title: Vitamin E-Induced Changes in Glutamate and GABA Metabolizing Enzymes of Chick Embryo Cerebrum.
abstract: Vitamin E exists in eight different forms, four tocopherols and four tocotrienols. It forms an important component of our antioxidant system. The structure of Vitamin E makes it unique and indispensable in protecting cell membranes. α -tocopherol, one of the forms of Vitamin E, is also known to regulate signal transduction pathways by mechanisms that are independent of its antioxidant properties. Vitamin E compounds reduce the production of inflammatory compounds such as prostaglandins. Swollen, dystrophic axons are considered as the hallmark of Vitamin E deficiency in the brains of rats, monkeys, and humans. The present work aimed to study the Vitamin E- ( α -tochopherol acetate-) induced alterations of enzymes involved in metabolism of Glutamate and GABA during developmental neurogenesis of cerebrum. Therefore, cytosolic and crude mitochondrial enzyme activities of glutamine synthetase, aspartate transaminase, alanine transaminase, GABA transaminase, succinic Semialdehyde dehydrogenase, glutamic dehydrogenase, and α -Ketoglutarate dehydrogenase were analysed. Vitamin E induced significant changes in these enzymes thus altering the normal levels of glutamate and GABA during developmental neurogenesis. Such changes are surely to disturb the expression and/or intensity of neurotransmitter signaling during critical periods of brain development.
authors: Physiology and Biochemistry Laboratory, Department of Zoology, Goa University, Panaji, Goa 403206, India.
authors: Ivy
authors: I
authors: Pereira
authors: Shanti N
authors: SN
authors: Dessai
authors: Annaliza
authors: A
authors: Pinto
references: Neurosci Lett. 1987 Jul 9;78(1):7-11
references: 3614773
references: Brain Res Mol Brain Res. 1989 Dec;6(4):223-32
references: 2574402
references: Neuroscience. 2005;130(3):567-80
references: 15590141
references: Comp Biochem Physiol C Toxicol Pharmacol. 2003 Sep;136(1):29-45
references: 14522597
references: J Neural Transm Gen Sect. 1992;90(3):231-40
references: 1285951
references: Neuroscience. 2009 Jan 23;158(2):610-6
references: 18996448
references: Poult Sci. 2000 Apr;79(4):539-45
references: 10780651
references: Prog Neuropsychopharmacol Biol Psychiatry. 2002 Apr;26(3):427-35
references: 11999891
references: J Neurol Sci. 1984 Oct;66(1):27-32
references: 6151588
references: Int Rev Neurobiol. 2005;71:27-62
references: 16512345
references: Invest Ophthalmol. 1974 Jul;13(7):499-510
references: 4366000
references: Poult Sci. 2001 Oct;80(10):1496-505
references: 11599710
references: J Biol Chem. 1951 Nov;193(1):265-75
references: 14907713
references: Ann Neurol. 2000 Sep;48(3):297-303
references: 10976635
references: FEBS Lett. 2002 Oct 23;530(1-3):17-23
references: 12387859
references: Methods Enzymol. 1985;113:16-27
references: 4088065
references: Experientia. 1982 Oct 15;38(10):1199-202
references: 6128246
references: Arch Biochem Biophys. 1988 Nov 1;266(2):386-96
references: 3190233
references: Brain Res. 1968 Nov;11(2):412-30
references: 5701204
references: Crit Rev Neurobiol. 1990;5(3):239-63
references: 2204484
references: Prog Neurobiol. 2004 Aug;73(6):397-445
references: 15313334
references: Neurochem Int. 2002 Aug-Sep;41(2-3):123-42
references: 12020613
references: Brain Res Dev Brain Res. 1992 Sep 18;69(1):51-7
references: 1424089
references: Brain Res. 1983 Dec;313(1):67-74
references: 6661665
references: Int J Dev Neurosci. 1984;2(1):55-60
references: 24873852
references: Prog Neurobiol. 1997 Feb;51(3):337-61
references: 9089792
references: Ann N Y Acad Sci. 1989;570:146-55
references: 2483495
references: Invest Ophthalmol Vis Sci. 1980 Sep;19(9):1030-7
references: 7409996
references: Clin Chim Acta. 1988 Mar 31;173(1):43-55
references: 3289795
references: J Neuropathol Exp Neurol. 1981 Mar;40(2):166-86
references: 7463101
references: Neuroscience. 1994 Oct;62(4):1133-46
references: 7531302
references: Methods Enzymol. 1985;113:199-212
references: 2868384