BackgroundFor several years, cell-free DNA has been emerging as an important biomarker for non-invasive diagnostic in a wide range of clinical conditions and diseases. The limited information available on the genotoxic effects associated with occupational exposure to car paints, as well as the fact that up-to-date there are not reports about cell-free DNA measurements for assessing this condition, led us to evaluate the DNA damage caused by the occupational exposure to organic solvents contained in car paints, through the quantification of the cell-free DNA and the comet assay, in a sample of 33 individuals taken from 10 automobile paint shops located in Bogota DC, Colombia.ResultsBy applying the two methods, cell-free DNA and comet assay, we found a significant increase in the extent of DNA damage in the exposed individuals compared with the non-exposed ones within the control group.ConclusionsOur findings provide useful information about the cell-free DNA levels in this type of exposure and can be considered as a support tool that contributes to the diagnosis of genotoxic damage in individuals occupationally exposed to car paints.Electronic supplementary materialThe online version of this article (doi:10.1186/s12995-016-0123-8) contains supplementary material, which is available to authorized users.

BackgroundPainters are exposed to an extensive variety of harmful substances like aromatic hydrocarbons used as solvents and paint removers, some of which have shown clastogenic activity. These substances constitute a complex mixture of chemicals which contain well-known genotoxicants, such as Benzene, Toluene and Xylene. Thus, chronic occupational exposure to such substances may be considered to possess genotoxic risk. In Colombia the information available around the genotoxic damage (Chromosomal and DNA damage) in car paint shop workers is limited and the knowledge of this damage could contribute not only to a better understanding of the carcinogenic effect of this kind of substances but also could be used as biomarkers of occupational exposure to genotoxic agents.ResultsIn this study, the genotoxic effect of aromatic hydrocarbons was assessed in peripheral blood lymphocytes of 24 workers occupationally exposed and 24 unexposed donors, by using Cytogenetic analysis and comet assay. A high frequency of Chromosomal alterations was found in the exposed group in comparison with those observed in the unexposed group. Among the total of CAs observed in the exposed group, fragilities were most frequently found (100 %), followed by chromosomal breaks (58 %), structural (41.2 %) and numerical chromosomal alterations (21 %). Numerical chromosomal alterations, fragilities and chromosomal breaks showed significant differences between exposed and unexposed groups. Among the fragilities, fra(9)(q12) was the most frequently observed. DNA damage index was also significantly higher in the exposed group compared to the unexposed group (p < 0.000).ConclusionsOur results revealed that occupational exposure to aromatic hydrocarbons is significantly associated with Chromosomal and DNA damage in car paint shops workers and are also indicative of high chromosomal instability. The high frequency of both Chromosomal Alterations and DNA Damage Index observed in this study indicates an urgent need of intervention not only to prevent the increased risk of developing cancer but also to the application of strict health control and motivation to the use of appropriate protecting devices during work.

CHUAIRE-NOACK, L.; SÁNCHEZ-CORREDOR, M. C. & RAMÍREZ-CLAVIJO, S. The dual role of senescence in tumorigenesis. Int. J. Morphol., 28(1):37-50, 2010. SUMMARY:Senescence was rendered a tumor suppressor mechanism based on the observation of its protective effect against cancer in young organisms under conditions of oncogene activation or inactivation of tumor suppressor genes. In addition to this beneficial effect, senescence has been deemed to have age-associated deleterious effects because, apparently, senescence not only recapitulates aging and therefore loss of function and tissue regeneration capacity, but can also induce preneoplastic changes in adjacent stromal cells, provoke degenerative diseases or induce the production of tumor cell growth promoting factors. For that reason, senescence has become an attractive therapeutic target against cancer. This paper reviews some of the latest findings on the role of senescence in the malignant progression and analyzes them in relation to the concept of antagonistic pleiotropism, as well as its possible use as a therapeutic target against cancer.

X-chromosome inactivation is the genetic mechanism by which X-linked gene expression is equalized between the male and female genders of all placental mammal species. Given that the probability of mutant X-linked allele expression decreases as a result of the inactivation, it has been proposed that females have biological advantages relative to males. These advantages have grabbed the attention of the scientific community in recent years and have focused it on this topic and its clinical implications. To shed some new light on this intriguing phenomenon, this article reviews the most relevant molecular events involved in this process. These events include the role of Xist, the selection mechanism for future X-chromosome inactivation, the age-related inactivation skewing, and the relationship between inactivation and the emergence of X-linked diseases, possible treatments, and longevity.

caracteriza por la degeneración y pérdida de las neuronas dopaminérgicas en el cerebro. Existen factores genéticos involucrados en su desarrollo, en su forma de inicio temprano como el gen PARK2, codificante de la parkina, una E3 ubiquitín ligasa, lo que hace que en caso de mutaciones pierda su capacidad reguladora de degradación de proteínas causando estrés y muerte celular. Objetivo: determinar la presencia de cambios moleculares en los exones 3, 4, y 5 de PARK2 en un grupo de 29 pacientes y 21 controles colombianos con enfermedad de Parkinson de inicio temprano o con antecedentes familiares de ella y la posible correlación con las manifestaciones clínicas de los pacientes. materiales y métodos: estudio descriptivo observacional (entre junio de 2013 y noviembre de 2014) en donde se realizó extracción de ADN de sangre total y se utilizó la técnica de PCR para cada uno de los exones. Finalmente se procedió a la secuenciación automática, análisis de las secuencias con el software Sequencher y comparación con información de bases de datos. Resultados: se identificó una variante en estado homocigoto (Ala46Thr) en el exón 4 en un paciente no reportada anteriormente, posiblemente no patogénica y la variante Ser167Asn en estado heterocigoto en el mismo exón en otro paciente, considerada patogénica y reportada con anterioridad en poblaciones asiática y europea. No se identificaron variantes en los controles. Conclusiones: los cambios no descritos antes en la población colombiana,-Ala46Thr y Ser167Asn-, fueron identificados en el grupo de pacientes. mÉD.uIs. 2017;30(3):31-8.