Vitamin E and thyroid disease: a potential link that kindles hope.

Abstract

Vitamin E was discovered in 1922 and is the best known lipid-soluble antioxidant [1]. Natural vitamin E represents a complex of 8 tocopherol and tocotrienol isomers of which α-tocopherol (atoc) is predominant in most species and significantly more potent than any other naturally occurring tocopherol [2]. Vitamin E is considered the prototype of phenolic based chain-breaking antioxidants, its primary role consisting in preventing free radical initiated lipid peroxidation damage and thus in protecting the integrity of tissues [3]. Vitamin E is mainly distributed in adipose tissue and in the subcellular membrane fractions, the intracellular transport and release of α-tocopherol into the plasma involves via a Golgi-dependent pathway a specific protein, the α-tocopherol transfer protein [4]. Oxidative stress is defined as the overproduction of oxygen free radicals (OFR) that can no longer be compensated by the antioxidant defence system [5]. Oxidative stress appears to play a pivotal role in various diseases such as atherosclerosis, cancer and Alzheimer’s and is associated with diminution of antioxidant molecules. α-tocopherol decreases, in a specific and concentration dependent way, the proliferation of vascular smooth cells by interacting with the protein kinase C (PKC) [6]. The interaction with the cytosolic PKC results in inhibition of its membrane translocation and activation [7]. The PKC specific activity is diminished due to dephosphorylation following the activation of protein phosphatase 2A1 activity by α-tocopherol at a cellular level [8]. Thus, the diminution of a-toc in smooth muscle cells may consequently augment the PKC activity and lead to an increase in cell proliferation also by a non-antioxidant mechanism [8].