According to recent research from the United States published in the journal Brain Research, mitochondrially targeted vitamin E (MitoVit E), and vitamin E (VE) mitigate ethanol (EtOH)-mediated effects on cerebellar granule cell (CGC) antioxidant defense systems.
"EtOH disrupts the structure and function of the developing nervous system, sometimes leading to birth defects associated with fetal alcohol syndrome (FAS). Animal FAS models indicate that cellular membrane peroxidation, intracellular oxidant accumulation, and suppression of endogenous:antioxidant enzymes contribute to the toxic effects of EtOH," wrote K.I. Siler-Marsiglio and colleagues, University of Florida.
"MitoVit E, a chemically engineered form of VE designed to accumulate in the mitochondria, has been shown to inhibit intracellular oxidant accumulation and cell death more effectively than VE. In previous investigations, we have shown that, in vivo, VU reduces neuronal death in the developing cerebellum of EtOH-exposed animals, and, in vitro, VE prevents apoptotic and necrotic death of EtOH-exposed CGCs.
"The present investigation shows that, in a FAS CGC model, 1 nM MitoVit E renders significant neuroprotection against EtOH concentrations as high as 1600 mg/dL. The present study also demonstrates that, in this same model," the authors reported.
"MitoVit E mitigates EtOH-induced accumulation of intracellular oxidants and counteracts suppression of glutathione peroxidase/glutathione reductase (GSH-Px/GSSGR) functions, protein expression of gamma-glutamylcysteine synthetase (gamma-GCS), and total cellular glutathione (GSH) levels.
"In the presence and absence of EtOH, VE amplifies the protein expression levels of gamma-GCS, an enzyme that performs the rate-limiting step for GSH synthesis, and total GSH levels," continued the researchers.
"These results suggest that MitoVit E and VE ameliorate EtOH toxicity through non-oxidant mechanisms modulations of endogenous cellular proteins and antioxidant means," concluded the investigators.
Siler-Marsiglio and colleagues published their study in Brain Research (Mitochondrially targeted vitamin E and vitamin E mitigate ethanol-mediated effects on cerebellar granule cell antioxidant defense systems. Brain Res, 2005;1052(2):202-211).
For additional information, contact K.I. Silermarsiglio, University of Florida, McKnight Brain Institute, Department of Neuroscience, 100 S Newell Dr., Room L3-151, Gainesville, FL 32611, USA.
The publisher's contact information for the journal Brain Research is: Elsevier Science BV, PO Box 211, 1000 AE Amsterdam, Netherlands.
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