Estrés oxidativo y antioxidantes en la conservación espermática

El estrés oxidativo de los espermatozoides, se refiere al daño que pueden sufrir en la integridad de sus componentes estructurales y fisiológicos; cuyo efecto está directamente relacionado con la disminución de la sobrevivencia y capacidad fecundante después de ser eyaculados. El estrés oxidativo, es provocado por la formación de gran cantidad de especies reactivas al oxígeno (ROS) o moléculas que contienen radicales libres, las cuales se hacen presentes durante el manejo y manipulación del eyaculado, comprometiendo la viabilidad de los espermatozoides. La pérdida de la funcionalidad de los espermatozoides –capacidad fecundante- por la presencia de grandes cantidades de ROS, después de ser eyaculados, es motivo de gran interés y preocupación en el tema de la conservación seminal de machos reproductores, cuyo objetivo es mantener, mejorar y optimizar la eficiencia reproductiva en las Unidades de Producción Animal, en cualquier parte del mundo. En este trabajo se presenta una revisión sobre estrés oxidativo, antioxidantes, técnicas para valorar el estrés oxidativo en espermatozoides y al final un glosario de términos relacionados con el tema.Oxidative stress of spermatozoa, it refers to damage that may have on the integrity of their structural and physiological components, whose purpose is directly related to the decrease in the survival and fertilizing capacity after he ejaculates. Oxidative stress is caused by the formation of large amounts of reactive oxygen species (ROS), or molecules containing free radicals, which are present during the handling and manipulation of the ejaculate and jeopardize the viability of spermatozoa. The loss of the functionality of sperm-fertilizing capacity, the presence of large amounts of ROS, after he ejaculates, is of great interest and concern on the issue of preservation of seminal male breeding, which aims to maintain, improve and to optimize reproductive efficiency in animal production units, anywhere in the world. This paper presents an overview on oxidative stress, antioxidants, techniques for assessing oxidative stress in spermatozoa and in the end a glossary of terms related to the topic

Actores de la cadena productiva que deben participar para prevenir el uso de clembuterol en la engorda del ganado bovino en México

El clembuterol, Químicamente se describe como polvo blanco, anhidro, muy soluble en agua y altamente estable a temperatura ambiente, su punto de fusión es de 174 a 175.5 ºC. También es un derivado sintético perteneciente a una clase de medicamentos análogos fisiológicamente a la adrenalina, tiene la capacidad de interactuar con receptores adrenérgicos,  generalmente  del  tipo  ß2    (β  agonista),  es  uno  de  los  modificadores metabólicos más conocido en el área de producción de carne, debido al alto grado residual que deja esta sustancia en los tejidos comestibles y sus posibles repercusiones en la salud pública. En este trabajo, se describen los principales actores de la cadena productiva en la engorda  de  ganado  que  deben  participar  para  prevenir  el  uso  de  clembuterol.  La información fue recopilada de información científicas y publicaciones de las autoridades competentes, tales como: SENASICA, SAGARPA, COFEPRIS y Ley Federal de Sanidad Animal

Inborn errors of OAS–RNase L in SARS-CoV-2–related multisystem inflammatory syndrome in children

International audienceMultisystem inflammatory syndrome in children (MIS-C) is a rare and severe condition that follows benign COVID-19. We report autosomal recessive deficiencies of OAS1 , OAS2 , or RNASEL in five unrelated children with MIS-C. The cytosolic double-stranded RNA (dsRNA)–sensing OAS1 and OAS2 generate 2′-5′-linked oligoadenylates (2-5A) that activate the single-stranded RNA–degrading ribonuclease L (RNase L). Monocytic cell lines and primary myeloid cells with OAS1, OAS2, or RNase L deficiencies produce excessive amounts of inflammatory cytokines upon dsRNA or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) stimulation. Exogenous 2-5A suppresses cytokine production in OAS1-deficient but not RNase L–deficient cells. Cytokine production in RNase L–deficient cells is impaired by MDA5 or RIG-I deficiency and abolished by mitochondrial antiviral-signaling protein (MAVS) deficiency. Recessive OAS–RNase L deficiencies in these patients unleash the production of SARS-CoV-2–triggered, MAVS-mediated inflammatory cytokines by mononuclear phagocytes, thereby underlying MIS-C

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

International audienceSignificance There is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

International audienceSignificance There is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in similar to 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P=1.1x10(-4)) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70[95%CI 1.3-8.2], P=2.1x10(-4)). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR=19.65[95%CI 2.1-2635.4], P=3.4x10(-3)), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR=4.40[9%CI 2.3-8.4], P=7.7x10(-8)). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years; P=1.68x10(-5)).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old