Spermicides: a contraception alternative to consider

El objetivo de éste artículo fue realizar una revisión bibliográfica que permitiera referir algunos datos históricos, generalidades, uso, ventajas y desventajas sobre los espermicidas. Mediante el uso de diferentes bases de datos biomédicas, utilizando los términos Anticoncepción, Espermato-zoide, Espermicidas, Nonoxinol-9, Microbicida y Productos naturales se realizó una revisión de la literatura y para esto, se seleccionaron diferen-tes artículos científicos, documentos y manuales que permitieron la reali-zación del presente manuscrito, encontrando que desde hace muchos años la anticoncepción ha sido un tema de gran interés en el mundo tratando aspectos como el control de la natalidad y algunas infecciones de transmi-sión sexual. Con el tiempo se han desarrollado métodos anticonceptivos, entre ellos los espermicidas de origen sintético, que cuentan con una multiplicidad de ventajas y desventajas. Sin embargo, diferentes organi-zaciones han planteado la necesidad de buscar nuevos compuestos activos con propiedades espermicidas y microbicidas, que presenten mínimos efectos secundarios; entre estos nuevos compuestos, se destacan en el presente artículo aquellos espermicidas derivados de productos naturales.The aim of this manuscript was to show a review about historical data, uses, advantages and disadvantages of spermicidal products. Conducting a search in several biomedical databases and using some terms such as Contraception, Spermatozoa, Spermicides, Nonoxynol-9, Microbicide and Natural Products there was realized a literature review selecting different scientific articles, documents and guidelines that allowed the realization of this work. Contraception has been a worldwide interest subject since a long time ago, implicating aspects such as natality control and sexual transmitted infections. Eventually, due to the increased knowledge in contraception, some spermicidal products have been developed including the synthetic ones. However, different organizations have paid attention to the necessity for seeking new compounds with spermicidal and microbicidal activity, associated to minimal side effects; among these new molecules, the present article highlight those potential spermicides derived from natural products

Mitochondrial DNA methylation in metabolic associated fatty liver disease

INTRODUCTION: Hepatic lipid accumulation and mitochondrial dysfunction are hallmarks of metabolic associated fatty liver disease (MAFLD), yet molecular parameters underlying MAFLD progression are not well understood. Differential methylation within the mitochondrial DNA (mtDNA) has been suggested to be associated with dysfunctional mitochondria, also during progression to Metabolic Steatohepatitis (MeSH). This study further investigates whether mtDNA methylation is associated with hepatic lipid accumulation and MAFLD.METHODS: HepG2 cells were constructed to stably express mitochondria-targeted viral and prokaryotic cytosine DNA methyltransferases (mtM.CviPI or mtM.SssI for GpC or CpG methylation, respectively). A catalytically inactive variant (mtM.CviPI-Mut) was constructed as a control. Mouse and human patients' samples were also investigated. mtDNA methylation was assessed by pyro- or nanopore sequencing.RESULTS AND DISCUSSION: Differentially induced mtDNA hypermethylation impaired mitochondrial gene expression and metabolic activity in HepG2-mtM.CviPI and HepG2-mtM.SssI cells and was associated with increased lipid accumulation, when compared to the controls. To test whether lipid accumulation causes mtDNA methylation, HepG2 cells were subjected to 1 or 2 weeks of fatty acid treatment, but no clear differences in mtDNA methylation were detected. In contrast, hepatic Nd6 mitochondrial gene body cytosine methylation and Nd6 gene expression were increased in mice fed a high-fat high cholesterol diet (HFC for 6 or 20 weeks), when compared to controls, while mtDNA content was unchanged. For patients with simple steatosis, a higher ND6 methylation was confirmed using Methylation Specific PCR, but no additional distinctive cytosines could be identified using pyrosequencing. This study warrants further investigation into a role for mtDNA methylation in promoting mitochondrial dysfunction and impaired lipid metabolism in MAFLD.</p

