Wanderings in bioenergetics with Licio Azzone

Ernster, Lars

doi:10.1002/biof.5520080302

Cited by 2 publications

(5 citation statements)

References 26 publications

(27 reference statements)

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“…in mitochondrial and reconstituted liposomal membranes (34,35). Others, however, have reported that CoQ acts independently of a-TH in inhibiting lipid peroxidation (21,22,36).…”

Section: Discussionmentioning

confidence: 99%

“…Heart mitochondria, approximately 0.5 mg of mitochondrial protein/ml, were incubated at 37~ in a medium containing 25 mM Tris.HCI, pH 7.4, 150 mM KCI, 0.25 mM ascorbate and 1.0 mM ADP + 0.01 mM FeCI 3 to initiate the reaction (22). Assays were conducted over a time-course of 60 minutes and aliquots removed at intervals for the quantitation of thiobarbituric acid reactive products (TBARS) at 535 nm using an extinction value of 1.56 x 105.M-l.cm 1 (26).…”

Section: Lipid Peroxidation Assaymentioning

confidence: 99%

“…Equivocal results are particularly apparent when isolated mitochondrial preparations are used. A potential recycling of a-tocopherol (c(-TH) from the a-tocopheroxyl radical by the ubiquinones has also been the focus of recent research using liposomal and mitochondrial membrane systems (18)(19)(20)(21)(22)(23). Whereas interrelationships among antioxidants and antioxidant response to oxidant stress have been the focus of numerous studies with isolated liver mitochondria, relatively less has been reported for heart mitochondria.…”

Section: Introductionmentioning

confidence: 99%

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Effects of vitamin E and selenium on antioxidant defense in rat heart

1997

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Heart mitochondria, isolated from rats fed diets deficient or supplemented with vitamin E (E) and/or selenium (Se), were subjected to time-course assays of lipid peroxidation stimulated by ascorbate/ADP/Fe 3.. Mitochondria depleted of a-tocopherol (a-TH) peroxided rapidly as assessed by formation of thiobarbituric acid reactive substances (TBARS). Formation of TBARS was strongly inhibited in mitochondria from rats fed diets supplemented with E. Selenium deficiency, reduced glutathione (GSH), glutathione disulfide (GSSG) or GSH + GSSG did not affect the course of lipid peroxidation in mitochondda from rats supplemented or deficient in E. Combined E and Se deficiency resulted in significantly lower total (oxidized + reduced) mitochondrial coenzyme Q-9 (CoQ-9) concentration compared with control rats supplemented with dietary E and Se. Time-course changes in mitochonddal a-TH and total CoQ-9 during oxidizing conditions were minor in +E rats. Total CoQ-9 was reduced substantially, however, during the course of lipid peroxidation in mitochondria depleted of a-TH. Selenium-dependent glutathione peroxidase (Se-GSHPx) activity was reduced by approximately 96% in heart cytosol, and to a somewhat lesser extent in mitochondria, by dietary Se deficiency. Non-Se GSHPx activity was not detected in heart cytosol but was detected in very small amounts in heart mitochondria. Glutathione S-transferase activity of heart cytosol was decreased in E and/or Se deficiency. The results of these experiments indicate that membrane a-TH was most effective in inhibiting lipid peroxidation in heart mitochondria.

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“…in mitochondrial and reconstituted liposomal membranes (34,35). Others, however, have reported that CoQ acts independently of a-TH in inhibiting lipid peroxidation (21,22,36).…”

Section: Discussionmentioning

confidence: 99%

Section: Lipid Peroxidation Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of vitamin E and selenium on antioxidant defense in rat heart

1997

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“…Mitochondrial ubiquinone is a respiratory chain component buried within the lipid core of the inner membrane where it accepts two electrons from complexes I or II, becoming reduced to ubiquinol which then donates electrons to complex III 13. The ubiquinone pool in vivo is largely reduced, and ubiquinol is an effective antioxidant 14‐17. Ubiquinol acts as an antioxidant by donating a hydrogen atom from one of its hydroxyl groups to a lipid peroxyl radical, thereby decreasing lipid peroxidation within the mitochondrial inner membrane 17‐19.…”

Section: Introductionmentioning

confidence: 99%

“…The ubiquinone pool in vivo is largely reduced, and ubiquinol is an effective antioxidant 14‐17. Ubiquinol acts as an antioxidant by donating a hydrogen atom from one of its hydroxyl groups to a lipid peroxyl radical, thereby decreasing lipid peroxidation within the mitochondrial inner membrane 17‐19. The ubisemiquinone radicals thus formed disproportionate to ubiquinone and ubiquinol 16,19,20.…”

Section: Introductionmentioning

confidence: 99%

Prevention of Mitochondrial Oxidative Damage Using Targeted Antioxidants

Kelso

Porteous

Hughes

et al. 2002

Annals of the New York Academy of Sciences

121

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Mitochondrial-targeted antioxidants that selectively block mitochondrial oxidative damage and prevent some types of cell death have been developed. These antioxidants are ubiquinone and tocopherol derivatives and are targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation. Because of the large mitochondrial membrane potential, these cations accumulated within mitochondria inside cells, where the antioxidant moiety prevents lipid peroxidation and protects mitochondria from oxidative damage. The mitochondrially localized ubiquinone also protected mammalian cells from hydrogen peroxide-induced apoptosis while an untargeted ubiquinone analogue was ineffective against apoptosis. When fed to mice these compounds accumulated within the brain, heart, and liver; therefore, using these mitochondrial-targeted antioxidants may help investigations of the role of mitochondrial oxidative damage in animal models of aging.

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Wanderings in bioenergetics with Licio Azzone

Cited by 2 publications

References 26 publications

Effects of vitamin E and selenium on antioxidant defense in rat heart

Effects of vitamin E and selenium on antioxidant defense in rat heart

Prevention of Mitochondrial Oxidative Damage Using Targeted Antioxidants

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