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Effect of Early Iron Deficiency in Rat on the γ‐Aminobutyric Acid Shunt in Brain
Author(s) -
Taneja Veena,
Mishra Kamalapati,
Agarwal K. N.
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb08483.x
Subject(s) - glutamate decarboxylase , glutamic acid , medicine , endocrinology , glutamate receptor , isocitrate dehydrogenase , glutamate dehydrogenase , enzyme , chemistry , biochemistry , transaminase , gaba transaminase , biology , amino acid , receptor
Abstract: Early iron deficiency in rat does not affect the weight or the protein, DNA, and RNA content but results in a slight reduction in γ‐aminobutyric acid (GABA) (13%, p < 0.01) and glutamic acid (20%, p < 0.001) content of the brain. The activities of the two GABA shunt enzymes, glutamate dehydrogenase and GABA‐transaminase, and of the NAD + ‐linked isocitrate dehydrogenase (ICDH) were inhibited whereas the glutamic acid decarboxylase, mitochondrial NADP + ‐linked ICDH, and succinic dehydrogenase activities remained unaltered in brain. On rehabilitation with the iron‐supplemented diet for 1 week, these decreased enzyme activities in brain attained the corresponding control values. However, the hepatic nonheme iron content increased to about 80% of the control, after rehabilitation for 2 weeks. A prolonged iron deficiency resulting in decreased levels of glutamate and GABA may lead to endocrinological, neurological, and behavioral alterations.