Low zinc status in guinea pigs and chicks has no effect on reassembly rate of brain microtubules

Abstract

Zinc deficiency in guinea pigs and chicks results in peripheral neuropathy. Slowed reassembly of brain microtubules in zinc deficient rats has been reported, and such a defect might explain the neuropathy. To investigate this possibility, growing guinea pigs, chicks, and rats were fed a low zinc diet ad libitum (− Zn:AL), a control diet restricted (+ Zn:RF) to the intake of the − Zn:AL group, and the control diet ad libitum (+ Zn:AL). When the − Zn:AL guinea pigs and chicks exhibited neuropathy, at approximately 7 wk and 3 wk, respectively, a supernatant fraction of the brain was prepared and microtubule reassembly rates determined. Tubulin concentration and its sulfhydryl content were determined, as was the zinc content of the supernatant fraction. Similar measurements were made on rat brains taken after 3 wk, although the rats did not exhibit neurological signs. The reassembly rates of tubulin from the deficient guinea pigs and chicks were not decreased. That of the − Zn:AL rats was significantly less than that of the + Zn:AL group, but was not different from the + Zn:RF group. The tubulin sulfhydryl concentration was higher in deficient guinea pigs than in controls. There was no correlation between supernatant zinc concentration and the rate of reassembly. Because low zinc status had no effect in the guinea pig and chick, species susceptible to zinc deficiency neuropathy, it was concluded that the observed neuropathy is not the result of deranged properties of tubulin.