Mitochondrial DNA methylation in metabolic associated fatty liver disease

IntroductionHepatic lipid accumulation and mitochondrial dysfunction are hallmarks of metabolic associated fatty liver disease (MAFLD), yet molecular parameters underlying MAFLD progression are not well understood. Differential methylation within the mitochondrial DNA (mtDNA) has been suggested to be associated with dysfunctional mitochondria, also during progression to Metabolic Steatohepatitis (MeSH). This study further investigates whether mtDNA methylation is associated with hepatic lipid accumulation and MAFLD.MethodsHepG2 cells were constructed to stably express mitochondria-targeted viral and prokaryotic cytosine DNA methyltransferases (mtM.CviPI or mtM.SssI for GpC or CpG methylation, respectively). A catalytically inactive variant (mtM.CviPI-Mut) was constructed as a control. Mouse and human patients’ samples were also investigated. mtDNA methylation was assessed by pyro- or nanopore sequencing.Results and discussionDifferentially induced mtDNA hypermethylation impaired mitochondrial gene expression and metabolic activity in HepG2-mtM.CviPI and HepG2-mtM.SssI cells and was associated with increased lipid accumulation, when compared to the controls. To test whether lipid accumulation causes mtDNA methylation, HepG2 cells were subjected to 1 or 2 weeks of fatty acid treatment, but no clear differences in mtDNA methylation were detected. In contrast, hepatic Nd6 mitochondrial gene body cytosine methylation and Nd6 gene expression were increased in mice fed a high-fat high cholesterol diet (HFC for 6 or 20 weeks), when compared to controls, while mtDNA content was unchanged. For patients with simple steatosis, a higher ND6 methylation was confirmed using Methylation Specific PCR, but no additional distinctive cytosines could be identified using pyrosequencing. This study warrants further investigation into a role for mtDNA methylation in promoting mitochondrial dysfunction and impaired lipid metabolism in MAFLD

Experiencia del investigador y docente Fabian Maurico Cortés Mancera

El investigador y docente Fabian Maurico Cortés Mancera nos habla sobre su experiencia investigativa en los avances y resultados en el grupo de investigación e innovación de biomédica del ITM

Gene-Targeted DNA Methylation:Towards Long-Lasting Reprogramming of Gene Expression?

DNA methylation is an essential epigenetic mark, strongly associated with gene expression regulation. Aberrant DNA methylation patterns underlie various diseases and efforts to intervene with DNA methylation signatures are of great clinical interest. Technological developments to target writers or erasers of DNA methylation to specific genomic loci by epigenetic editing resulted in successful gene expression modulation, also in in vivo models. Application of epigenetic editing in human health could have a huge impact, but clinical translation is still challenging. Despite successes for a wide variety of genes, not all genes mitotically maintain their (de)methylation signatures after editing, and reprogramming requires further understanding of chromatin context-dependency. In addition, difficulties of current delivery systems and off-target effects are hurdles to be tackled. The present review describes findings towards effective and sustained DNA (de)methylation by epigenetic editing and discusses the need for multi-effector approaches to achieve highly efficient long-lasting reprogramming.</p

Gene-Targeted DNA Methylation: Towards Long-Lasting Reprogramming of Gene Expression?

DNA methylation is an essential epigenetic mark, strongly associated with gene expression regulation. Aberrant DNA methylation patterns underlie various diseases and efforts to intervene with DNA methylation signatures are of great clinical interest. Technological developments to target writers or erasers of DNA methylation to specific genomic loci by epigenetic editing resulted in successful gene expression modulation, also in in vivo models. Application of epigenetic editing in human health could have a huge impact, but clinical translation is still challenging. Despite successes for a wide variety of genes, not all genes mitotically maintain their (de)methylation signatures after editing, and reprogramming requires further understanding of chromatin context-dependency. In addition, difficulties of current delivery systems and off-target effects are hurdles to be tackled. The present review describes findings towards effective and sustained DNA (de)methylation by epigenetic editing and discusses the need for multi-effector approaches to achieve highly efficient long-lasting reprogramming