α-Tocopherol incorporation in mitochondria and microsomes upon supranutritional vitamin E supplementation

Abstract

Vitamin E (a-tocopherol) is a major lipid-soluble chain-breaking antioxidant in humans and mammals and plays an important role in normal development and physiology. The localization of a-tocopherol within the highly unsaturated phospholipid bilayer of cell membranes provides a means of controlling lipid oxidation at the initiation site. Mitochondria are the site for major oxidative processes and are important in fat oxidation and energy production, but a side effect is leakage of reactive oxygen species. Thus, incorporation of a-tocopherol and other antioxidants into mitochondria and other cellular compartments is important in order to maintain oxidative stability of the membranebound lipids and prevent damage from the reactive oxygen species. Many studies regarding mitochondrial disease and dysfunction have been performed in relation to deficiency of vitamin E and other antioxidants, whereas relatively sparse information is available regarding the eventual beneficial effects of antioxidant-enriched mitochondria in terms of health and function. This may be due to the fact that only little scientific information is available concerning the effect of supranutritional supplementation with antioxidants on their incorporation into mitochondria and other cellular membranes. The purpose of this review is therefore to briefly summarize experimental data performed with dietary vitamin E treatments in relation to the deposition of a-tocopherol in mitochondria and microsomes.

Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review

“…Such studies showed that increased vitamin E concentration seems to be able to protect livestock muscle from oxidation [45][46][47]. In addition, vitamin E preferentially incorporates into the plasma membrane and the membranes of microsomes and mitochondria [44]. Although the mechanism of vitamin E delivery to cellular organelles has not been defined, its preferential distribution to mitochondria concurs with the observation of the existence of a cytosolic binding protein able to transfer the vitamin from liposomes to mitochondria [40].…”

“…Few data exist on the effect of in vivo vitamin E supplementation in mitochondria. Some information is available on the changes in mitochondrial vitamin E levels from studies on skeletal muscle of livestock, performed to improve food muscle resistance to lipid oxidation [44]. Such studies showed that increased vitamin E concentration seems to be able to protect livestock muscle from oxidation [45][46][47].…”

The Effect of LDL-Apheresis and Rheohaemapheresis Treatment on Vitamin E

“…A study by Rajasekaran et al proposed that the regulation of a-tocopherol levels in membranes is critically important to maintain the erythrocyte membrane structure and function (42). Recently, it has been hypothesized that a-tocopherol partitions into domains of membranes that are rich in polyunsaturated phospholipids, amplifying the concentration of the vitamin where it is most needed (43). The presented results indicated that vitamin E in erythrocytes did not change after LDL-apheresis and showed only a slight increase (although it was significant) after rheohaemapheresis.…”

Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

“…The main antioxidant enzymes include thioredoxin 2 (TRX2), thioredoxin reductase (TXNRD2), the glutaredoxins 2 (GLRX2) and 5 (GLRX5), the peroxiredoxins 3 (PRDX3) and 5 (PRDX5), GSH peroxidase 1 (GPX1), oxidized glutathione (GSSG) reductase (GSR), and the copper/zinc (SOD1)-and manganese (SOD2)-containing SODs (Kalinina et al, 2008). The major non-enzymatic antioxidants are GSH, coenzyme A (CoA-SH; for more details, see The Redox Metabolism of PeroxisomesAntioxidant Systems), ubiquinol (Maroz et al, 2009), vitamin C, andvitamin E (Sagun et al, 2005;Marí et al, 2009;Lauridsen and Jensen, 2012). Vitamin E, a fat-soluble nutrient, is present in relatively low concentrations in mitochondria, and its main function is to trap LOO • , thereby preventing the propagation of lipid peroxidation (Forkink et al, 2010).…”