Oxidative Medicine and Cellular Longevity / 2018 / Article / Tab 2

Research Article

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 mop66Shc(−/−) 24 mo

A. Oxygen consumption rate
 1. Malate + glutamate
  State 3 (ng at O/min/mg protein)102 ± 3.674 ± 2.4a125 ± 4.6b
  Respiratory control (RC)4.3 ± 0.23.3 ± 0.1a4.4 ± 0.2
 2. Succinate
  State 3 (ng at O/min/mg protein)116 ± 4.484 ± 3.5a109 ± 5a
  Respiratory control (RC)4.1 ± 0.13.1 ± 0.1a5 ± 0.1a
B. Respiratory chain complex activity
 1. Complex I (nmol/min/mg protein)78.4 ± 4.737.5 ± 3.1a51.8 ± 5.2b
 2. Complex II–III (nmol/min/mg protein)98.2 ± 9.151.1 ± 6.7a48.4 ± 4.1a
 3. Complex IV (/min/mg protein)23 ± 0.7519.1 ± 0.45a15.8 ± 1b
C. ATP synthesis rate (nmol/min/mg protein)125 ± 142 ± 3a81 ± 2b
D. NAD+/NADH+H ratio5.3 ± 0.71.2 ± 0.4a2.7 ± 0.5b
E. Mitochondrial potential, ∆Ψ (AFU)601 ± 15414 ± 25a520 ± 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.