Ruthenium-based catalysts including monometallic Ru, bimetallic Ru-Cu and Ru-Co were prepared using spheric active carbon (SAC) as the support, and their catalytic performance was assessed for the acetylene hydrochlorination reaction, characterized by BET, TG, TEM, TPR and XPS. It is suggested that using cobalt as the additive can significantly enhance the catalytic activity of the Ru/SAC catalyst for the acetylene hydrochlorination reaction. Over the 1%Ru1Co3/SAC catalyst the acetylene conversion is maintained above 95% with 48 h on stream under reaction conditions of 170 C, C 2 H 2 hourly space velocity ¼ 180 h À1 and the feed HCl/C 2 H 2 volume ratio ¼ 1.1; while the addition of copper results in a lower acetylene conversion. It is illustrated that the cobalt additive can greatly influence the amount of ruthenium species involved in RuO 2 , Ru 0 , RuO x and RuCl 3 in the catalyst, which results in good catalytic activity and capability to inhibit coking of the 1%Ru1Co3/SAC catalyst. The optimal 1%Ru1Co3/SAC catalyst is a promising non-mercuric catalyst for PVC manufacture, with the advantages of both good stability and low cost.

This study aimed to evaluate how excess selenium induces oxidative stress by determining antioxidant enzyme activity and changes in expression of selected selenoproteins in mice. BALB/c mice (n = 20 per group) were fed a diet containing 0.045 (Se-marginal), 0.1 (Se-adequate), 0.4 (Se-supernutrition), or 0.8 (Se-excess) mg Se/kg. Gene expression was quantified in RNA samples extracted from the liver, kidney, and testis by real-time quantitative reverse transcription-polymerase chain reaction. We found that glutathione peroxidase (GPx) and catalase activities decreased in livers of mice fed the marginal or excess dose of Se as compared to those in the Se-adequate group. Additionally, superoxide dismutase and glutathione reductase activities were significantly reduced only in mice fed the excess Se diet, compared to animals on the adequate Se diet. Se-supernutrition had no effect on hepatic mRNA levels of GPx isoforms 1 and 4 (GPx1 and GPx4), down-regulated GPx isoform 3 (GPx3), and upregulated selenoprotein W (SelW) mRNA expression. The excess Se diet led to decreased hepatic mRNA levels of GPx1, GPx3 and GPx4 but no change in testicular mRNA levels of GPx1, GPx3 or SelW. Dietary Se had no effect on testicular mRNA levels of GPx4. Thus, our results suggest that Se exposure can reduce hepatic antioxidant capacity and cause liver dysfunction. Dietary Se was found to differentially regulate mRNA levels of the GPx family or SelW, depending on exposure. Therefore, these genes may play a role in the toxicity associated with Se.

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