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Resumen El sentido del gusto tiene un papel importante porque ha permitido discriminar entre lo que puede ser alimento y lo que no, e incluso en lo que puede ser tóxico o peligroso al ingerirlo. La búsqueda de nuevos sabores está presente en toda la historia de la humanidad. Desde la antigüedad, las especias aportaron nuevas experiencias gustativas para hacer más palatables los alimentos o incluso para conservarlos durante más tiempo. La búsqueda de especias fue una motivación para realizar viajes que llevaron a descubrimiento de nuevas tierras y continentes. Más recientemente, la pandemia por un virus que altera los sentidos del olfato y del gusto, nos ha hecho recordar la importancia de estos sentidos. El sentido del gusto está determinado por unas pequeñas estructuras que se ubican en las papilas linguales. Hay cuatro tipos que definen cinco sabores y uno que aún está en duda. Las alteraciones de este sentido tienen varios posibles orígenes que se comentan en esta revisión.

Abstract Taste is relevant because it has allowed us to discriminate between what is food and what is not, and even what can be toxic or dangerous when ingested. The search for new flavors is present in history of mankind. Since ancient times, the spices provided new taste experiences to make meals more palatable or as a means of preserving food; the search for spices was a motivation to make voyages that led to the discovery of new lands and continents. More recently, a viral pandemic that damages the olfaction and taste senses made us to remember the relevance of the senses. Small structures, called taste buds, located in the papillae of the tongue are responsible of the sense of taste. There are four types of taste buds that identify five tastes and one whose existence has not yet been fully proven. Taste alterations have different etiologies which will be commented on this review.

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Resumen Se calcula que el cuerpo humano está conformado por billones de células, las cuales sufren cientos de miles de lesiones al día en su DNA. Aunque el DNA no es la única biomolécula que sufre daños, su importancia radica en que es la única que no puede ser sustituida por la célula, así que, cuando esta sufre daños, la célula debe repararlos, tolerarlos o, en el caso extremo, activar las vías que la llevarán a la muerte, ya que lo importante es mantener la integridad celular y la homeostasis del organismo. Hay miles de agentes que pueden dañar al DNA, algunos los produce la misma célula y se les denomina 'agentes endógenos', mientras que otros son agentes externos y se les conoce como 'agentes exógenos'. La célula no puede evitar el daño causado por los agentes endógenos, ya que son productos de la actividad metabólica, por ejemplo; así que, cuando suceden se activan de forma inmediata los mecanismos celulares para mitigarlos. Lo mismo pasa con los daños causados por agentes exógenos, ya que la célula hará todo lo posible por disminuir los efectos adversos que pueden causar. El problema se pone de manifiesto cuando la célula no puede reparar los daños o los repara mal o son tantos que los mecanismos de reparación se ven rebasados, es entonces cuando el daño permanece en el DNA y se genera un estado de inestabilidad cromosómica que puede conducir a la célula a la disfunción y a la malignización. Este estado de inestabilidad cromosómica se puede ver reflejado en el aumento de rompimientos de DNA o de micronúcleos en las células expuestas, lo que se puede cuantificar por medio de métodos especiales como el 'Ensayo Cometa' y el 'Ensayo de Micronúcleos', ya que identificar el daño en el DNA es una forma de evaluar el potencial tóxico que tienen los agentes a los que están expuestas las poblaciones, permite conocer los mecanismos de acción que tienen y, además, ayuda a comprender los factores que influyen en el detrimento de la salud poblacional.

Abstract It is estimated that the human body is made of trillions of cells, which suffer hundreds of thousands of DNA lesions every day. Although DNA is not the only biomolecule that suffers damage, its importance lies in the fact that it is the only biomolecule that cannot be replaced by the cell, so when it suffers damage, the cell must repair it, tolerate or, in a extreme case, activate pathways that will lead to death, since the objective is to maintain cell integrity and the homeostasis of the organism.There are thousands of agents that can damage DNA, some are produced by the cell and are called 'endogenous, while others are external agents and are known as 'exogenous. The cell cannot avoid the damage caused by endogenous agents, since they are products of its metabolic activity, for example, so when they occur, cellular mechanisms are immediately activated to mitigate them. The same happens with the damage caused by exogenous agents, since the cell will do everything possible to diminish the adverse effects they can cause. The problem becomes apparent when the cell is unable to repair the damage or poorly repairs it, or repairs so much that the mechanisms are overwhelmed, when the damage remains in the DNA and a state of chromosomal instability is generated that can lead the cell to dysfunction and malignization. This state of chromosomal instability can be reflected in increased DNA breaks or micronuclei in exposed cells, which can be quantified by special methods such as the 'Comet Assay' and the 'Micronucleus Assay'. Since identifying DNA damage is a way of evaluating the toxic potential of the agents to which populations are exposed, it allows us to know their mechanisms of action and helps to understand the factors that influence the detriment in population's health.

