Coupling of Semiconductor Nanowires with Neurons and Their Interfacial Structure

We report on the compatibility of various nanowires with hippocampal neurons and the structural study of the neuron–nanowire interface. Si, Ge, SiGe, and GaN nanowires are compatible with hippocampal neurons due to their native oxide, but ZnO nanowires are toxic to neuron due to a release of Zn ion. The interfaces of fixed Si nanowire and hippocampal neuron, cross-sectional samples, were prepared by focused ion beam and observed by transmission electron microscopy. The results showed that the processes of neuron were adhered well on the nanowire without cleft

Over-expression of phenol-oxidising peroxidases alters the UV-susceptibility of transgenic Nicotiana tabacum

* Class III peroxidases catalyse the oxidative crosslinking of UV-absorbing phenolics. The effect of changes in the activity of phenol oxidising peroxidases (EC 1.11.1.7) on UV-tolerance in Nicotiana tabacum plants has been determined. * The UV-sensitivity of transgenic N. tabacum lines, altered in their peroxidase expression pattern, was studied by measuring radiation effects on photosynthetic efficiency. * Analysis of the effect of UV-radiation on the relative variable chlorophyll fluorescence showed that the SPI-2 line, which over-expresses a defence-related cationic peroxidase, is markedly UV-tolerant. By contrast, the ROPN3-line, which overexpresses a synthetic horseradish peroxidase-C gene, was found to be UV-sensitive. The increased activity of indole-3-acetic acid (IAA) inducible peroxidases in homozygous IAA-overproducing transgenic plants was also found to correlate with UV-sensitivity. * It is concluded that only specific peroxidase isozymes, through their effects on phenolic metabolism, contribute to the UV protection response. Thus, the analysis of the role of isozymes in UV-protection addresses fundamental questions of isozyme diversity and/or redundancy in relation to phenolic substrate

Mechanisms of Rapid Reactive Oxygen Species Generation in Response to Cytosolic Ca2+ or Zn2+ Loads in Cortical Neurons

Excessive “excitotoxic” accumulation of Ca(2+) and Zn(2+) within neurons contributes to neurodegeneration in pathological conditions including ischemia. Putative early targets of these ions, both of which are linked to increased reactive oxygen species (ROS) generation, are mitochondria and the cytosolic enzyme, NADPH oxidase (NOX). The present study uses primary cortical neuronal cultures to examine respective contributions of mitochondria and NOX to ROS generation in response to Ca(2+) or Zn(2+) loading. Induction of rapid cytosolic accumulation of either Ca(2+) (via NMDA exposure) or Zn(2+) (via Zn(2+)/Pyrithione exposure in 0 Ca(2+)) caused sharp cytosolic rises in these ions, as well as a strong and rapid increase in ROS generation. Inhibition of NOX activation significantly reduced the Ca(2+)-induced ROS production with little effect on the Zn(2+)- triggered ROS generation. Conversely, dissipation of the mitochondrial electrochemical gradient increased the cytosolic Ca(2+) or Zn(2+) rises caused by these exposures, consistent with inhibition of mitochondrial uptake of these ions. However, such disruption of mitochondrial function markedly suppressed the Zn(2+)-triggered ROS, while partially attenuating the Ca(2+)-triggered ROS. Furthermore, block of the mitochondrial Ca(2+) uniporter (MCU), through which Zn(2+) as well as Ca(2+) can enter the mitochondrial matrix, substantially diminished Zn(2+) triggered ROS production, suggesting that the ROS generation occurs specifically in response to Zn(2+) entry into mitochondria. Finally, in the presence of the sulfhydryl-oxidizing agent 2,2'-dithiodipyridine, which impairs Zn(2+) binding to cytosolic metalloproteins, far lower Zn(2+) exposures were able to induce mitochondrial Zn(2+) uptake and consequent ROS generation. Thus, whereas rapid acute accumulation of Zn(2+) and Ca(2+) each can trigger injurious ROS generation, Zn(2+) entry into mitochondria via the MCU may do so with particular potency. This may be of particular relevance to conditions like ischemia in which cytosolic Zn(2+) buffering is impaired due to acidosis and oxidative stress