Highly efficient xylem transport of arsenite in the arsenic hyperaccumulator Pteris vittata.

The hyperaccumulator Pteris vittata translocates arsenic (As) from roots to fronds efficiently, but the form of As translocated in xylem and the main location of arsenate reduction have not been resolved. Here, P. vittata was exposed to 5 microM arsenate or arsenite for 1-24 h, with or without 100 microM phosphate. Arsenic speciation was determined in xylem sap, roots, fronds and nutrient solutions by high-performance liquid chromatography (HPLC) linked to inductively coupled plasma mass spectrometry (ICP-MS). The xylem sap As concentration was 18-73 times that in the nutrient solution. In both arsenate- and arsenite-treated plants, arsenite was the predominant species in the xylem sap, accounting for 93-98% of the total As. A portion of arsenate taken up by roots (30-40% of root As) was reduced to arsenite rapidly. The majority (c. 80%) of As in fronds was arsenite. Phosphate inhibited arsenate uptake, but not As translocation. More As was translocated to fronds in the arsenite-treated than in the arsenate-treated plants. There was little arsenite efflux from roots to the external solution. Roots are the main location of arsenate reduction in P. vittata. Arsenite is highly mobile in xylem transport, possibly because of efficient xylem loading, little complexation with thiols in roots, and little efflux to the external medium.

Field evaluation of in situ remediation of a heavy metal contaminated soil using lime and red-mud.

We evaluated the effectiveness of lime and red mud (by-product of aluminium manufacturing) to reduce metal availability to Festuca rubra and to allow re-vegetation on a highly contaminated brown-field site. Application of both lime and red mud (at 3 or 5%) increased soil pH and decreased metal availability. Festuca rubra failed to establish in the control plots, but grew to a near complete vegetative cover on the amended plots. The most effective treatment in decreasing grass metal concentrations in the first year was 5% red mud, but by year two all amendments were equally effective. In an additional pot experiment, P application in combination with red mud or lime decreased the Pb concentration, but not total uptake of Pb in Festuca rubra compared to red mud alone. The results show that both red mud and lime can be used to remediate a heavily contaminated acid soil to allow re-vegetation.

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice.

Effects of maternal dietary zinc deficiency on prenatal and postnatal brain development were investigated in ICR strain mice. From d 1 of pregnancy (E0) until postnatal d 20 (P20), maternal mice were fed experimental diets that contained 1 mg Zn/kg/day (severe zinc deficient, SZD), 5 mg Zn/kg/day (marginal zinc deficient, MZD), 30 mg Zn/kg/day (zinc adequately supplied, ZA) or 100 mg Zn/kg/day (zinc supplemented, ZS and pair-fed, PF). Brains of offspring from these dietary groups were examined at various developmental stages for expression of nestin, an intermediate filament protein found in neural stem cells and young neurons. Immunocytochemistry showed nestin expression in neural tube 10.5 d post citrus (dpc) as well as in the cerebral cortex and neural tube from 10.5 dpc to postnatal d 10 (P10). Nestin immunoreactivities in both brain and neural tube of those zinc-supplemented control groups (ZA, ZS, PF) were stronger than those in zinc-deficient groups (SZD and MZD). Western blot analysis confirmed that nestin levels in pooled brain extracts from each of the zinc-supplemented groups (ZA, ZS, PF) were much higher than those from the zinc-deficient groups (SZD and MZD) from 10.5 dpc to P10. Immunostaining and Western blots showed no detectable nestin in any of the experimental and control group brains after P20. These observations of an association between maternal zinc deficiency and decreased nestin protein levels in brains of offspring suggest that zinc deficiency suppresses development of neural stem cells, an effect which may lead to neuroanatomical and behavioral abnormalities in adults.

Cellular compartmentation of cadmium and zinc in relation to other elements in the hyperaccumulator Arabidopsis halleri.

The cellular compartmentation of elements was analysed in the Zn hyperaccumulator Arabidopsis halleri (L.) O'Kane & Al-Shehbaz (=Cardaminopsis halleri) using energy-dispersive X-ray microanalysis of frozen-hydrated tissues. Quantitative data were obtained using oxygen as an internal standard in the analyses of vacuoles, whereas a peak/background ratio method was used for quantification of elements in pollen and dehydrated trichomes. Arabidopsis halleri was found to hyperaccumulate not only Zn but also Cd in the shoot biomass. While large concentrations of Zn and Cd were found in the leaves and roots, flowers contained very little. In roots grown hydroponically, Zn and Cd accumulated in the cell wall of the rhizodermis (root epidermis), mainly due to precipitation of Zn/Cd phosphates. In leaves, the trichomes had by far the largest concentrations of Zn and Cd. Inside the trichomes there was a striking sub-cellular compartmentation, with almost all the Zn and Cd being accumulated in a narrow ring in the trichome base. This distribution pattern was very different from that for Ca and P. The epidermal cells other than trichomes were very small and contained lower concentrations of Zn and Cd than mesophyll cells. In particular, the concentrations of Cd and Zn in the mesophyll cells increased markedly in response to increasing Zn and Cd concentrations in the nutrient solution. This indicates that the mesophyll cells in the leaves of A. halleri are the major storage site for Zn and Cd, and play an important role in their hyperaccumulation.

[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.