Highly effective decontamination in a hospital environment: An easy-to-operate, low-cost prototype.

Healthcare-associated infections (HAI) are illnesses acquired during healthcare and are often the most important adverse event during healthcare. With the aim of increasing the effectiveness of disinfection/decontamination processes in the health service with safe and not promote microbial resistance, we propose the development of portable equipment associated with type C ultraviolet light (UVC). The efficiency of the irradiance emitted by the equipment (at dosages 3.5, 5.0, and 60 mJ/cm2) was determined by the action exerted after exposure against four different bacterial (Acinetobacter baumannii, Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus) and three different fungi (Candida albicans, C. parapsilosis, and Aspergillus section Fumigati). It was possible to observe that all treatments were capable of inactivating the bacterial species evaluated (p < 0.05), causing the irreversible death of these microorganisms. The most effective elimination of fungal agents was at a dose of 60 mJ/cm2 of UVC radiation, with a decrease in the fungal inoculum varying between 94% and 100% in relation to the control without exposure. Thus, our study showed that the application of the portable prototype with UVC light (254 nm) at a distance of 48 mm, allowed an average irradiance of 3.5 mW/cm2, with doses of 3.5 ≈ 60 mJ/cm2 (from 1 to 60 s of exposure), which can promote the total reduction of the bacteria evaluated and significantly reduce fungal growth. Therefore, this prototype could be used safely and effectively in the hospital environment, considerably reducing contamination and contributing to the reduction of healthcare-associated infection risk.

C-Phycocyanin: Cellular targets, mechanisms of action and multi drug resistance in cancer.

C-Phycocyanin (C-PC) has been shown to be promising in cancer treatment; however, although several articles detailing this have been published, its main mechanisms of action and its cellular targets have not yet been defined, nor has a detailed exploration been conducted of its role in the resistance of cancer cells to chemotherapy, rendering clinical use impossible. From our extensive examination of the literature, we have determined as our main hypothesis that C-PC has no one specific target, but rather acts on the membrane, cytoplasm, and nucleus with diverse mechanisms of action. We highlight the cell targets with which C-PC interacts (the MDR1 gene, cytoskeleton proteins, and COX-2 enzyme) that make it capable of killing cells resistant to chemotherapy. We also propose future analyses of the interaction between C-PC and drug extrusion proteins, such as ABCB1 and ABCC1, using in silico and in vitro studies.

Anti-MDR and antitumoral action of acetylsalicylic acid on leukaemic cells.

ASA (acetylsalicylic acid) is an NSAID (non-steroidal anti-inflammatory drug). ASA has gained attention as a potential chemopreventive and chemotherapeutic agent for several neoplasms. The aim of this study was to analyse the possible antitumoural effects of ASA in two erythroleukaemic cell lines, with or without the MDR (multidrug resistance) phenotype. The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression. ASA inhibited the cellular proliferation or induced toxicity in K562 and Lucena cell lines, irrespective of the MDR phenotype. The ASA treatment provoked death by apoptosis and necrosis in K562 cells and only by necrosis in Lucena cells. ASA also showed antioxidant activity in both cell lines. The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression. However, normal lymphocytes treated with the same ASA concentrations were more resistant than tumoral cells. The results of this work show that both cell lines responded to treatment with ASA, demonstrating a possible antitumoral and anti-MDR role for this drug.

Nitric oxide-dependent pigment migration induced by ultraviolet radiation in retinal pigment cells of the crab Neohelice granulata.

The purpose of this study was to verify the occurrence of pigment dispersion in retinal pigment cells exposed to UVA and UVB radiation, and to investigate the possible participation of a nitric oxide (NO) pathway. Retinal pigment cells from Neohelice granulata were obtained by cellular dissociation. Cells were analyzed for 30 min in the dark (control) and then exposed to 1.1 and 3.3 J cm(-2) UVA, 0.07 and 0.9 J cm(-2) UVB, 20 nmß-PDH (pigment dispersing hormone) or 10 µm SIN-1 (NO donor). Histological analyses were performed to verify the UV effect in vivo. Cultured cells were exposed to 250 µm L-NAME (NO synthase blocker) and afterwards were treated with UVA, UVB or ß-PDH. The retinal cells in culture displayed significant pigment dispersion in response to UVA, UVB and ß-PDH. The same responses to UVA and UVB were observed in vivo. SIN-1 did not induce pigment dispersion in the cell cultures. L-NAME significantly decreased the pigment dispersion induced by UVA and UVB but not by ß-PDH. All retinal cells showed an immunopositive reaction against neuronal nitric oxide synthases. Therefore, UVA and UVB radiation are capable of inducing pigment dispersion in retinal pigment cells of Neohelice granulata and this dispersion may be nitric oxide synthase dependent.

Influence of the dark/light rhythm on the effects of UV radiation in the eyestalk of the crab Neohelice granulata.

Crustaceans are interesting models to study the effects of ultraviolet (UV) radiation, and many species may be used as biomarkers for aquatic contamination of UV radiation reaching the surface of the Earth. Here, we investigated cell damage in the visual system of crabs Neohelice granulata that were acclimated to either 12L:12D, constant light, or constant dark, and were exposed to UVA or UVB at 12:00h (noon). The production of reactive oxygen species (ROS), antioxidant capacity against peroxyl radicals (ACAP), lipid peroxidation (LPO) damage, catalase activity, and pigment dispersion in the eye were evaluated. No significant differences from the three groups of controls (animals acclimated to 12L:12D, or in constant light, or not exposed to UV radiation) were observed in animals acclimated to 12L:12D, however, crabs acclimated to constant light and exposed to UV radiation for 30min showed a significant increase in ROS concentration, catalase activity, and LPO damage, but a decrease in ACAP compared with the controls. Crabs acclimated to constant darkness and exposed to UV for 30min showed a significantly increased ROS concentration and LPO damage, but the ACAP and catalase activity did not differ from the controls (animals kept in the dark while the experimental group was being exposed to UV radiation). Pigment dispersion in the pigment cells of eyes of animals acclimated to constant light was also observed. The results indicate that UVA and UVB alter specific oxidative parameters; however, the cell damage is more evident in animals deviated from the normal dark/light rhythm.

Photodynamic action of benzo[a]pyrene in K562 cells.

Benzo[a]pyrene (BaP) is ubiquitously distributed in the environment, being considered the most phototoxic element among polycyclic aromatic hydrocarbon (PAHs). In presence of oxygen, PAHs can act as a photosensitizer by means of promoting photo-oxidation of biological molecules (photodynamic action, PDA). Thus, the present study analyzed the photodynamic action of BaP under UVA irradiation (BaP + UVA) and its oxidative effects on K562 cells. The evaluation of BaP kinetics showed that the highest intracellular concentration occurred after 18 h of incubation. Cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, DNA damage (breaks and DNA-protein cross-link [DNAPC]) were assessed after exposure to BaP, UVA and BaP plus UVA irradiation (BaP + UVA). Cell viability was decreased just after exposure to BaP + UVA. Lipid peroxidation and DNA breaks increased after BaP + UVA exposure, while the DNAPC increased after BaP, UVA and BaP + UVA exposure, suggesting that BaP + UVA effects were a consequence of both type II (producing mainly singlet oxygen) and type I (producing others ROS) mechanisms of PDA.