Reports on the effects of PM2.5 from dust storm on lung cells are limited. We compared the effects of PM2.5 collected in dust storm days (dust storm PM2.5) with that in sunshiny and non-dust storm days (normal PM2.5) on cell proliferation and cell cycle in human lung fibroblasts. Our results showed that both dust storm and normal PM2.5 had biphasic effects on cell proliferation, namely, stimulated cell proliferation at lower concentrations while inhibited it at higher concentrations. On the contrary, the organic and inorganic extracts from dust storm and normal PM2.5 significantly inhibited the proliferation in human lung fibroblasts at the concentrations corresponding to their mass contents in PM2.5 samples. The flow cytometry showed that the number of cells in G2/M phase increased significantly after treatment with the dust storm and normal PM2.5. The inorganic and organic extracts from PM2.5, however, induced cell arrest in S phase and G0/G1 phase, respectively. It seems that the biphasic effects of both dust storm and normal PM2.5 on cell proliferation may not be related to their inorganic or organic extractable components.
"Möller and colleagues  reported effects on phagocytosis, phagosome transport mechanisms and cytoskeletal integrity. PAHs-rich PM0.2, produced by combustion of solid fuels, induced G2/M arrest in macrophages , while organic extracts from PM2.5 and PM10 arrested the cell cycle of different human cell lines in G0/G1 [22,51]. Several PAHs are able to alter the cell cycle in various ways; dibenzo[a,l]pyrene induces G2/M arrest in human mammary carcinoma MCF-7 cells , while it delays HEL fibroblasts in the S phase . "
[Show abstract][Hide abstract] ABSTRACT: This study explores and characterizes cell cycle alterations induced by urban PM2.5 in the human epithelial cell line BEAS-2B, and elucidates possible mechanisms involved.
The cells were exposed to a low dose (7.5 mug/cm2) of Milan winter PM2.5 for different time points, and the cell cycle progression was analyzed by fluorescent microscopy and flow cytometry. Activation of proteins involved in cell cycle control was investigated by Western blotting and DNA damage by 32P-postlabelling, immunostaining and comet assay. The formation of reactive oxygen species (ROS) was quantified by flow cytometry. The role of PM organic fraction versus washed PM on the cell cycle alterations was also examined. Finally, the molecular pathways activated were further examined using specific inhibitors.
Winter PM2.5 induced marked cell cycle alteration already after 3 h of exposure, represented by an increased number of cells (transient arrest) in G2. This effect was associated with an increased phosphorylation of Chk2, while no changes in p53 phosphorylation were observed at this time point. The increase in G2 was followed by a transient arrest in the metaphase/anaphase transition point (10 h), which was associated with the presence of severe mitotic spindle aberrations. The metaphase/anaphase delay was apparently followed by mitotic slippage at 24 h, resulting in an increased number of tetraploid G1 cells and cells with micronuclei (MN), and by apoptosis at 40 h. Winter PM2.5 increased the level of ROS at 2 h and DNA damage (8-oxodG, single- and double stand breaks) was detected after 3 h of exposure. The PM organic fraction caused a similar G2/M arrest and augmented ROS formation, while washed PM had no such effects. DNA adducts were detected after 24 h. Both PM-induced DNA damage and G2 arrest were inhibited by the addition of antioxidants and alpha-naphthoflavone, suggesting the involvement of ROS and reactive electrophilic metabolites formed via a P450-dependent reaction.
Milan winter PM2.5 rapidly induces severe cell cycle alterations, resulting in increased frequency of cells with double nuclei and MN. This effect is related to the metabolic activation of PM2.5 organic chemicals, which cause damages to DNA and spindle apparatus.
[Show abstract][Hide abstract] ABSTRACT: Silver nanoparticles (Ag NPs) are increasingly being used in wound dressings, medical settings, and various household products due to their unique properties and antimicrobial activity. Despite the widespread use of Ag NP products, the molecular mechanisms underlying the biological effects of Ag NPs remain unclear. Gap junctional intercellular communication (GJIC), formed by the connexin protein family, plays a critical role in the maintenance of tissue and organ homeostasis. This study was undertaken to investigate the effects of well characterized, PVP-coated Ag NPs (69 +/- 3 nm) and silver nitrate on GJIC and connexin43 (Cx43) expression in human lung adenocarcinoma cell line A549. Our results showed that Ag NPs increased GJIC in A549 cells as assayed by dye transfer method. Western blot analysis showed that incubation of cells with Ag NPs significantly increased the expression of Cx43 protein. In addition, Ag NPs up-regulated expression of Cx43 mRNA in a dose-dependent manner. Silver nitrate failed to increase GJIC and the expression of Cx43 protein. It, however, increased Cx43 mRNA expression in A549 cells. Taken together, our results provide the first evidence that Ag NPs induced the increase of GJIC activity in A549 cells through up-regulation of Cx43 protein, suggesting that Cx43 and GJIC may be one of the targets for Ag NPs biological effects.
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