (a and b), to the activity of the citrate synthase measured at the same temperature (c and d), or as the % of electrons leaking from the electron transfer system toward the formation of H₂O₂ (e and f). M: malate; G: glutamate; Rot: rotenone; S: succinate. Significant differences between species were assessed using t tests, with *p < 0.05, **p < 0.01, and ***p < 0.001. For mouse, n = 4 for M and MG, n = 9 for MGS and MGS + ADP, and n = 7 for all conditions with succinate. For NMR, n = 6 for all conditions except at 37°C (n = 2). Data are mean ± SEM, except for NMR at 37°C where bars represent range