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Contexto: en la obesidad, se observa una disfunción mitocondrial y un aumento del estrés oxidativo, caracterizado por cambios en la estructura de las mitocondrias, acumulación de mutaciones en el ADN mitocondrial y una sobreproducción de especies reactivas de oxígeno (ROS, según sus siglas en inglés), lo que resulta en una respuesta ineficiente en la producción de ATP. Objetivo: el objetivo principal de esta investigación fue evaluar los niveles de estrés oxidativo y su impacto sobre la morfología mitocondrial en placentas a término de gestantes obesas. Metodología: estudio de cohorte transversal retrospectivo analítico. Se obtuvieron 30 muestras de placenta de gestantes a término, sin antecedentes patológicos previos, que asistieron a una IPS de Cali. Se dividieron en tres grupos de estudio: grupo control (CO) = 10 (IMC = 18,5 kg/m2-24,9 kg/m2); obesidad pregestacional (OP) = 10 (IMC > 30 kg/m2); obesidad gestacional (OG) = 10 (IMC ? 29,9 kg/m2 con aumento > 13 kg). El análisis de daño por estrés oxidativo fue evaluado por medio de anticuerpo antinitrotirosina, donde la morfología mitocondrial fue analizada con microscopía electrónica de transmisión (MET). Resultados: los residuos de nitrotirosina (NT) se presentaron en mayor cantidad en las placentas de las madres con obesidad, en comparación con el grupo control (CO = 11,64 ± 0,40; OG = 14,7 ± 0,92; OP = 17,44 ± 2,13; p ? 0,02). Las mitocondrias presentes en las vellosidades terminales del sincitiotrofoblasto de los grupos OP y OG mostraron cambios en su número, tamaño y forma. Además, se identificó una alteración en las crestas mitocondriales, pérdida de las membranas mitocondriales interna y externa, y fragmentación de mitocondrias en el citoplasma de la célula placentaria. Conclusiones: la obesidad materna ocasionó cambios significativos en los niveles de estrés oxidativo, evaluados mediante residuos de NT, así como daño severo en la morfología mitocondrial. Estos cambios podrían afectar negativamente el metabolismo de biomoléculas y el funcionamiento placentario, induciendo un proceso inflamatorio persistente mediado por radicales libres de oxígeno.

La EW es causada por las variantes de ATP7B que alteran el eflujo de cobre y provocan una acumulación excesiva de cobre, principalmente en el hígado y el cerebro. El diagnóstico de la EW se ve dificultado por su evolución clínica variable, su aparición, su morbilidad y el tipo de variante ATP7B. Actualmente se diagnostica mediante una combinación de síntomas/signos clínicos, parámetros aberrantes del metabolismo del cobre (por ejemplo, niveles séricos bajos de ceruloplasmina y concentraciones elevadas de cobre urinario y hepático) y cuando están disponibles, a través de pruebas genéticas de mutaciones ATP7B. Dado que el diagnóstico y el tratamiento precoces son clave para obtener resultados favorables, es fundamental identificar a los sujetos antes de la aparición de manifestaciones clínicas manifiestamente perjudiciales. Con este fin, tratamos de mejorar el diagnóstico de la EW mediante algoritmos de redes neuronales artificiales (parte de la inteligencia artificial) integrando los parámetros clínicos y moleculares disponibles. Sorprendentemente, el diagnóstico de la EW se basó en los niveles plasmáticos de glutamato, asparagina, taurina y el cociente de Fischer. Dado que estos aminoácidos están relacionados con los ciclos urea-Krebs, nuestro estudio no sólo subraya el papel central de las mitocondrias hepáticas en la patología de la EW, sino también que la mayoría de los pacientes con EW presentan una disfunción hepática subyacente. Nuestro estudio aporta pruebas novedosas de que la inteligencia artificial utilizada para el análisis integrado de la EW puede dar lugar a un diagnóstico más precoz y a tratamientos mecánicamente relevantes para los pacientes con EW.

