p66^Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain

Table 1

Oxidative parameters in isolated brain mitochondria of wild-type and p66^Shc(−/−) aged mice.

	Control (WT 3 mo)	WT 24 mo	p66^Shc(−/−) 24 mo
A. H2O2 production rate (nmoles/min/mg prot)
1. Malate + glutamate	1.66 ± 0.05	2.22 ± 0.1^a	0.97 ± 0.03^b
2. Succinate	1.08 ± 0.05	1.35 ± 0.09^a	0.8 ± 0.1^b
B. Superoxide anion level (AFU)	101 ± 8	194 ± 4.5^a	140 ± 14^b
C. ROS level (AFU)	76 ± 3	111 ± 8^a	82 ± 4^a
D. SOD activity (pmoles/min/mg prot)	2824 ± 309	2305 ± 153^a	2468 ± 94^a
E. Catalase activity (units/mg prot)	32 ± 5	29 ± 4	27 ± 3

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 the 24-month-old WT and p66^Shc(−/−) groups (b). a and b represent , one-way analysis of variance (ANOVA) and Bonferroni post hoc test.