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Vitamin E Research Today is a free monthly online journal that collates and summarizes the latest research about Vitamin E, including details on benefits, dosage, supplements, antioxidants.


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The effects of ellagic acid and vitamin E succinate on antioxidant enzymes activities and glutathione levels in different brain regions of rats after subchronic exposure to TCDD.

Hassoun EA, Vodhanel J, Holden B, Abushaban A

College of Pharmacy, University of Toledo, Toledo, Ohio 43606,, USA. ezdihar.hassoun@utoledo.edu

Ellagic acid (EA) and vitamin E succinate (VES) were previously shown to protect against 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-induced reactive oxygen species (ROS) overproduction in certain brain regions of rats after subchronic exposure. The current study was designed to assess the modulation of antioxidant enzyme activities and glutathione (GSH) levels as protective measures for VES and EA against TCDD-induced ROS overproduction in four regions of rat brain. TCDD was administered to groups of rats at a daily dose of 46 ng/kg for 90 d. EA and VES were administered to some other groups of rats either alone or simultaneously with TCDD, every other day for 90 d. At the end of the treatment period, animals were sacrificed and brain regions were dissected, including cerebral cortex (Cc), hippocampus (H), cerebellum (C), and brainstem (Bs), for assay of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH levels. While treatment of rats with VES alone or in combination with TCDD resulted in significant increases in SOD and CAT activities in different brain regions, treatment with EA resulted in a significant rise in total GSH levels and GSH-Px activity in those regions. Results may suggest antioxidant modulation by VES and EA as a mechanism for the previously observed protection by these compounds against TCDD-induced ROS overproduction in brain. Data also indicate there are two different pathways in the protection provided by the two antioxidants.

Published 3 February 2006 in J Toxicol Environ Health A, 69(5): 381-93.
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