The ROS generation was evidenced here for HepG2 cells and PBMC incubated with both types of nanoparticles for 24 h, as shown in Fig. 3a and b, respectively. For both PBMC and HepG2 cells, a significant increase in the ROS generation was observed
upon incubation with citrate and PAMAM-covered AuNps (Fig. 3a and b). The cellular oxidative stress increased in both cell lines may be directly correlated with AuNps exposure, homologous Ribociclib mouse to an increase in cytotoxicity. Taken together, our findings suggest that the exposure of HepG2 cells and PBMC to AuNps-PAMAM and AuNps-citrate might lead to the disturbance of cells with cytotoxic effects and DNA damage. The correlation between the toxic effects of Au nanoparticles with their physico-chemical and surface properties may be an important step forward to the application of these nanomaterials in cancer treatment. Our results from the comet assay, for example, revealed that the immune system cells (PBMC) were less sensitive to DNA damage than cancer
HepG2 cells, upon exposure to AuNps. The latter is an indicative that nanoparticulate systems may be applied in cancer therapy with reduced side effects in the future studies. The authors declare that there is no conflict of interest regarding the work reported in this paper. The authors are grateful to Mrs. Derminda Isabel de Moraes, Ms. Andressa Patricia Alves Pinto (IFSC-USP), Mrs. Joana Darc Castania Darin and Dr. Regislaine Valeria Burim (FCFRP-USP) for their excellent technical assistance. Dr. Ana M Souza is also acknowledged for her assistance on the flow cytometry analyses. This work was supported by CNPq and FAPESP. “
“The authors of the above Enzalutamide order article would like to apologise for a mistake which is present in Fig. 1B. In Fig. 1B, the data for fetal CORT should be multiplied by 15. A
corrected version of this figure is below: “
“Carcinogenesis is recognized as a multi-stage process (Yamasaki, 1986, Trosko et al., 2004 and Sun and Liu, 2005). The operational process of tumor development comprises three stages: exposure to an initiating substance, which has a mutagenic effect on DNA (initiation stage); proliferation of the cells with the mutated genome (promotion stage); deregulated cellular proliferation, PRKACG resulting in an invasive and metastatic tumor profile (progression stage) (Trosko et al., 2004). A breakdown of cellular communication during the promotion stage has been linked to the later progression of tumors. Specifically, a breakdown in gap-junctional intercellular communication (GJIC) will remove a cell from the growth suppression influence of its neighboring cells (Chipman et al., 2003), leading to the deregulated cell proliferation (Sun and Liu, 2005 and Yamasaki et al., 1999) and metastatic profile (Trosko et al., 2004) characteristic of the progression stage of carcinogenesis. Moreover, the inhibition of GJIC is a typical feature of non-genotoxic carcinogens (i.e., TPA).