The intrinsic mechanisms sensing the imbalance of energy in cells are pivotal for cell survival under various environmental insults. AMP-activated protein kinase (AMPK) serves as a central guardian maintaining energy homeostasis by orchestrating diverse cellular processes, such as lipogenesis, glycolysis, TCA cycle, cell cycle progression and mitochondrial dynamics. Given that AMPK plays an essential role in the maintenance of energy balance and metabolism, managing AMPK activation is considered as a promising strategy for the treatment of metabolic disorders such as type 2 diabetes and obesity. Since AMPK has been attributed to aberrant activation of metabolic pathways, mitochondrial dynamics and functions, and epigenetic regulation, which are hallmarks of cancer, targeting AMPK may open up a new avenue for cancer therapies. Although AMPK is previously thought to be involved in tumor suppression, several recent studies have unraveled its tumor promoting activity. The double-edged sword characteristics for AMPK as a tumor suppressor or an oncogene are determined by distinct cellular contexts. In this review, we will summarize recent progress in dissecting the upstream regulators and downstream effectors for AMPK, discuss the distinct roles of AMPK in cancer regulation and finally offer potential strategies with AMPK targeting in cancer therapy. [ABSTRACT FROM AUTHOR]

Mitochondria are complex organelles that play a critical role within the cell; mitochondrial dysfunction can result in significant cell damage or death. Previous studies have demonstrated the promising therapeutic effects of autologous mitochondria transplantation into ischemic cardiac tissue; however, few studies have examined the in vivo effects of mitochondria infusion into the brain. The aim of this study is to report a procedure for carotid infusion of autologous mitochondria into porcine brains. By using this infusion technique, we propose that a selective and minimally invasive administration is feasible and may provide benefits in the treatment of various central nervous system disorders.

Introduction: Sperm sexing allows the production of offspring of a desired sex. Justification: Recognizing the characteristics of porcine sperm with X and Y chromosomes could favor the generation of strategies aimed at improving sperm sexing. Objective: To evaluate the association of mitochondrial activity and sperm viability (VE) with the distribution of boar sperm populations with X and Y chromosomes. Methods: Ten ejaculates from three male boars were used to perform 100 sessions of detection of the sperm populations X and Y, by flow cytometry with the Hoechst-33342 probe. The mitochondrial membrane potential (ΔΨM) and VE of spermatozoa X and Y were evaluated by flow cytometry with the JC-1 and SYBR14/Propidium iodide probes, respectively. Linear models, correlation analysis and comparison of means by Tukey test were performed. Results and Discussion: The proportion of sperm with high-ΔΨM (dimers) was 76.2 ± 1.0 % for X, and 45.0 ± 2.0 % for Y. VE was 84.1 ± 1.6 % for X, and 38.8 ± 2.8 % for Y (p<0.05). A positive correlation was found between high-ΔΨM and VE for X of 0.38 (P<0.001), and for Y of 0.54 (P<0.0001). The difference found between the vitality and mitochondrial activity of porcine sperm with X and Y chromosomes could be explained by particular characteristics of the sperm, as well as by a differentiated sensitivity between both to the conditions of flow cytometry. Conclusion: Porcine sperm populations X and Y may differ in their levels of mitochondrial activity and viability, as well as in the degree of association between both parameters. [ABSTRACT FROM AUTHOR]

Usually sexual hormones have been linked to its role in reproduction and development of sexual secondary characteristics. This has changed in time, nowadays it is known that they are involved in development and maturation of muscle, bone in neuronal and cognitive processes, and even in bioenergetic processes through the control that are capable to exert over mitocondria the organelle that produces the bioenergetic coin in the body, adenosin tryphosphate (ATP). These mitochondrion are specially numerous in organs with high metabolism such as liver and heart, in the last one is where the experimental evidence has revealed that the presence or absence of estrogens, could have a big impact in its function. [ABSTRACT FROM AUTHOR]

Objective: Contributing to elucidate the pathophysiology of dyspnoea and exertion intolerance in post-COVID syndrome patients with normal cardiopulmonary imaging and functional tests at rest, while determining their fitness and level of endurance in order to individualize working parameters for physical rehabilitation., Material and Methods: After an anamnesis and clinical examination at rest, 27 subjects (50±11.9 years) (14 women) with post-COVID syndrome of more than 6 months of evolution performed a continuous maximal-incremental graded cardiopulmonary exercise test (CPET) with breath-by-breath gas-exchange monitoring and continuous ECG registration, on an electromagnetically braked cycle ergometer. The values obtained were compared with those of reference, gender or controls, using the Chi-square, t-Student or ANOVA test., Results: The clinical examination at rest and the CPET were clinically normal and without adverse events. Reasons for stopping exercise were leg discomfort. It is only worth noting a BMI=29.9±5.8kg/m 2 and a basal lactate concentration of 2.1±0.7mmol/L. The physiological assessment of endurance showed the following results relative to predicted VO 2máx : 1)peakVO 2 =80.5±18.6%; 2)VO 2 at ventilatory threshold1 (VO 2 VT1): 46.0±12.9%; 3)VO 2 VT2: 57.2±16.4%; 4)working time in acidosis: 5.6±3,0minutes; and 5)maximum lactate concentration: 5.1±2.2mmol/L., Conclusions: The CPET identified limited aerobic metabolism and early increase in glycolytic metabolism as causes of dyspnoea and exercise intolerance, determined fitness for physical rehabilitation, and individualized it based on the level of endurance., (Copyright © 2024 Sociedad Española de Médicos de Atención Primaria (SEMERGEN). Publicado por Elsevier España, S.L.U. All rights reserved.)

