RESUMO
Urban yellow dust deposition is a common phenomenon in many parts of the world, which is sometimes called "sulfur shower," "sulfur rain," or "pollen storm." Most people, especially those living in the vicinity of industrial facilities, wrongly perceive the yellow dust as sulfur when in fact it is pollen. The misunderstanding increases risk perception as people believe the "yellow powder" is a serious threat to their health. Based on simple observations, it is virtually impossible to differentiate sulfur from pollen, so risk communication should consider the chemical, biological, and toxicological aspects of these agents. In this review, we clarify that industrial emissions of sulfur are under the form of sulfides, oxides, and other volatile compounds which are gaseous and noncolored, and we explain that it is chemically impossible for gaseous sulfur to become solid yellow sulfur under normal environmental conditions. We also describe pollen and its release from trees, shrubs, and herbs a process influenced by atmospheric conditions. We suggest take-home messages that risk communicators may use when explaining the phenomenon to their communities.
Assuntos
Poluentes Atmosféricos/toxicidade , Poeira/análise , Pólen/química , Enxofre/toxicidade , Poluentes Atmosféricos/análise , Comunicação , Humanos , Pólen/efeitos adversos , Chuva , Enxofre/análiseRESUMO
Few vaccine adjuvants have been approved for human use although several are currently being studied in preclinical and clinical trial. MPL is a toll-like receptor agonist able to trigger a high and persistent antibody response via-TLR-4 while QS-21 activates the NLRP3 inflammasome. Data suggest that there is a cross-talk between Notch and TLR signaling pathways modulating the polarization of the immune response in a MyD88-dependent manner. However, the role of Notch on the mechanism action of immunogenic adjuvants has not been addressed yet. This study aims to evaluate the in vitro toxicity and inflammatory response triggered by MPL and QS-21 using an in vitro human cell co-culture model and to determine whether NFκB or Notch signaling pathways are involved in their mechanism of immunotoxicity. In order to do this, we evaluated the effect of QS- 21/MPL alone or in combination using a co-culture of PBMC and HUVEC using cytotoxicity, surface expression of ECAMs, cell adhesion and cytokine release, NF-κB activation and NOTCH1 expression as observation endpoints. We found that both MPL and QS-21 were cytotoxic at concentrations over 5 µg/mL. Both adjuvants were able to trigger the expression of ECAMs and induce firm adhesion of PBMC to the endothelium. QS-21 and MPL combination demonstrated a synergistic effect on cellular recruitment and cytokine release generating a switch from Th2 to Th1 cytokine profile. Both MPL and QS-21 by themselves were able to generate significant NF-κB activation. However, this effect was not observed when both adjuvants were combined. On the contrary, the adjuvants alone and combined induced an overexpression of NOTCH-1. This is an important finding, as it provides new evidence that these adjuvants could modulate reactogenicity of vaccines through Notch signaling.
Assuntos
Adjuvantes Imunológicos/toxicidade , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Leucócitos Mononucleares/efeitos dos fármacos , Lipídeo A/análogos & derivados , Receptor Notch1/genética , Saponinas/toxicidade , Adesão Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Técnicas de Cocultura , Citocinas/metabolismo , Interações Medicamentosas , Células Endoteliais da Veia Umbilical Humana/fisiologia , Humanos , Leucócitos Mononucleares/fisiologia , Lipídeo A/toxicidade , NF-kappa B/metabolismoRESUMO
BACKGROUND: Epanorin (EP) is a secondary metabolite of the Acarospora lichenic species. EP has been found in lichenic extracts with antimicrobial activity, and UV-absorption properties have been described for closely related molecules; however, its antiproliferative activity in cancer cells has not yet been explored. It has been hypothesized that EP inhibits cancer cell growth. MCF-7 breast cancer cells, normal fibroblasts, and the non-transformed HEK-293 cell line were exposed to increasing concentrations of EP, and proliferation was assessed by the sulforhodamine-B assay. RESULTS: MCF-7 cells exposed to EP were examined for cell cycle progression using flow cytometry, and DNA fragmentation was examined using the TUNEL assay. In addition, EP's mutagenic activity was assessed using the Salmonella typhimurium reverse mutation assay. The data showed that EP inhibits proliferation of MCF-7 cells, and it induces cell cycle arrest in G0/G1 through a DNA fragmentation-independent mechanism. Furthermore, EP's lack of overt cytotoxicity in the normal cell line HEK-293 and human fibroblasts in cell culture is supported by the absence of mutagenic activity of EP. CONCLUSION: EP emerges as a suitable molecule for further studies as a potential antineoplastic agent.
