p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain
Table 2
Bioenergetic parameters of isolated brain mitochondria of wild-type and p66Shc(−/−) aged mice.
Control (WT 3 mo)
WT 24 mo
p66Shc(−/−) 24 mo
A. Oxygen consumption rate
1. Malate + glutamate
State 3 (ng at O/min/mg protein)
102 ± 3.6
74 ± 2.4a
125 ± 4.6b
Respiratory control (RC)
4.3 ± 0.2
3.3 ± 0.1a
4.4 ± 0.2
2. Succinate
State 3 (ng at O/min/mg protein)
116 ± 4.4
84 ± 3.5a
109 ± 5a
Respiratory control (RC)
4.1 ± 0.1
3.1 ± 0.1a
5 ± 0.1a
B. Respiratory chain complex activity
1. Complex I (nmol/min/mg protein)
78.4 ± 4.7
37.5 ± 3.1a
51.8 ± 5.2b
2. Complex II–III (nmol/min/mg protein)
98.2 ± 9.1
51.1 ± 6.7a
48.4 ± 4.1a
3. Complex IV (/min/mg protein)
23 ± 0.75
19.1 ± 0.45a
15.8 ± 1b
C. ATP synthesis rate (nmol/min/mg protein)
125 ± 1
42 ± 3a
81 ± 2b
D. NAD+/NADH+H ratio
5.3 ± 0.7
1.2 ± 0.4a
2.7 ± 0.5b
E. Mitochondrial potential, ∆Ψ (AFU)
601 ± 15
414 ± 25a
520 ± 16b
Note: data are expressed as the of the different groups (). Results were contrasted in pairs between the 3-month-old WT control group and the two aged groups (a) as well as between both the 24-month old WT and p66Shc(−/−) groups (b). a and b represent , one-way analysis of variance (ANOVA) and Bonferroni post hoc test. AFU: arbitrary fluorescence units.