Premium
Zinc homeostasis in the brain of adult rats fed zinc‐deficient diet
Author(s) -
Takeda Atsushi,
Minami Akira,
Takefuta Sachiyo,
Tochigi Minori,
Oku Naoto
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20010301)63:5<447::aid-jnr1040>3.0.co;2-c
Subject(s) - zinc , hippocampal formation , endocrinology , medicine , zinc deficiency (plant disorder) , hippocampus , chemistry , homeostasis , metallothionein , biology , organic chemistry
Zinc concentration and 65 Zn uptake in the brain of rats fed zinc‐deficient diet for 12 weeks were examined, based on a previous finding of the impairment of learning behavior by the zinc deprivation. Zinc concentrations in the brain, except for the hippocampal formation, did not decrease significantly in zinc‐deficient rats, whereas zinc concentration in the liver of the zinc‐deficient rats was approximately half that of control rats. When zinc‐deficient rats were subjected to brain autoradiography with 65 Zn, 65 Zn concentration in any brain region of zinc‐deficient rats was significantly higher than in control rats 6 days after injection of 65 ZnCl 2 . The increase rate of 65 Zn concentration in the brain by the zinc deprivation was approximately 150%, and was similar to those in the liver and serum, suggesting that dietary zinc deprivation may cause a scarcity of zinc in the brain, in addition to the peripheral tissues such as the liver. These results indicate that the adult brain is responsive to dietary zinc deprivation. In the brain of zinc‐deficient rats, the increase rate of 65 Zn concentration in the hippocampal formation seemed to be low compared to those in other brain regions. The hippocampal formation may be the most responsive to dietary zinc deprivation in the adult brain. The present finding demonstrates that zinc homeostasis in the brain is altered by chronically dietary zinc deprivation. J. Neurosci. Res. 63:447–452, 2001. © 2001 Wiley‐Liss, Inc.