Autoxidation and antioxidant activity of ubiquinol homologues in large unilamellar vesicles

Cipollone, Marta; Fiorentini, Diana; Galli, Maria Cristina; Sechi, A. M.; Landi, Laura

doi:10.1016/0009-3084(94)90030-2

Cited by 14 publications

(8 citation statements)

References 29 publications

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“…Liposome Preparation and Fluorescence Assay. Liposomes were prepared by an adaptation of previously reported protocols (Cipollone et al, 1994;Frei et al, 1990). An aliquot of a PC stock solution (125 mM in chloroform) was mixed with 2 mL of methanol and Q 6 H 2 (0.3-144 µM), when present, and dried by rotary evaporation.…”

Section: Methodsmentioning

confidence: 99%

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Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

et al. 1996

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Ubiquinone (Q) is an essential, lipid soluble, redox component of the mitochondrial respiratory chain. Much evidence suggests that ubiquinol (QH 2 ) functions as an effective antioxidant in a number of membrane and biological systems by preventing peroxidative damage to lipids. It has been proposed that superoxide dismutase (SOD) may protect QH 2 from autoxidation by acting either directly as a superoxide-semiquinone oxidoreductase or indirectly by scavenging superoxide. In this study, such an interaction between QH 2 and SOD was tested by monitoring the fluorescence of cis-parinaric acid (cPN) incorporated phosphatidylcholine (PC) liposomes. Q 6 H 2 was found to prevent both fluorescence decay and generation of lipid peroxides (LOOH) when peroxidation was initiated by the lipid-soluble azo initiator DAMP, dimethyl 2,2′-azobis (2-methylpropionate), while Q 6 or SOD alone had no inhibitory effect. Addition of either SOD or catalase to Q 6 H 2 -containing liposomes had little effect on the rate of peroxidation even when incubated in 100% O 2 . Hence, the autoxidation of QH 2 is a competing reaction that reduces the effectiveness of QH 2 as an antioxidant and was not slowed by either SOD or catalase. The in ViVo interaction of SOD and QH 2 was also tested by employing yeast mutant strains harboring deletions in either CuZnSOD and/or MnSOD. The sod mutant yeast strains contained the same percent Q 6 H 2 per cell as wild-type cells. These results indicate that the autoxidation of QH 2 is independent of SOD.

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Section: Methodsmentioning

confidence: 99%

“…Q 6 was reduced for the liposome experiments as described by Cipollone et al (1994). A 5 mg sample of Q 6 in 2.5 mL of ethanol was combined with 15 mL of a solution of 0.1 M phosphate, pH 7.4, 0.2 M sucrose, and 0.2 g of sodium dithionite, and the mixture was vortexed for 1 min.…”

Section: Methodsmentioning

confidence: 99%

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

et al. 1996

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“…Amounts of Q 6 H 2 and Q 6 were determined directly from the ECD results by comparison to external standards. Q 6 was reduced with dithionite and stored in acidic-ethanol [5,24]. Values represent an average of three separate experiments, and each experiment was analyzed in triplicate.…”

Section: Measurement Of Qmentioning

confidence: 99%

Characterization of Saccharomyces cerevisiae ubiquinone‐deficient mutants

Schultz

Clarke

1999

BioFactors

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Ubiquinol (QH2) is a lipid-soluble molecule that participates in cellular redox reactions. Previous studies have shown that yeast mutants lacking QH2 are hypersensitive to treatment with polyunsaturated fatty acids (PUFAs) indicating that QH2 can function as an antioxidant in vivo. In this study the effect of 1 mM linolenic acid on levels of Q6 and Q6H2 is assessed in both wild-type and respiration-deficient (atp2 delta) strains. The response of Q-deficient mutants to other forms of oxidative stress is further characterized to define those conditions where QH2 acts as an antioxidant. Endogenous antioxidant defense systems were also assessed in wild-type, Q-deficient, and atp2 delta strains. Superoxide dismutase (SOD) activity decreased and catalase activity increased in both Q-deficient and atp2 delta mutants compared to wild-type cells, suggesting that such changes result from the loss of respiration rather than the lack of Q.

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“…As shown in Figure 3 , the lipid peroxidation was initiated by an azo initiator, based on approaches described in [ 18 , 76 , 77 ], similarly as in our previous study [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

“…To avoid protein-due effects, we initiated the oxidation of CL by an azo initiator 2,2′-azobis(4-methoxy-2,4-dimethylvaleronitrile), or MeO-AMVN [ 18 ]. The formation of primary oxidation products, conjugated dienes (see Figure 1 ), was followed, in real time, by measuring their accumulation at 234 nm [ 18 , 76 , 77 ]. The high efficiency of the hydrophobic initiator MeO-AMVN at low temperatures [ 18 ] allowed us to use low amounts of the initiator, which decreased the possible influence of the initiator on the structure of the liposomes.…”

Section: Introductionmentioning

confidence: 99%

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

Lokhmatikov

Voskoboynikova

Cherepanov

et al. 2016

Oxidative Medicine and Cellular Longevity

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Molecules of mitochondrial cardiolipin (CL) get selectively oxidized upon oxidative stress, which triggers the intrinsic apoptotic pathway. In a chemical model most closely resembling the mitochondrial membrane—liposomes of pure bovine heart CL—we compared ubiquinol-10, ubiquinol-6, and alpha-tocopherol, the most widespread naturally occurring antioxidants, with man-made, quinol-based amphiphilic antioxidants. Lipid peroxidation was induced by addition of an azo initiator in the absence and presence of diverse antioxidants, respectively. The kinetics of CL oxidation was monitored via formation of conjugated dienes at 234 nm. We found that natural ubiquinols and ubiquinol-based amphiphilic antioxidants were equally efficient in protecting CL liposomes from peroxidation; the chromanol-based antioxidants, including alpha-tocopherol, were 2-3 times less efficient. Amphiphilic antioxidants, but not natural ubiquinols and alpha-tocopherol, were able, additionally, to protect the CL bilayer from oxidation by acting from the water phase. We suggest that the previously reported therapeutic efficiency of mitochondrially targeted amphiphilic antioxidants is owing to their ability to protect those CL molecules that are inaccessible to natural hydrophobic antioxidants, being trapped within respiratory supercomplexes. The high susceptibility of such occluded CL molecules to oxidation may have prompted their recruitment as apoptotic signaling molecules by nature.

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Autoxidation and antioxidant activity of ubiquinol homologues in large unilamellar vesicles

Cited by 14 publications

References 29 publications

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

Characterization of Saccharomyces cerevisiae ubiquinone‐deficient mutants

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

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