Background: Ascending Thoracic Aortic Aneurysm (ATAA) is a progressive dilation of the aorta that can be complicated by its dissection leading to death in 80-90% of the patients. When associated with aging and atherosclerosis, the outcome is worse and reconstructive surgery is the only effective therapy. Our objective was to characterize differential expressed genes (DEG) involved in endoplasmic reticulum (ER) and mitochondria dysfunction in patients with degenerative ATAA., Methods: A transcriptomic analysis was performed by RNA sequencing using RNA isolated from ATAA of patients classified as degenerative (n=13) and multi-organ healthy donors (n=6). DEGs related to ER stress and mitochondrial dysfunction were identified with the DESeq2 package. Enriched pathway (Reactome) and protein interaction (PPI) analysis was performed with the clusterProfiles package. PPI of the selected DEGs was analyzed based on the string database and visualized by Cytoscape software., Results: Histology revealed a complete disorganization of the extracellular matrix (ECM) and cell loss in the aortic wall of ATAA patients where the upregulation of 15 DEGs and the downregulation of 13 DEGs that encode proteins related to ER stress (ATF4, EIF2AK3, HSPA5, ERN1, SEL1L), mitochondrial dysfunction (DNML1, IMMT, MT-CO3, MT-CYB, MT ND2, TIMM17B, MT-ERF1, TOMM5) and ECM was detected. The results of GO term and enriched pathway analysis indicated that these DEGs are mainly enriched in pathways related to aortic diseases., Conclusions: Our data show that proteins related to mitochondrial dysfunction and ER stress might be therapeutic targets for the treatment of ATAA., (Copyright © 2024 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.)

A Produção in vitro de embriões (PIVE) depende das etapas de maturação, fertilização e cultivo in vitro, sendo a maturação a etapa decisiva para o oócito atingir o estádio de mórula e blastocisto. Neste trabalho objetivou-se avaliar a qualidade de maturação in vitro, de acordo com a distribuição mitocondrial de oócitos provenientes de ovários de fêmeas de abatedouro, com baixa ou alta contagem de folículos antrais (CFA). Foram aspirados 243 ovários dos quais selecionou-se 334 oócitos perante de cinco repetições para cada grupo. Os ovários foram separados em dois grupos: 1- baixa CFA (n=19), 2- alta CFA (n= 53) e os oócitos recuperados corados com a sonda MitoTracker Red. Os dados obtidos foram analisados pelo teste não paramétrico exato de Fisher (α=5%) mediante o software Statistical Analysis System for Windows (SAS Inst., Inc., Cary, NC). Em relação a localização das mitocôndrias o presente trabalho apresentou diferenças (p

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Copyright of Revista Brasileira de Reprodução Animal is the property of Revista Brasileira de Reproducao Animal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Universitas Médica is the property of Pontificia Universidad Javeriana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introdução: Como parte da Edição Especial de 2020 I, a Revista de Educação Física / Journal of Physical Education (REF/JPE) está trazendo aspectos científicos da prática de atividade física relacionados à pandemia de CoViD-19. Objetivo: Apresentar e indicar aos leitores da REF/JPE, a leitura da revisão integrativa de Nunn et al., publicado em um periódico internacional, que analisou a literatura a respeito da relação da saúde mitocondrial nos contextos de estilo de vida e envelhecimento e potenciais associações com desfechos de CoViD-19. Conclusão: Após a profunda e abrangente discussão sobre o que a literatura apresenta sobre o tema abordado, os autores apontaram que a ideia de que a saúde mitocondrial, induzida por um estilo de vida saudável, pode ser um fator fundamental na resistência ao vírus SARS-CoV2. Além disso, apontaram que, para pessoas que não estejam em ótima saúde, tratamentos que apoiem a função mitocondrial podem ser essenciais para a recuperação a longo prazo.

