Synthesis, characterization, and evaluation of antimicrobial and cytotoxic effect of silver and titanium nanoparticles.

Microbial resistance represents a challenge for the scientific community to develop new bioactive compounds. Nosocomial infections represent an enormous emerging problem, especially in patients with ambulatory treatment, which requires that they wear medical devices for an extended period of time. In this work, an evaluation of the antimicrobial activity of both silver and titanium nanoparticles was carried out against a panel of selected pathogenic and opportunistic microorganisms, some of them commonly associated with device-associated infections. Cytotoxicity assays monitoring DNA damage and cell viability were evaluated using human-derived monocyte cell lines. We show that silver-coated nanoparticles having a size of 20-25 nm were the most effective among all the nanoparticles assayed against the tested microorganisms. In addition, these nanoparticles showed no significant cytotoxicity, suggesting their use as antimicrobial additives in the process of fabrication of ambulatory and nonambulatory medical devices. FROM THE CLINICAL EDITOR: In this study, antimicrobial activity of silver and titanium nanoparticles was evaluated against a panel of selected pathogenic and opportunistic microorganisms. Silver-coated nanoparticles of 20-25 nm size were the most effective among all the nanoparticles without significant cytotoxicity, suggesting their use as antimicrobial additives in the process of fabrication of ambulatory and nonambulatory medical devices.

Neocarzinostatin induces an effective p53-dependent response in human papillomavirus-positive cervical cancer cells.

Human papillomavirus (HPV) E6 viral oncoprotein plays an important role during cervical carcinogenesis. This oncoprotein binds the tumor suppressor protein p53, leading to its degradation via the ubiquitin-proteasome pathway. Therefore, it is generally assumed that in HPV-positive cancer cells p53 function is completely abolished. Nevertheless, recent findings suggest that p53 activity can be recovered in cells expressing endogenous E6 protein. To investigate whether p53-dependent functions controlling genome integrity, cell proliferation, and apoptosis can be reactivated in cervical cancer cells, we examined the capacity of HeLa, INBL, CaSki, C33A, and ViBo cell lines to respond to neocarzinostatin (NCS), a natural product which induces single- and double-strand breaks in DNA. We found that NCS treatment inhibits cellular proliferation through G2 cell cycle arrest and apoptosis induction. This effect was preceded by nuclear accumulation of p53 protein and by an increase of p21 transcripts. Although apoptosis was blocked in ViBo cells (HPV-negative), nuclear accumulation of transcriptionally active p53 and inhibition of cell proliferation are observed after NCS treatment. These results suggest that HPV-positive cervical cancer cells are capable of responding efficiently to DNA damage provoked by NCS treatment through a p53-dependent pathway in spite of the presence of E6 protein.