Lysosome and proteasome pathways are distributed in laticifers of Euphorbia helioscopia L.

At present, the lysosome pathway (LP) and proteasome pathway (PP) are known as major clearance systems in eukaryotic cells. The laticifer, a secretory tissue, degrades some cytoplasm during development. In this study, we investigated the distribution of LP and PP in non-articulated laticifers of Euphorbia helioscopia L. Electron microscopy revealed that, plastids, mitochondria and some cyotsol were degraded in the late development laticifers, where there were numerous vesicles originated from dicytosomes. Accordingly, some key proteins in LP and PP were detected in E. helioscopia latex using isobaric tags for relative and absolute quantitation (iTRAQ) proteomics. Further immunohistochemistry analysis revealed that the clathrin heavy chain (CHC) belonging to LP and the ubiquitin-mediated proteasome degradation increases gradually as the laticifer develops. Immuno-electron microscopy revealed that the cysteine protease, CHC and AP-2 complex subunit beta-1 belonging to LP were mainly distributed in vesicles deriving from dicytosomes, which we called lysosome-like vesicles. Ubiquitin was widely distributed in the cytosol, and proteasome activity was significantly reduced when various concentrations of the inhibitor MG132 were added to the latex total protein. We hypothesize that LP and PP are distributed in E. helioscopia laticifers; and it was speculated that LP and PP might be involved in the degradation of organelles and some cytoplasmic matrix in E. helioscopia laticifers.

Single-wall carbon nanotubes induce oxidative stress in rat aortic endothelial cells.

Oxidative stress is a major factor contributing to endothelial cell damage. Single-wall carbon nanotubes (SWCNTs) have oxidative properties; however, the oxidative effects of SWCNTs on endothelial cells are not fully understood. In the present study, we investigated the effects of oxidative stress induced by SWCNTs on rat aortic endothelial cells (RAECs). Various markers of cellular damage were assessed, such as biochemical and ES immunity indexes, and DNA and protein damage. Our findings suggest that RAEC endured oxidative damage following SWCNT exposure. Specifically, after SWCNTs exposure, non-enzymatic antioxidant glutathione was activated prior to superoxide dismutase activation in order to defend against oxidative stress. Additionally, it was found that as SWCNT concentration increased, so did the stress protein, heme oxygenase-1 (HO-1), expression levels. These changes may induce RAEC damage, and result in many serious diseases.

Single-walled carbon nanotube induction of rat aortic endothelial cell apoptosis: Reactive oxygen species are involved in the mitochondrial pathway.

The use of nano-sized materials offers exciting new options in technical and medical applications. Single-walled carbon nanotubes are emerging as technologically important in different industries. However, adverse effects on cells have been reported and this may limit their use. We previously found that 200µg/mL of single-walled carbon nanotubes induce apoptosis in rat aorta endothelial cells. The current study aimed to determine the signaling pathway involved in this process. We found that reactive oxygen species generation was involved in activation of the mitochondria-dependent apoptotic pathway. The finding of apoptosis was supported by a number of morphological and biochemical hallmarks, including chromatin condensation, internucleosomal DNA fragmentation, and caspase-3 activation. In conclusion, our results demonstrate that single-walled carbon nanotubes induce apoptosis in rat aorta endothelial cells and that reactive oxygen species are involved in the mitochondrial pathway.