Linking Material Flow Analysis with Environmental Impact Potential

Technology transition can have significant implications on the evolution of environmental impact potential of disposed electronics over time. Considering technology transition, we quantify the temporal behavior of ecological and human health impact potential from select heavy metals in electronic waste (e‐waste). The case study analyzes product substitution effects in two electronic cohorts from the U.S. market: (1) computers (laptops substituting for desktops) and (2) televisions (flat‐panel liquid crystal displays [LCDs] and plasma displays substituting for cathode‐ray tubes [CRTs]). Quantities of end‐of‐life (EoL) units to year 2030 are forecasted by the unique combination of dynamic material flow analysis, logistic trend analysis, and product lifespan calibration methods. Metal content from EoL units are assessed via a pathway and effect model using USETox? characterization factors to determine the toxicity potential attributed to heavy metal releases into different media (e.g., air, water, and soil) as an indicator of environmental burden. Results show high impact materials such as lead, nickel, and zinc cause changes in human health toxicity potential and copper causes changes in ecological toxicity potential. Effects of dematerialization, such as reduced metal content in laptops over desktops, provide some positive benefits in toxicity potential per product. However, from a market perspective, emerging e‐waste quantities created by increasing per capita penetration rates of electronics and increasing population will offset gains in environmental performance at the product level. The resulting analysis provides guidance on the timing expected for emerging EoL units and an indication of high impact potential materials requiring pollution prevention as product substitution occurs.     

Association between Gene Polymorphism of Manganese Superoxide Dismutase and Prostate Cancer Risk

Manganese superoxide dismutase (MnSOD) is the most effective antioxidant enzyme in mitochondria and protects cells from reactive oxygen species‐induced oxidative damage. The aim of this study was to investigate the association between MnSOD Ala‐9Val gene polymorphism and prostate cancer (PCa) risk in Turkish men with prostate cancer. 33 patients with PCa and 81 control individuals were included in the study. We observed an association between MnSOD Ala/Ala frequency and a higher PCa risk. In addition, we found that the increased risk of early‐onset PCa (under age of 65) in the men homozygous for Ala allele was higher than the men homozygous for Val allele. However, we determined that MnSOD Ala‐9Val genotype was not associated with the aggressiveness of the disease. The results of our study suggest that MnSOD Ala/Ala genotype may influence on early‐onset of PCa patients, but no effect on subsequent development of the disease in Turkish men. However, our study has a limitation that is small numbers of individuals for cases and controls. Therefore, the presented study limited our statistical power to fully investigate the gene polymorphism on cancer risk. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:213‐218, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21472     

The Cytotoxic and Proapoptotic Activities of Hypnophilin are Associated with Calcium Signaling in UACC‐62 Cells

Hypnophilin (HNP) is a sesquiterpene that is isolated from Lentinus cf. strigosus and has cytotoxic activities. Here, we studied the calcium signaling and cytotoxic effects of HNP in UACC‐62 cells, a human skin melanoma cell line. HNP was able to increase the intracellular calcium concentration in UACC‐62 cells, which was blocked in cells stimulated in Ca²⁺‐free media. HNP treatment with BAPTA‐AM, an intracellular Ca²⁺ chelator, caused an increase in calcium signals. HNP showed cytotoxicity against UACC‐62 cells in which it induced DNA fragmentation and morphological alterations, including changes in the nuclear chromatin profile and increased cytoplasmatic vacuolization, but it had no effect on the plasma membrane integrity. These data suggest that cytotoxicity in UACC‐62 cells, after treatment with HNP, is associated with Ca²⁺ influx. Together, these findings suggest that HNP is a relevant tool for the further investigation of new anticancer approaches. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:479‐485, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21507     

Periostin Mediates the Increased Pro‐Angiogenic Activity of Gastric Cancer Cells under Hypoxic Conditions

This study was conducted to investigate the biological role of periostin in gastric cancer (GC) under hypoxia. Western blot analysis revealed that along with an upregulation of hypoxia‐inducible factor‐1alpha, there was a time‐dependent induction of periostin in MKN‐45 cells under hypoxia (2% O₂), increasing by eightfold as compared to normoxic cells. Pretreatment with 30 µM PD98059, an inhibitor of ERK1/2, significantly reduced hypoxia‐stimulated periostin expression (P < 0.01). Periostin knockdown in MKN‐45 cells was achieved by specific small interfering RNA (siRNA). The conditioned medium from periostin siRNA‐transfected MKN‐45 cells induced significantly less (P < 0.01) endothelial tube formation than control siRNA‐transfected cells. Additionally, periostin silencing markedly decreased the mRNA expression and secretion of vascular endothelial growth factor (VEGF) in hypoxic MKN‐45 cells. Thus, our data suggest that periostin is a hypoxia‐response gene and mediates a cross talk between GC and endothelial cells under hypoxia, partially through regulation of the VEGF expression. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:364‐369, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21498     

Mitochondrial reactive oxygen species originating from Romo1 exert an important role in normal cell cycle progression by regulating p27Kip1 expression

Reactive oxygen species (ROS) steady-state levels are required for entry into the S phase of the cell cycle in normal cells, as well as in tumour cells. However, the contribution of mitochondrial ROS to normal cell proliferation has not been well investigated thus far. A previous report showed that Romo1 was responsible for the high ROS levels in tumour cells. Here, we show that endogenous ROS generated by Romo1 are indispensable for cell cycle transition from G1 to S phase in normal WI-38 human lung fibroblasts. The ROS level in these cells was down-regulated by Romo1 knockdown, resulting in cell cycle arrest in the G1 phase. This arrest was associated with an increase in the level of p27^Kip1. These results demonstrate that mitochondrial ROS generated by Romo1 expression is required for normal cell proliferation and it is suggested that Romo1 plays an important role in redox signalling during normal cell proliferation.