• magnetic resonance imaging (MRI);
  • magnetic resonance spectroscopy (MRS);
  • brain development;
  • in vivo


In humans, zinc deficiency is characterized by a broad spectrum of neurological clinical syndromes. It is known that vesicular zinc-enriched areas of the brain, such as the hippocampus, are responsive to zinc deprivation, which may result in learning impairment. Recent findings show that zinc deficiency may cause alterations in neurochemical activity. In this study we used contrast-enhanced magnetic resonance imaging (MRI) to monitor disruptions to the blood–brain barrier (BBB) and image-guided MR spectroscopy to follow alterations in brain metabolites as a result of zinc-deficiency and/or hyperoxia-induced oxidative stress. Gadolinium-diethylaminetriaminopentaacetic acid, an extracellular T1 relaxation contrast agent, increases tissue water signal in the brain if the BBB is damaged. A significant increase in postcontrast T1-weighted MR image intensity was observed in the brain of zinc-deficient or hyperoxia-exposed rats, as well as zinc-deficient rats exposed only to hyperoxia when compared with zinc-adequate rats. From single-voxel image-guided MR spectroscopy results, significant decreases in the ratio of N-acetyl aspartate, a neuronal-specific compound, to total choline levels were found when comparing controls (zinc-adequate or zinc pair-fed) with zinc-deficiency or hyperoxia groups alone, and when zinc-deficiency was combined with hyperoxia. This study demonstrates the sensitivity of MR techniques in the ability to monitor the effect of zinc deficiency combined with oxidative stress on BBB permeability as well as detect alterations in brain metabolites. This will further aid in our understanding of the possible cellular and molecular mechanisms involved in zinc deficiency pathology associated with the brain. J. Trace Elem. Exp. Med. 17:161–174, 2004. © 2004 Wiley-Liss, Inc.