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Resumen El endotelio es una monocapa formada por células aplanadas llamadas w, que revisten la parte más interna del corazón, los vasos sanguíneos y los linfáticos. Es considerado un órgano que tiene una función de barrera, pero además se encarga de regular la permeabilidad y tono vascular, hemostasia, inflamación y angiogénesis. Esta revisión se centra sobre todo en las generalidades del endotelio vascular sano y su disfunción. Se analizan los conceptos de activación y disfunción, en donde la activación se considera como un proceso autolimitado, indispensable para la hemostasia y la inflamación. La disfunción endotelial, en cambio, es un proceso patológico, de mayor duración y que se presenta cuando el endotelio ya no puede autorregularse y cambia a un fenotipo proinflamatorio y protrombótico permanente. Esta disfunción es el primer cambio que lleva a la ateroesclerosis y al aumento del riesgo cardiovascular, por esta razón se revisan los principales biomarcadores de disfunción endotelial y riesgo cardiovascular. A medida que se avance en el conocimiento básico del endotelio y su disfunción, será posible diseñar nuevas medidas preventivas o terapéuticas que puedan disminuir dicho riesgo.

Abstract The endothelium is a monolayer of flatten cells named endothelial cells that form the inner layer of the heart, blood, and lymphatic vessels. Its function is not just as a barrier, but it is a regulator of vascular permeability and tone, hemostasis, inflammation, and angiogenesis. This review is about the general aspects of vascular endothelium and endothelial dysfunction that leads to increased vascular risk. Activation and dysfunction are discussed, considering the endothelial activation as a self-limiting process, necessary to promote inflammation and hemostasis. Endothelial dysfunction is a pathological process in which the endothelium loses its ability for self-regulation and acquires a prothrombotic and proinflammation phenotype. Endothelial dysfunction is the initial step for atherosclerosis and increased cardiovascular risk, so the main biomarkers of endothelial dysfunction are reviewed. As basic knowledge about endothelium increases, preventive or therapeutic measures can be designed as treatment or prevention the risk of its dysfunction.

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Environmental pollution is a worldwide problem recognized by the World Health Organization as a major health risk factor that affects low-, middle- and high-income countries. Suspended particulate matter is among the most dangerous pollutants, since it contains toxicologically relevant agents, such as metals, including vanadium. Vanadium is a transition metal that is emitted into the atmosphere especially by the burning of fossil fuels to which dwellers are exposed. The objective of this literature review is to describe the toxic effects of vanadium and its compounds when they enter the body by inhalation, based especially on the results of a murine experimental model that elucidates the systemic effects that vanadium has on living organisms. To achieve this goal, we reviewed 85 articles on the relevance of vanadium as a component of particulate matter and its toxic effects. Throughout several years of research with the murine experimental model, we have shown that this element generates adverse effects in all the systems evaluated, because it causes immunotoxicity, hematotoxicity, neurotoxicity, nephrotoxicity and reprotoxicity, among other noxious effects. The results with this experimental model add evidence of the effects generated by environmental pollutants and increase the body of evidence that can lead us to make more intelligent environmental decisions for the welfare of all living beings.

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The aim of this report was to evaluate the morphological and biochemical changes in the liver by the inhalation of vanadium and consumption of sweetened beverages in a subchronic murine model. Forty CD-1 male mice were randomly divided into four groups: control, vanadium (V), sucrose 30% (S), and vanadium-sucrose (V + S). V was inhaled (1.4 mg/m3) for 1h, twice/week; 30% sucrose solution was given orally ad libitum. Blood samples were obtained for AST, ALT, and LDH determination. Liver samples were processed for histological and oxidative stress immunohistochemical evaluation with 4-hydroxynonenal at weeks 4 and 8 of exposure. Regarding liver function tests, a statistically significant increase (P < 0.05) was observed in groups V, S, and V + S at weeks 4 and 8 compared to the control group. A greater number of hepatocytes with meganuclei and binuclei were observed in V and V + S at week 8 compared to the other groups. Steatosis and regenerative changes were more extensive in the eighth week V + S group. 4-Hydroxynonenal immunoreactivity increased in the V + S group at both exposure times compared to the other groups; however, the increment was more evident in the V + S group at week 4 compared to the V + S group at week 8. An increase in De Ritis ratio (>1) was noticed in experimental groups at weeks 4 and 8. Findings demonstrate that in the liver, V, S, and V + S induced oxidative stress and regenerative changes that increased with the length of exposure. Results support possible potentiation of liver damage in areas with high air pollution and high-sweetened beverage consumption.

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Air pollution is a worldwide public health issue and it is associated with millions of premature deaths due to cancer, thrombosis, and pulmonary and cardiovascular diseases. Thrombosis is the excessive clotting that blocks a blood vessel, and its etiology is multifactorial. In recent years, growing evidence has linked air pollution, especially particulate matter (PM) and metals, to the development of thrombosis. PM and metals induce lung and systemic inflammation and oxidative stress that are frequent mechanisms in thrombosis. Platelets are important effectors of physiological hemostasis and pathological thrombosis. They are responsible for the formation of the initial plug and are important in the cellular model of coagulation. Therefore, any changes in their morphology or function or an increase in activation could be extremely relevant in thrombosis. Megakaryocytes (MKs) in the bone marrow and in the lungs are the precursor cells of platelets, and the latter is the first organ injured by air pollution. There is substantial evidence of the effect that PM and metals have on platelets, but there is almost no research about the effect of PM and metals on MKs. It is very likely that the alterations produced by air pollution originate in these cells. In this article, we review the biology of MKs and platelets and their role in particulate air pollution-related thrombosis to emphasize the need for further research in this field.

