Non‐small lung cell carcinoma has a high morbidity and mortality rates. The elective treatment for stage III and IV is cisplatinum that conveys serious toxic side effects. Vanadium compounds are metal molecules with proven antitumor activity that depends on its valence. Therefore, a better understanding of the mechanism of action of vanadium compounds is required. The aim of our study was to investigate the mechanisms of cell death induced by sodium metavanadate (NaVO3 [V(+5)]) and vanadyl sulfate (VOSO4 [(+4)]), both of which have reported apoptotic‐inducing activity. We exposed the A549 cell line to various concentrations (0‐100 μM) and to different exposure times to each compound and determined the cell viability and expression of caspases, reactive oxygen species (ROS) production, Bcl2, Bax, FasL and NO. Our results showed that neither compounds modified the basal expression of caspases or pro‐ and anti‐apoptotic proteins. The only change observed was the 12‐ and 14‐fold significant increase in ROS production induced by NaVO3 and VOSO4, respectively, at 100 μm concentrations after 48 hours. Our results suggest that classical apoptotic mechanisms are not related to the cell death induced by the vanadium compounds evaluated here, and showed that the higher ROS production was induced by the [(+4)] valence compound. It is possible that the difference will be secondary to its higher oxidative status and thus higher ROS production, which leads to higher cell damage. In conclusion, our results suggest that the efficacy of the cell death mechanisms induced by vanadium compounds differ depending on the valence of the compound.
Exposure to arsenic in drinking water is a worldwide health problem. This pollutant is associated with increased risk of developing chronic diseases, including metabolic diseases. Metabolic syndrome (MS) is a complex pathology that results from the interaction between environmental and genetic factors. This condition increases the risk of developing type 2 diabetes, cardiovascular diseases, and cancer. The MS includes at least three of the following signs, central obesity, impaired fasting glucose, insulin resistance, dyslipidemias, and hypertension. Here, we summarize the existing evidence of the multiple mechanisms triggered by arsenic to developing the cardinal signs of MS, showing that this pollutant could contribute to the multifactorial origin of this pathology.
Air pollution is a worldwide health problem, and metals are one of the various air pollutants to which living creatures are exposed. The pollution by metals such as: lead, cadmium, manganese, and vanadium have a common mechanism of action: the production of oxidative stress in the cell. Oxidative stress favors the production of free radicals, which damage biomolecules such as: DNA, proteins, lipids, and carbohydrates; these free radicals produce changes that are observed in different organs and systems. Vanadium is a transition element delivered into the atmosphere by the combustion of fossil fuels as oxides and adhered to the PM enters into the respiratory system, then crosses the alveolar wall and enters into the systemic circulation. In this chapter, we will review the oxidative stress induced by vanadium-as a common mechanism of metal pollutants-; in addition, we will review the protective effect of the antioxidants (carnosine and ascorbate).
Se evaluó la cito/genotoxicidad en sangre periférica de ratones CD-1 expuestos a diferentes variedades de vino tinto (Cabernet Sauvignon, Merlot, Carménère y Cabernet Sauvignon/Nebbiolo). Grupos de cinco organismos fueron tratados: a) con el vehículo, b) vino tinto o etanol (diluidos al 75 y 10%, respectivamente) ad libitum, y c) vino tinto sin diluir o etanol diluido al 13.5% (dos dosis diarias-0.25 ml, vía i.g.). La genotoxicidad se evaluó con los micronúcleos (MN) y la citotoxicidad con la relación entre eritrocitos policromáticos/normocromáticos (EPC/ENC) a las 0, 24, 48 y 72 h. Solo se observaron incrementos significativos en los MN con los tratamientos i.g de Cabernet Sauvignon, Merlot y etanol, siendo mayor para el etanol. La administración ad libitum de los vinos tintos redujo los MN. Nuestros hallazgos sugieren que los efectos genotóxicos del vino tinto podrían estar relacionados con la biodisponibilidad, farmacodinámica y farmacocinética del etanol. No se observaron efectos citotóxicos.
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