Impact of Antioxidants on Cardiolipin Oxidation in Liposomes: Why Mitochondrial Cardiolipin Serves as an Apoptotic Signal?

Table 1

Relative efficiencies of various antioxidants in CL liposomes (note the split -axis). The values for oxidation rates were obtained from the data in Figures 6, 7, and 10 and analogous repetitive experiments as described in Section 2. The chain propagation length for pure CL and each antioxidant was calculated using the radical production rate of 11.8 nM/min, as derived from the α-tocopherol run; see Section 4. The inhibition efficiencies were calculated as ratios of the respective uninhibited and inhibited oxidation rates. The inhibition duration rates were determined from the data in Figures 5–7 and 10.

Antioxidant	CL oxidation rate, nM/min	Chain propagation length	Inhibition efficiency	Inhibition duration (min)
Pure CL	334 ± 32	28	—	—
decPQH2	3.28 ± 1.1	0.28	102	48.7 ± 2.1
SkQ1H2	3.87 ± 0.6	0.33	86	58.7 ± 5.7
decUQH2	4.49 ± 1.2	0.38	74	114 ± 4.4
MitoQH2	6.70 ± 2.0	0.57	50	91 ± 8.9
Q6H2	4.05 ± 0.5	0.34	82	124 ± 9
Q10H2	4.55 ± 0.4	0.39	73	104 ± 1
α-Tocopherol	10.6 ± 0.5	0.90	32	171 ± 1
HPMC	8.62 ± 1.8	0.73	39	N.A.

The duration of action varied dramatically in the case of HPMC because of its variable loss upon the incorporation into liposomes; see Section 4.