Our previous study showed that dietary
zinc restriction induces depression-like behavior with concomitant up-regulation of the
N-methyl-D-aspartate receptor (NMDAR). Because
metal ions, oxidative stress, and
inflammation are involved in depression/NMDAR function, in the present study, bio-elements (
zinc,
copper,
iron,
magnesium, and
calcium), oxidative (
thiobarbituric acid-reactive substances;
protein carbonyl content), and inflammatory (IL-1α, IL-1β) factors were measured in serum, hippocampus (Hp), and prefrontal cortex (PFC) of male Sprague-Dawley rats subjected to a
zinc-adequate (ZnA) (50 mg Zn/kg) or a
zinc-deficient (ZnD) (3 mg Zn/kg) diet for 4 or 6 weeks. Both periods of dietary
zinc restriction reduced serum
zinc and increased serum
iron levels. At 4 weeks, lowered
zinc level in the PFC and Hp as well as lowered
iron level in the PFC of the ZnD rats was observed. At 6 weeks, however,
iron level was increased in the PFC of these rats. Although at 6 weeks
zinc level in the PFC did not differ between the ZnA and ZnD rats, extracellular
zinc concentration after 100 mM KCl stimulation was reduced in the PFC of the ZnD rats and was accompanied by increased extracellular
iron and
glutamate levels (as measured by the in vivo microdialysis). The examined oxidative and inflammatory parameters were generally enhanced in the tissue of the ZnD animals. The obtained data suggest dynamic redistribution of bio-elements and enhancement of oxidative/inflammatory parameters after dietary
zinc restriction, which may have a link with depression-like behavior/NMDAR function/neurodegeneration.