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Resumen La pandemia de la enfermedad COVID-19, ocasionada por el virus Sars-CoV-2, ha preocupado al personal de salud, entre otras cosas, por la alta incidencia de coagulopatía asociada a aumento en la mortalidad que se presenta en los pacientes. La coagulopatía es principalmente trombótica, inicialmente en pulmón y posteriormente sistémica, macro y microvascular, asociada al daño endotelial, inflamación, trampas extracelulares de neutrófilos (NETs), activación de macrófagos y tormenta de citocinas que perpetúan el círculo vicioso de trombosis e inflamación. Se ha reportado el aumento de factores protrombóticos en los pacientes: aumento del factor tisular, factor de Von Willebrand, fibrinógeno, factor VIII, entre otros y, además, la disminución de algunos anticoagulantes naturales como la proteína S y la antitrombina. Además, se menciona la insuficiencia de la fibrinólisis, asociada con el aumento del PAI-1 (inhibidor del activador tisular de plasminógeno). Durante la enfermedad, hay depósito de fibrina intraalveolar que también es degradada. Tanto la fibrinólisis del trombo, como la degradación de fibrina intraalveolar, hacen que aumenten los dímeros D y, por esta razón, este es uno de los mejores predictores de la severidad de la enfermedad COVID-19. En este artículo se revisa la fisiología de la hemostasia, la tromboinflamación secundaria a la infección por el virus Sars-Cov-2, la evidencia clínica y lo que se sabe de la fisiopatología de la coagulopatía en COVID-19, para tratar de entenderla desde la mirada de la ciencia básica.

Abstract COVID-19 global pandemic caused by Sars-CoV-2 virus, has worried to health care providers due to the high mortality rate related to coagulopathy in many patients. COVID-19 coagulopathy is mainly thrombotic, first locally in lungs but later on it becomes micro and macrovascular systemic coagulopathy. It has been associated to endothelial damage, inflammation, neutrophil-extracellular traps, monocyte and macrophage activation, cytokines storm that induce a vicious cycle of thrombosis and inflammation. The increased levels of prothrombotic factors as tissue factor, Von Willebrand factor, fibrinogen, VIII factor and the decreased levels of antithrombotic factos, such as: antithrombin and Protein S have been reported in COVID-19 patients. Insufficiency of fibrinolysis because of the increased levels of PAI-1 (plasminogen activator inhibitor 1) have been reported also. During this disease there are intraalveolar fibrin deposits that needs to be degraded. Fibrinolysis of thrombus and fibrin intraalveolar degradation are responsible for the high increase of D-dimers levels that are an important predictor of severity of the disease. In this report, the physiology of hemostasis, thromboinflamation secondary to Sars-CoV-2 infection are reviewed, as well as the clinical evidence and the physiopathology of COVID-19 coagulopathy from the basic sciences point of view.

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The Non-Ciliated Bronchiolar Cell (NCBC) is responsible for the defense and maintenance of the bronchiolar epithelium. Several cellular defense mechanisms have been associated with an increase in the secretion of CC16 and changes in the phenotype of the cell; these mechanisms could be linked to tolerance to the damage due to exposure to inhaled Particulate Matter (PM) of the epithelium. These defense mechanisms have not been sufficiently explored. In this article, we studied the response of the NCBC to inhaled vanadium, an element which adheres to PM. This response was measured by the changes in the phenotype of the NCBC and the secretion of CC16 in a mouse model. Mice were exposed in two phases to different vanadium concentrations; 1.27 mg/m³ in the first phase and 2.56 mg/m³ in the second phase. Mice were sacrificed on the 2nd, 4th, 5th, 6th and 8th weeks. In the second phase, we observed the following: sloughing of the NCBC, hyperplasia and small inflammatory foci remained without changes and that the expression of CC16 was higher in this phase than in phase I. We also observed a change in the phenotype with a slow decrease in both phases. The increase in the secretion of CC16 and the phenotype reversion could be due to the anti-inflammatory activity of CC16. The changes observed in the second phase could be attributed to the tolerance to inhaled vanadium.

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Vanadium is a metal present in particulate matter and its reprotoxic effects have been demonstrated in males and pregnant females in animal models. However, the effects of this metal on the reproductive organs of nonpregnant females have not been sufficiently studied. In a vanadium inhalation model in nonpregnant female mice, we found anestrous and estrous cycle irregularity, as well as low serum concentrations of 17ß-estradiol and progesterone. A decrease in the diameter of secondary and preovulatory follicles, as well as a thickening of the myometrium and endometrial stroma, was observed in the vanadium-treated mice. There was no difference against the control group with respect to the presence of the estrogen receptor α in the uterus of the animals during the estrous stage. Our results indicate that when vanadium is administered by inhalation, effects are observed on the female reproductive organs and the production of female sex hormones.

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