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

Abstract

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.

Pine Bark Extract Protects Against Oxidative Stress Induced By Recurrent Hypoglycemia In Rats.

“…The results of this study are concomitant with the results of the study carried out by the [2] which showed that hypoglycemia may cause an increase in oxidative stress in the brain tissue, and also with the study carried out by [8] which stated that hypoglycemia has led to an increase in the level of MDA with the decreased activity of SOD and GSH content of the brain's cortex and is also consistent with studies conducted by [32], [33], [34] and [35]. The accumulation of large quantities of zinc in neurons as a well as the result of decreased glucose level; has led to an increase in the production of ROS in the nerve cells which led to increased oxidative stress in the brain cortex and the hypothalamus and hypoglycemic coma and brain injury are complications.…”

Preventive Effects of Ellagic Acid on Nucleus Tractus Solitarius Electrical Activity and Oxidative Stress Altered by Cerebral Global Ischemia/Reperfusion in Rat

“…With respect to numerous reports in antioxidant role of EA on neuodegeneration [47][48][49][50], we can confirm anti-oxidative profile of EA. The SOD enzyme produces substrate for GPx activity in the brain under stressful situations [51,52].…”

“…However, the long-time study in reperfusion phase to show more specific role and perceive mechanism of EA effect should be designed in future studies. Several line of evidences consistently supports the claim that ellagic acid improves antioxidant enzymes and subsequently these enzymes might defend neuronal cells against produced free radicals in brain injuries [47,48,49]. Herein, we detected the two antioxidant enzymes (SOD and GPx) in the present or absence of ellagic acid in ischemic rats' tissues.…”

Modulation by ellagic acid of DCA-induced developmental toxicity in the zebrafish (Danio rerio)

“…Four hydroxyl groups are attached to the ring system of the compound and may play a role in complex formation with free radicals [20]. EA was found to provide protection against many conditions associated with free radical formation including hemorrhage in rodents, skin tumorigenicity in mice, Aflatoxin B1-induced mutagenicity in rats, 2,3,7,8-tertrachlorodibenzo-p-dioxin (TCDD)-induced oxidative stress in rats, and TCDD-induced developmental toxicity in mice [20][21][22][23][24]. This study tested the possible protection by EA of both DCAinduced production of developmental toxic effects and DCA-induced production of ROS in zebrafish embryos.…”