RESUMEN
The objective of this study is to investigate the contributions of Mikania micrantha (chinese creeper) to remediate heavy metal pollutants present in an e-waste-contaminated soil. Different proportions of e-waste soil (0%, 25%, 50%, 75%, and 100% w/w) planted with Cynodon dactylon together with the test species were prepared for testing relative seed germination (RSG), relative root growth (RRG), and germination index (GI) tests. A significant higher value of GI (77.8%) was found in M. micrantha than that of the other species when planting in 100% e-waste-contaminated soil. A significant correlation (< 0.05) was found between heavy metal concentration and germination assays in M. micrantha. A significant decrease in heavy metal concentration of the polluted soil after the experiment indicated that biomolecule development studies to determine the aggregate benefit of M. micrantha for phytoremediation remain to be studied in future.
Asunto(s)
Residuos Electrónicos , Metales Pesados/metabolismo , Mikania/metabolismo , Contaminantes del Suelo/metabolismo , Biodegradación Ambiental , Germinación , Metales Pesados/análisis , Suelo , Contaminantes del Suelo/análisisRESUMEN
2-Deoxyglucose (2DG) is a non-metabolizable glucose analog currently in clinical trials to determine its efficacy in enhancing the therapeutic effects of radiotherapy and chemotherapy of several types of cancers. It is thought to preferentially kill cancer cells by inhibiting glycolysis because cancer cells are more dependent on glycolysis for their energy needs than normal cells. However, we found that the toxicity of 2DG in cancer cells is mediated by the enzymatic activities of AKR1B1 and/or AKR1B10 (AKR1Bs), which are often overexpressed in cancer cells. Our results show that 2DG kills cancer cells because, in the process of being reduced by AKR1Bs, depletion of their cofactor NADPH leads to the depletion of glutathione (GSH) and cell death. Furthermore, we showed that compounds that are better substrates for AKR1Bs than 2DG are more effective than 2DG in killing cancer cells that overexpressed these 2 enzymes. As cancer cells can be induced to overexpress AKR1Bs, the anticancer mechanism we identified can be applied to treat a large variety of cancers. This should greatly facilitate the development of novel anticancer drugs.