{"title":"第六章。生育酚磷酸","authors":"A. Azzi","doi":"10.1039/9781788016216-00075","DOIUrl":null,"url":null,"abstract":"Older studies of the phosphoric acid ester of α-tocopherol (TP) in enzymes and animal models have given no conclusive results. More recently, the molecule has been the object of new scientific attention as an extension to the renewed popularity of vitamin E (α-tocopherol). α-Tocopherol is a micronutrient that is needed to prevent a form of cerebellar ataxia, but several alleged functions have been attributed to it, including protection against neurodegeneration, atherosclerosis, cancer and aging. Initially, the biological function of TP was seen as a pro-vitamin E capable of releasing α-tocopherol in the body. Subsequent studies have indicated that the nanomolar amount of TP in the body is not compatible with functioning as a reserve of vitamin E, whose concentration in plasma is in the micromolar order. On the other hand, its existence in humans, animals and plants has prompted studies on TP's molecular functions, and these have revealed that it can be synthesized and hydrolyzed in cells and in animals. The enzymes responsible for α-tocopherol kinase and tocopheryl phosphate phosphatase cellular activities have not been purified. TP inhibits cell proliferation and regulates gene expression more potently than α-tocopherol; furthermore, some genes are exclusively regulated by TP. These signaling effects of TP are in connection with phosphatidyl inositol kinase. In animal models, TP has shown more potency than α-tocopherol against atherosclerosis and inflammation. TP has been proposed to be an activated form of α-tocopherol.","PeriodicalId":23674,"journal":{"name":"Vitamin E","volume":"42 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"CHAPTER 6. Tocopheryl Phosphate\",\"authors\":\"A. Azzi\",\"doi\":\"10.1039/9781788016216-00075\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Older studies of the phosphoric acid ester of α-tocopherol (TP) in enzymes and animal models have given no conclusive results. More recently, the molecule has been the object of new scientific attention as an extension to the renewed popularity of vitamin E (α-tocopherol). α-Tocopherol is a micronutrient that is needed to prevent a form of cerebellar ataxia, but several alleged functions have been attributed to it, including protection against neurodegeneration, atherosclerosis, cancer and aging. Initially, the biological function of TP was seen as a pro-vitamin E capable of releasing α-tocopherol in the body. Subsequent studies have indicated that the nanomolar amount of TP in the body is not compatible with functioning as a reserve of vitamin E, whose concentration in plasma is in the micromolar order. On the other hand, its existence in humans, animals and plants has prompted studies on TP's molecular functions, and these have revealed that it can be synthesized and hydrolyzed in cells and in animals. The enzymes responsible for α-tocopherol kinase and tocopheryl phosphate phosphatase cellular activities have not been purified. TP inhibits cell proliferation and regulates gene expression more potently than α-tocopherol; furthermore, some genes are exclusively regulated by TP. These signaling effects of TP are in connection with phosphatidyl inositol kinase. In animal models, TP has shown more potency than α-tocopherol against atherosclerosis and inflammation. TP has been proposed to be an activated form of α-tocopherol.\",\"PeriodicalId\":23674,\"journal\":{\"name\":\"Vitamin E\",\"volume\":\"42 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-02-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Vitamin E\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1039/9781788016216-00075\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Vitamin E","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1039/9781788016216-00075","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Older studies of the phosphoric acid ester of α-tocopherol (TP) in enzymes and animal models have given no conclusive results. More recently, the molecule has been the object of new scientific attention as an extension to the renewed popularity of vitamin E (α-tocopherol). α-Tocopherol is a micronutrient that is needed to prevent a form of cerebellar ataxia, but several alleged functions have been attributed to it, including protection against neurodegeneration, atherosclerosis, cancer and aging. Initially, the biological function of TP was seen as a pro-vitamin E capable of releasing α-tocopherol in the body. Subsequent studies have indicated that the nanomolar amount of TP in the body is not compatible with functioning as a reserve of vitamin E, whose concentration in plasma is in the micromolar order. On the other hand, its existence in humans, animals and plants has prompted studies on TP's molecular functions, and these have revealed that it can be synthesized and hydrolyzed in cells and in animals. The enzymes responsible for α-tocopherol kinase and tocopheryl phosphate phosphatase cellular activities have not been purified. TP inhibits cell proliferation and regulates gene expression more potently than α-tocopherol; furthermore, some genes are exclusively regulated by TP. These signaling effects of TP are in connection with phosphatidyl inositol kinase. In animal models, TP has shown more potency than α-tocopherol against atherosclerosis and inflammation. TP has been proposed to be an activated form of α-tocopherol.