The loss of dopaminergic (DA) neurons in the substantia nigra leads to a progressive, long-term decline of movement and other non-motor deficits. The symptoms of Parkinson’s disease (PD) often appear later in the course of the disease, when most of the functional dopaminergic neurons have been lost. The late onset of the disease, the severity of the illness, and its impact on the global health system demand earlier diagnosis and better targeted therapy. PD etiology and pathogenesis are largely unknown. There are mutations in genes that have been linked to PD and, from these complex phenotypes, mitochondrial dysfunction emerged as central in the pathogenesis and evolution of PD. In fact, several PD-associated genes negatively impact on mitochondria physiology, supporting the notion that dysregulation of mitochondrial signaling and homeostasis is pathogenically relevant. Derangement of mitochondrial homeostatic controls can lead to oxidative stress and neuronal cell death. Restoring deranged signaling cascades to and from mitochondria in PD neurons may then represent a viable opportunity to reset energy metabolism and delay the death of dopaminergic neurons. Here, we will highlight the relevance of dysfunctional mitochondrial homeostasis and signaling in PD, the molecular mechanisms involved, and potential therapeutic approaches to restore mitochondrial activities in damaged neurons.

The loss of functional capacities, aging and death are inherent to all living matter due to metabolism and other factors causing the formation of substances which damage irreversibly cell structure components. With the objective of updating about the last findings which explain the role of oxidative stress on cell aging, a bibliographic review is done. It is concluded that oxygen which is necessary for cell viability and other exogenous substances show toxicity since they lead to the formation of free radicals whose action is the main cause of aging. In addition, the administration of anti- oxidants is very important to prevent aging and improve the population´s quality of life.

The Viperidae venoms are composed of a mixture of constituents with enzymatic and non-enzymatic actions, which act on ultrastructural components of cells and tissues. Here, the number of mitochondria, mitochondrial area and the number of mitochondrial cristae from adrenal glands cortex treated with snake venoms were tested after 3, 6 and 24 hours of venom injections. The mitochondria quantitative changes showed a statistically significant decrease, in the number of mitochondria past 3, 6 and 24 h. There was an increase in the mitochondrial area after 6 h, where Crotalus vegrandis venom did not present significant differences with Crotalus pifanorum or Bothrops venezuelensis venoms. After 24 h, there was an escalation of mitochondrial area in all tested venoms. The number of mitochondrial cristae after 3 h did not present important differences with the control treatment. After 6 h, the number of mitochondrial cristae initiated to decrease under the activities of the 3 venoms action, until 24 h of observation. In the qualitative observations it was possible to witness an intense damage of the mitochondria, with loss and swelling of membranes, disappearance of cristae and the appearance of myelin figures, which started at 3 h after the Crotalus and Bothrops venoms injections. These damages probably were due to cytotoxic effects of phospholipases, metalloproteases and/or other proteolytic activities present in Viperidae snake venoms, being more evident in Crotalus venoms. As far as we know, these results define a novel finding that suggest that Viperidae snake venoms are extremely toxic to mammalian mitochondria. [ABSTRACT FROM AUTHOR]

The loss of dopaminergic (DA) neurons in the substantia nigra leads to a progressive, long-term decline of movement and other non-motor deficits. The symptoms of Parkinson's disease (PD) often appear later in the course of the disease, when most of the functional dopaminergic neurons have been lost. The late onset of the disease, the severity of the illness, and its impact on the global health system demand earlier diagnosis and better targeted therapy. PD etiology and pathogenesis are largely unknown. There are mutations in genes that have been linked to PD and, from these complex phenotypes, mitochondrial dysfunction emerged as central in the pathogenesis and evolution of PD. In fact, several PD-associated genes negatively impact on mitochondria physiology, supporting the notion that dysregulation of mitochondrial signaling and homeostasis is pathogenically relevant. Derangement of mitochondrial homeostatic controls can lead to oxidative stress and neuronal cell death. Restoring deranged signaling cascades to and from mitochondria in PD neurons may then represent a viable opportunity to reset energy metabolism and delay the death of dopaminergic neurons. Here, we will highlight the relevance of dysfunctional mitochondrial homeostasis and signaling in PD, the molecular mechanisms involved, and potential therapeutic approaches to restore mitochondrial activities in damaged neurons. [ABSTRACT FROM AUTHOR]

