Abstract
In addition to exhibiting antioxidant properties, conjugated linoleic acid (CLA) and vitamin E may modulate gene expression of endogenous antioxidant enzymes. Depending on cellular microenvironments, such modulation reflects either antioxidant or prooxidant outcomes. Although epidemiological/experimental studies have indicated that CLA and vitamin E have health promoting properties, recent findings from clinical trials have been inconclusive. Discrepancies between the results found from prospective studies and recent clinical trials might be attributed to concentration-dependent cellular microenvironment alterations. We give a perspective of possible molecular mechanisms of actions of these lipophilic compounds and their implications for interventions of reactive oxygen species (ROS)-related diseases.
Highlights
Depending on cellular microenvironments, such modulation reflects either antioxidant or prooxidant outcomes
The antioxidant defense system consists of endogenous enzymes, including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and endogenous/exogenous compounds, including glutathione, vitamins A, C, and E
In this article two lipophilic compounds, conjugated linoleic acid (CLA) and vitamin E (α-tocopherol), and the potential interventions of such compounds are discussed in relation to the antioxidant defense system and atherosclerosis prevention
Summary
Depending on cellular microenvironments, such modulation reflects either antioxidant or prooxidant outcomes. In this article two lipophilic compounds, conjugated linoleic acid (CLA) and vitamin E (α-tocopherol), and the potential interventions of such compounds are discussed in relation to the antioxidant defense system and atherosclerosis prevention. Isomers may be involved in regulation of genes, whose products influence ROS generation, such as antioxidant enzymes, through redox-sensitive transcription factors [41].
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