Relations Between Tocopherol Depletion and Coenzyme Q During Lipid Peroxidation in rat Liver Mitochondria

Abstract

In order to evaluate different mitochondrial antioxidant systems, the depletion of alpha-tocopherol and the levels of the reduced and oxidized forms of CoQ were measured in rat liver mitochondria during Fe++/ascorbate and NADPH/ADP/Fe++ induced lipid peroxidation. During the induction phase of malondialdehyde formation, alpha-tocopherol declined moderately to about 80% of initial contents, whereas the total CoQ pool remained nearly unchanged, but reduced CoQ9 continuously declined. At the start of massive malondialdehyde formation, CoQ9 reaches its fully oxidized state. At the same time alpha-tocopherol starts to decline steeply, but never becomes fully exhausted in both experimental systems. Evidently the oxidation of the CoQ9 pool constitutes a prerequisite for the onset of massive lipid peroxidation in mitochondria and for the subsequent depletion of alpha-tocopherol. Trapping of the GSH by addition of dinitrochlorbenzene (a substrate of the GSH transferase), results in a moderate acceleration of lipid peroxidation, but alpha-tocopherol and ubiquinol levels remained unchanged when compared with the controls. Addition of succinate to GSH depleted mitochondria effectively suppressed MDA formation as well as alpha-tocopherol and ubiquinol depletion. The data support the assumption that the protective effect of respiratory substrates against lipid peroxidation in the absence of mitochondrial GSH is mediated by the regeneration of the lipid soluble antioxidants CoQ and alpha-tocopherol.

Coenzyme Q 10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects

“…Coenzyme Q also serves as an important antioxidant in both mitochondria and lipid membranes (4,5). Coenzyme Q, which also is known as ubiquinone, is a lipid-soluble compound composed of a redox active quinoid moiety and a hydrophobic ''tail.''…”

Thirteen-Week Repeated Dose Oral Toxicity Study of Coenzyme Q10 in Rats

“…CoQ 10 was also found to be an important antioxidant, which protects cell and mitochondria membranes against oxidization and regenerates α-tocopherol (Noack et al, 1994;Nohl et al, 1999;Mukai et al, 1990). A number of preclinical and clinical reports on the antioxidant effect of CoQ 10 following oral supplementation were published, including reports on the prevention of LDL peroxidation (Mohr et al, 1992), administration to a patient with cardiovascular disease (Singh et al, 2003), hypertension (Rosenfeldt et al, 2007), angina pectoris (Singh et al, 1998), and neurodegenerative disorders (Parkinson's disease and Huntington's disease) (Young et al, 2007).…”

Protective Role of .ALPHA.-Tocopherol Acetate against Thioacetamide-Induced Mitochondrial Dysfunction.

“…Dietary supplementation of vitamin E prior to thioacetamide treatment prevented the toxicity induced by thioacetamide and lessened the reduction in values of all the mitochondrial parameters studied. The induction of lipid peroxidation in vitro in rat liver mitochondria by Fee /ascorbate and NADPH/ADP/Fe2+ caused an 80% decrease in a-tocopherol concentrations accompanied by an increase in lipid peroxide levels [34]. Thomas et al [35] showed that vitamin E deficiency led to reduced stability of mitochondrial membranes and decreased the rate of oxygen utilization with both NADH-and FADH2-linked substrates.…”