Abstract
It is well known that vitamin E functions as an antioxidant, and it is expected to exert an antioxidant effect when taken as a supplement. However, a number of cohort studies have shown that vitamin E does not alleviate oxidative stress and could even worsen it. Recently, Wang et al. investigated whether vitamin E intake was associated with amyotrophic lateral sclerosis (ALS) based on data from 5 cohort studies with 1,055,546 participants, of which 805 of them had developed ALS. They concluded in this large pooled prospective study, in which long-term vitamin E supplementation was associated with lower ALS rates, and therefore, a possible protective effect of vitamin E deserves further consideration. Performing further large cohort studies may reveal similar findings for other oxidative stressrelated diseases. It is still controversial if antioxidants such as vitamin E provide a clinical therapeutic effect against oxidative stressrelated diseases. If effective, the dose at which they should be administered and the duration of supplement exposure should be of interest. Vitamin E reduces production of reactive oxygen species by mitochondria and elicits further reactions in cells. It should be noted that mitochondria are important targets for vitamin E and its homologues. Therefore, a proper usage of vitamin E in subjects under high oxidative stress, due to its individually targeting property, will arise its importance in healthy life.
Keywords: Antioxidant, Vitamin E, MnSOD, Mitochondria, ROS, Oxidative Disease, apoptosis, diabetes mellitus, glioma cells, submitochondrial particles
Current Pharmaceutical Design
Title: Mitochondria as Possible Pharmaceutical Targets for the Effects of Vitamin E and its Homologues in Oxidative Stress-Related Diseases
Volume: 17 Issue: 21
Author(s): Hideyuki J. Majima, Hiroko P. Indo, Shigeaki Suenaga, Hirofumi Matsui, Hsiu-Chuan Yen and Toshihiko Ozawa
Affiliation:
Keywords: Antioxidant, Vitamin E, MnSOD, Mitochondria, ROS, Oxidative Disease, apoptosis, diabetes mellitus, glioma cells, submitochondrial particles
Abstract: It is well known that vitamin E functions as an antioxidant, and it is expected to exert an antioxidant effect when taken as a supplement. However, a number of cohort studies have shown that vitamin E does not alleviate oxidative stress and could even worsen it. Recently, Wang et al. investigated whether vitamin E intake was associated with amyotrophic lateral sclerosis (ALS) based on data from 5 cohort studies with 1,055,546 participants, of which 805 of them had developed ALS. They concluded in this large pooled prospective study, in which long-term vitamin E supplementation was associated with lower ALS rates, and therefore, a possible protective effect of vitamin E deserves further consideration. Performing further large cohort studies may reveal similar findings for other oxidative stressrelated diseases. It is still controversial if antioxidants such as vitamin E provide a clinical therapeutic effect against oxidative stressrelated diseases. If effective, the dose at which they should be administered and the duration of supplement exposure should be of interest. Vitamin E reduces production of reactive oxygen species by mitochondria and elicits further reactions in cells. It should be noted that mitochondria are important targets for vitamin E and its homologues. Therefore, a proper usage of vitamin E in subjects under high oxidative stress, due to its individually targeting property, will arise its importance in healthy life.
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Cite this article as:
J. Majima Hideyuki, P. Indo Hiroko, Suenaga Shigeaki, Matsui Hirofumi, Yen Hsiu-Chuan and Ozawa Toshihiko, Mitochondria as Possible Pharmaceutical Targets for the Effects of Vitamin E and its Homologues in Oxidative Stress-Related Diseases, Current Pharmaceutical Design 2011; 17 (21) . https://dx.doi.org/10.2174/138161211796957490
DOI https://dx.doi.org/10.2174/138161211796957490 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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