The elegant paper on zinc effects in neuronal cultures (1) clarifies the entry of its ions by a specific channel in the cells. The results are, however, difficult to evaluate in view of limited neurotoxicity of zinc salts in adult animals. In our study on adult rabbits, the animals did not display obvious neurotoxicity in a peroral exposure through drinking water up to 4 weeks (2).
Specifically, the motor conduction velocity in sciatic nerve did not decrease while a concomitant exposure to lead acetate caused a decrease (2). At the same time, the blood zinc concentration increased very significantly while that in brain or in sciatic nerve was less marked. This could be caused by the induction of the metallothionein, its carrier, by zinc (3) and by the efficiency of the blood brain and blood nerve barriers in preventing its entry in the nervous system.
References
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