Assuntos
Antineoplásicos/uso terapêutico , Apoptose/efeitos dos fármacos , Neoplasias da Mama/tratamento farmacológico , Proliferação de Células/efeitos dos fármacos , Líquens/química , Antineoplásicos/isolamento & purificação , Fragmentação do DNA , Feminino , Citometria de Fluxo , Humanos , Células MCF-7RESUMO
BACKGROUND: Epanorin (EP) is a secondary metabolite of the Acarospora lichenic species. EP has been found in lichenic extracts with antimicrobial activity, and UV-absorption properties have been described for closely related molecules; however, its antiproliferative activity in cancer cells has not yet been explored. It has been hypothesized that EP inhibits cancer cell growth. MCF-7 breast cancer cells, normal fibroblasts, and the non-transformed HEK-293 cell line were exposed to increasing concentrations of EP, and proliferation was assessed by the sulforhodamine-B assay. RESULTS: MCF-7 cells exposed to EP were examined for cell cycle progression using flow cytometry, and DNA fragmentation was examined using the TUNEL assay. In addition, EP's mutagenic activity was assessed using the Salmonella typhimurium reverse mutation assay. The data showed that EP inhibits proliferation of MCF-7 cells, and it induces cell cycle arrest in G0/G1 through a DNA fragmentation-independent mechanism. Furthermore, EP's lack of overt cytotoxicity in the normal cell line HEK-293 and human fibroblasts in cell culture is supported by the absence of mutagenic activity of EP. CONCLUSION: EP emerges as a suitable molecule for further studies as a potential antineoplastic agent.
Assuntos
Humanos , Feminino , Neoplasias da Mama/tratamento farmacológico , Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Líquens/química , Antineoplásicos/uso terapêutico , Fragmentação do DNA , Células MCF-7 , Citometria de Fluxo , Antineoplásicos/isolamento & purificaçãoRESUMO
The use of statistical distributions to predict air quality is valuable for determining the impact of air chemical contaminants on human health. Concentrations of air pollutants are treated as random variables that can be modeled by a statistical distribution that is positively skewed and starts from zero. The type of distribution selected for analyzing air pollution data and its associated parameters depend on factors such as emission source and local meteorology and topography. International environmental guideline use appropriate distributions to compute exceedance probabilities and percentiles for setting administrative targets and issuing environmental alerts. The distribution bears a relationship to the normal distribution, and there are theoretical - and physical-based mechanistic arguments that support its use when analyzing air-pollutant data. Others distribution have also been used to model air population data, such as the beta, exponential, gamma, Johnson, log-logistic, Pearson, and Weibull distribution. One model also developed from physical-mechanistic considerations that has received considerable interest in recent year is the Birnbaum-Saunders distribution. This distribution has theoretical arguments and properties similar to those of the log-normal distribution, which renders it useful for modeling air contamination data. In this review, we have addressed the range of common atmospheric contaminants and the health effects they cause. We have also reviewed the statistical distributions that have been use to model air quality, after which we have detailed the problem of air contamination in Santiago, Chile. We have illustrated a methodology that is based on the Birnbaum-Saunders distributions to analyze air contamination data from Santiago, Chile. Finally, in the conclusions, we have provided a list of synoptic statements designed to help readers understand the significance of air pollution in Chile, and in Santiago, in particular, but that can be useful to other cites and countries.
Assuntos
Poluentes Atmosféricos/química , Tamanho da Partícula , Poluentes Atmosféricos/toxicidade , Chile , HumanosRESUMO
BACKGROUND: Approximately 15% of misoprostol-induced-abortions may not be successful, leading to in utero exposure to the drug and to the induction of a series of defects including central nervous system, limb and visceral defects. A common proposal is that the drug causes disruption of the fetal vasculature leading to embryonic or fetal hypoxia. AIM: To evaluate the teratogenicity of misoprostol using the rat post-implantation embryo culture. MATERIAL AND METHODS: Rat embryos were collected at the beginning of organogenesis and cultured in rat serum containing misoprostol at concentrations of 200, 2,000 or 20,000 pg/ml. Functionality, morphology and morphometry parameters were evaluated. RESULTS: Misoprostol induced a dose-dependent embryotoxic effect causing a decrease in embryo viability and function (poor vascular development and survival) and morphometry (alterations in branchial arches, heart and cephalic portions of the neural tube, among others). CONCLUSIONS: All the manifestations observed are indicative of the ability of misoprostol to directly induce developmental retardation and alterations.
Assuntos
Anormalidades Induzidas por Medicamentos/embriologia , Abortivos não Esteroides/toxicidade , Embrião de Mamíferos/efeitos dos fármacos , Misoprostol/toxicidade , Animais , Embrião de Mamíferos/anormalidades , Feminino , Testes de Mutagenicidade/métodos , Gravidez , Ratos , Ratos Sprague-DawleyRESUMO
Background: Approximately 15 percent of misoprostol-induced-abortions may not be successful, leading to in utero exposure to the drug and to the induction of a series of defects including central nervous system, limb and visceral defects. A commonproposal is that the drug causes disruption of the fetal vasculature leading to embryonic or fetal hypoxia. Aim: To evaluate the teratogenicity of misoprostol using the rat post-implantation embryo culture. Material and Methods: Rat embryos were collected at the beginning of organogenesis and cultured in rat serum containing misoprostol at concentrations of 200, 2,000 or 20,000 pg/ml. Functionality, morphology and morphometry parameters were evaluated. Results: Misoprostol induced a dose-dependent embryotoxic effect causing a decrease in embryo viability and function (poor vascular development and survival) and morphometry (alterations in branchial arches, heart and cephalic portions of the neural tube, among others). Conclusions: All the manifestations observed are indicative of the ability of misoprostol to directly induce developmental retardation and alterations.