[Mechanism of impairment to microtubule polymerization resulting from zinc deficiency during pregnancy and lactation in mice].

To probe into the mechanism of zinc deficiency on microtubule polymerization impairment, the learning ability and the levels of alpha-tubulin, beta-tubulin and microtubule-associated protein 2 expression in the brain of zinc deficient offsprings, maternal ICR mice were fed with experiment diets containing different levels of zinc(1, 5, 30 and 100 mg/kg) during pregnancy and lactation respectively. On the postnatal day 70 of offsprings, the learning ability and the expression of alpha-tubulin, beta-tubulin and microtubule-associated protein 2 in the brain were examined by shuttle box and Western blot assays respectively. The results showed that the number of trials needed to reach the learning criterion for zinc deficient groups (1 and 5 mg/kg) was much higher than that for non zinc deficient groups (30 and 100 mg/kg). The levels of alpha-tubulin, beta-tubulin and microtubule-associated protein 2 expression in the brain of zinc deficient offsprings (1 and 5 mg/kg) were lower than those in the brain of offsprings whose dams fed with zinc adequately supplied diet (30 mg/kg) and zinc supplemented supplied diet (100 mg/kg) respectively. These results suggested that the inhibition of alpha-tubulin, beta-tubulin and microtubule-associated protein 2 expression might be the most important mechanism of microtubule polymerization decline resulting from zinc deficiency, which had close relationship with brain function impairment.