Sid Ahmed-Adrar, N., Collin, F., Couturier, M., Vitrac, H., Bonnefont-Rousselot, D., Jore, D. and Gardès-Albert, M. Radiolytic Yield of Cardiolipin Peroxidation by Gamma Rays in Large Unilamellar Vesicles of Phosphatidylcholine. Radiat. Res. 171, 622–630 (2009).
Large unilamellar vesicles of 1-hexanoyl-2-(9Z-12Z-octadecadienoyl)-sn-glycero-3-phosphocholine (PLPC) have been used as model membrane to investigate the effect of increasing amount of cardiolipin (1′,3′-bis-[1,2-Di-(9Z-12Z-octadecadienoyl)-sn-glycero-3-phospho]-sn-glycerol, CL) on the peroxidizability of the lipid phase. Hydroxyl radicals generated by gamma radiolysis of water initiated the lipid peroxidation. Both peroxidation products (conjugated dienes and hydroperoxides of PLPC, mono- and dihydroperoxides of CL) and disappearance of CL and PLPC were assessed as a function of the radiation dose (25 to 400 Gy, I = 10 Gy min−1). Our results show that the addition of 5% to 15% CL to large unilamellar vesicles (concentration ratio) produces almost complete inhibition of PLPC peroxidation. Thus, for 15% CL (known to be the proportion of CL in the inner mitochondrial membrane), the radiolytic yield of formation of PLPC hydroperoxides is reduced to zero, whereas it is equal to (3.1 ± 0.2) × 10−7 mol J−1 for CL hydroperoxides, showing the importance of the targeted CL. For this concentration ratio (CL/ PLPC 15%), we have established the balance equation between the consumption of CL [G(–CL) = (2.8 ± 0.1) × 10−7 mol J−1] and the formation of CL hydroperoxides [G(CLOOHT) = (3.1 ± 0.2) × 10−7 mol J−1]. In addition, the radiolytic yields of disappearance of PLPC and CL have been determined [(1.5 ± 0.1) × 10−7 mol J−1 and (2.8 ± 0.1) × 10−7 mol J−1, respectively], their sum [(4.3 ± 0.2) × 10−7 mol J−1] being higher than GHO· (2.8 × 10−7 mol J−1). However, there is no balance between the radiolytic yield of formation of PLPC hydroperoxides [G (PCOOHT) ∼ 0] and the yield of disappearance of PLPC [(1.5 ± 0.1) × 10−7 mol J−1], likely because lipid fragments (not measured in this work) could be generated from HO· reaction on the polar head of PLPC. These results have been interpreted by assuming that the hydroxyl radicals attack in competition both lipid targets, i.e. PLPC and CL, with a higher sensitivity to CL oxidation. It can be concluded that a little amount of CL (10–15% CL/ PLPC concentration ratio) may exert a strong protective effect against the HO·-induced peroxidation of PLPC.