TiO 2 doped with Cu 2+ initiates the formation of brookite phase along with anatase. Doping of Cu 2+ introduces structural defects into TiO 2 . The direct evidence is the low intense and broad diffraction peaks. Raman peaks of doped TiO 2 are also broad and are blueshifted. Pure TiO 2 exhibits an absorption in the UV region, the position of which is shifted towards the visible region on incorporation of Cu into it. The visible absorption peaks arise due to the

To understand the molecular mechanisms that upregulate the activities of pulmonary antioxidant enzymes in adult rats during exposure to 85% oxygen, the relative contents of corresponding mRNA in normal and hyperoxic lungs were determined. Hyperoxic exposure drastically induced the expression of lung manganese-containing superoxide dismutase (MnSOD) mRNA. Maximal induction of MnSOD mRNA occurred at days 3 and 5 of exposure to hyperoxia, reaching a 600 and a 340% increase over the levels of air-exposed rats, respectively. In addition, hyperoxia induced lung mRNA for glucose-6-phosphate dehydrogenase, glutathione peroxidase, glyceraldehyde-3-phosphate dehydrogenase, alpha-tubulin, and gamma-actin to different extends at various days of exposure. Hyperoxia had little or no effect on the levels of mRNA for copper/zinc-containing superoxide dismutase (CuZnSOD), catalase, heat shock protein (HSP70), and creatine kinase. Nuclear run-on experiments showed that the transcriptional rate of the MnSOD gene is enhanced in hyperoxic rat lungs by approximately 400% at day 3 of exposure compared with that of controls. The specific activities of CuZnSOD and MnSOD in these lung samples per unit of lung protein or DNA were also determined. The activity of CuZnSOD in hyperoxic lungs was found to be unchanged compared with controls, except a 20% decrease at day 7 of exposure when standardized against protein content of lung homogenate. Changes of CuZnSOD activity were more dramatic in hyperoxic lungs (a 40% increase at days 3, 5, 7, and 14 of exposure) when enzyme activity was normalized using lung DNA content. Surprisingly, no proportional increase of lung MnSOD enzyme activity was observed at days 3 and 5 of oxygen exposure. The increase of MnSOD activity per unit of lung protein also did not parallel the increase in MnSOD protein content at days 5, 7, and 14 of exposure. These data suggest that, in addition to transcriptional activation, translational and/or posttranslational regulation of the MnSOD gene expression may play a critical role in controlling lung MnSOD activity on hyperoxic exposure.

TiO 2 nanoparticles with 2 and 4 % Cu are synthesized by sol-gel method. The crystalline phase and size of the nanoparticles are investigated with X-ray diffraction and transmission electron microscope. Cu-doped TiO 2 has an extended absorption ranging from UV to visible region. Doping of Cu disturbs the arrangement of oxygen ions around Ti 4? and generates oxygen vacancies. These oxygen vacancies capture electrons and form some ionized oxygen vacancy centers or F centers. These F centers form subband states extending from shallow to the deep level in the band gap of TiO 2 . The visible emission peaks of pure and doped TiO 2 are mainly associated with self-trapped excitons (STEs) and F centers. We have observed that Auger type nonradiative recombination is responsible for the quenching of the UV and STE emission peak in the doped samples. The intense visible emission peaks in pure TiO 2 are due to shallow type centers whereas deep trap emission is predominant in doped samples. The intensity of UV and visible emission peaks are quenched with the increase in the doping level of Cu. Defects, Cu dstates, band structure of TiO 2 and low mobility of the carriers are responsible for the quenching of the emission peaks.

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