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Unequivocal role of \u03b1T in the prevention of these deficits is confounded by possible neurotoxic oxidant products generated, <jats:italic>ex vivo<\/jats:italic> in \u03b1T\u2010depleted diets. The discovery that large doses of \u03b1T could ameliorate neuromuscular deficits, attributed to very low serum \u03b1T caused by mutations in either the microsomal triglyceride transfer protein or the \u03b1T\u2010transfer protein (\u03b1TTP), underscores the necessity of \u03b1T for neuromuscular health in humans. The discovery of human \u03b1TTP provided physiological relevance to biochemical data from rodents documenting \u03b1T\u2013binding transfer protein, expressed exclusively in liver. The cloning of \u03b1TTP gene and the creation of \u03b1TTP\u2010knockout mice allowed to achieve severe systemic \u03b1T deficiency in brain and muscles, possibly at birth, eliminating the possible confounding effects of <jats:italic>ex vivo<\/jats:italic>\u2010generated oxidant products in vitamin E\u2010stripped diets. \u03b1TTP\u2010knockout mice have proven useful models to discover \u03b1T\u2010regulated phenotypes and molecular actions of \u03b1T <jats:italic>in vivo<\/jats:italic>. The results suggest that antioxidant and non\u2010antioxidant actions of \u03b1T <jats:italic>in vivo<\/jats:italic> may not be mutually exclusive. These studies also suggest that low levels of dietary \u03b1T can achieve in excess of nanomolar \u03b1T levels in tissues and maintain normal neuromuscular functions. This is consistent with biochemical and crystallographic data of \u03b1\u2010TTP and of other \u03b1T\u2010binding proteins that have dissociation constants in nanomolar range. Molecular mechanisms that cause a long delay for the development of deficiency symptoms remain enigmatic. It is likely that \u03b1T is metabolically stable in post\u2010mitotic neurons and myocytes and, if it undergoes redox\u2010cycling <jats:italic>in vivo<\/jats:italic>, a large repertoire of \u03b1T\u2010regenerating systems maintains its biological activity before it is totally depleted.<\/jats:p>","DOI":"10.1002\/mnfr.200900575","type":"journal-article","created":{"date-parts":[[2010,2,25]],"date-time":"2010-02-25T17:08:03Z","timestamp":1267117683000},"page":"693-709","source":"Crossref","is-referenced-by-count":41,"title":["Dietary \u03b1\u2010tocopherol and neuromuscular health: Search for optimal dose and molecular mechanisms continues!"],"prefix":"10.1002","volume":"54","author":[{"given":"Kishorchandra","family":"Gohil","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vihas T.","family":"Vasu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carroll E.","family":"Cross","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2010,5,10]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.56.1458.650"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.105.043018"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1373\/clinchem.2003.022681"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1753-4887.1993.tb03064.x"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1136\/vr.150.10.307"},{"key":"e_1_2_7_7_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.nutr.20.1.663"},{"key":"e_1_2_7_8_2","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/2.12.2109"},{"key":"e_1_2_7_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1439810"},{"key":"e_1_2_7_10_2","first-page":"548","article-title":"Isolated vitamin E deficiency in the absence of fat malabsorption\u2010\u2010familial and sporadic cases: characterization and investigation of causes","volume":"111","author":"Sokol R. 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