[Effect of dietary zinc on microtubule-associated protein 2 expression in the brain of mice]

Zinc deficiency could result in reduction of microtubule polymerization, which may cause impairment of brain development and function. The relationship between zinc deficiency and microtubules polymerization is still unclear. In this paper, microtubule-associated protein 2 (MAP2) expression in the brain was examined in order to explore the mechanism of zinc regulated microtubule polymerization. 80 pregnant ICR mice, randomized into 5 groups, were fed with experimental diets of different zinc levels (from 1 to 100 mg/kg) during pregnancy and lactation. The MAP2 expression in the brain of offsprings was examined by Western blot assays. The results showed that MAP2, including MAP2a, MAP2b and MAP2c, were expressed in brain from embryonic day 15, but not found on embryonic day 10. The high molecular weight of MAP2a and MAP2b expressed continuously from embryonic day 15 to postnatal day 70 (adult). While the low molecular weight of MAP2c was down-regulated from embryonic day 15 to non-existing on postnatal day 70. The expression of MAP2 in cerebrum and cerebellum kept closely at the positive dependence with dietary zinc level. The order of the levels of expression of MAP2 of the various groups administrated with different amounts of zinc is as follows: 1 mg/kg < 5 mg/kg < 30 mg/kg < 100 mg/kg. The above results suggest that zinc deficiency may inhibit the MAP2 expression, while zinc supplement exerts much improvement. The lowered level of MAP2 expression is one of important mechanisms underlying impairments of microtubule polymerization, as a result of zinc deficiency.