Nrf2 regulates redox homeostasis in cells by coordinately regulating a range of antioxidant enzymes and proteins. An increase in oxidative stress is one of the hallmarks of aging, and Nrf2 protein levels and activity decrease with aging. Decreased mitochondrial functions, such as decreased ATP production, also occur with aging, leading to the increased generation of reactive oxygen species (ROS) and oxidative stress. Thus, understanding the relationships between Nrf2 and the mitochondria is important for clarifying the regulatory mechanisms of aging. It is becoming clear that Nrf2 is activated in a tissue-specific manner in response to mitochondrial or NADPH oxidase-generated ROS. As the heart consists of postmitotic cells that utilize ATP produced mainly by mitochondrial oxidative phosphorylation, cardiomyocytes are equipped with highly sophisticated mitochondrial quality control mechanisms. Consistent with these findings, it has been reported that Nrf2 in the heart is regulated via a specific translational mechanism and that Nrf2 activation confers cardioprotective effects in various disease models. Thus, Nrf2 is a promising target for anti-aging strategies to combat age-related heart diseases, such as age-related cardiomyopathy. [ABSTRACT FROM AUTHOR]

El choque séptico es una patología que involucra alteraciones hemodinámicas y compromiso de la microvasculatura que derivan en una disfunción celular que conlleva a la falla orgánica múltiple propia de esta enfermedad. Los protocolos de manejo actuales se centran en la normalización de variables macrohemodinámicas y biomarcadores relacionados con la hipoxia tisular, convirtiéndose en un desafío clínico que requiere el reconocimiento temprano, el control de la infección y la optimización del estado hemodinámico del paciente. En los últimos años se ha identificado que la disfunción multiorgánica que se observa en el choque séptico se encuentra relacionada con el desarrollo de disfunción mitocondrial. Se han planteado dos posibilidades para explicar el surgimiento de esta disfunción mitocondrial, que son el convectivo e inmunometabólico. Dentro del contexto metabólico se observa que el ciclo de Krebs puede funcionar en un entorno de hipoxia mediante la fragmentación y reorientación de sus reacciones enzimáticas, permitiendo la adaptación al metabolismo intermediario a la noxa séptica.

Mitochondria (m) are responsible for the energy availability of cells, and their analysis is indicated for example, in studies related to metabolism and oxidative stress. The direct measurement of mitochondria (morphometry) is biased because of the section obliquity and position relative to the mitochondria length (non-equatorial cut). Therefore, stereology is an appropriate technique to evaluate mitochondria. However, before beginning the study, it is necessary to consider the premises to obtain random and uniform samples to be analyzed stereology. Mitochondria must have the chance to appear in all the possibilities of cut and orientation in the micrographs. The number of micrographs to be analyzed will depend on the distribution and occupation of mitochondria in the cell. After this is resolved, a proposal is the estimation of the following stereological data: volume density (Vv), surface density (Sv), and mean cross-sectional area (A). Overlapping a known test area at each micrograph, the density by area of mitochondria is estimated (NAT). Vv [m] can easily be estimated by point-counting (Vv = Pp/PT; Pp are the points hitting the structure, PT are the number of points of the test system). Sv is estimated overlaying a test-line (LT) on the micrographs and counting the intersections of the lines (I) with the outer membrane (om), inner membrane (im), and crests (c), thus, Sv [om], Sv [im], Sv [c] (Sv = 2I / LT). A [m] is obtained as the ratio: A = Vv / 2NAT. [ABSTRACT FROM AUTHOR]

In vitro embryo production (PIVE) depends on the stages of maturation, fertilization and in vitro cultivation, being the decisive stage for the oocyte to reach the morula and blastocyst stage. This study aimed to evaluate the quality of in vitro maturation, according to the mitochondrial distribution of oocytes from ovaries of slaughter females with low or high antral follicle count (CFA). A total of 243 ovaries were aspirated from which 334 oocytes were selected for five replicates for each group. The ovaries were separated into two groups: 1- low CFA (n = 19) 2- high CFA (n = 53) and stained with the Mito Traker Red probe. Data obtained were analyzed by Fisher's exact nonparametric test (a = 5%) using the Statistical Analysis System for Windows software (SAS Inst., Inc., Cary, NC). Regarding the location of mitochondria, the present study showed significant differences (p <0.001) between immature and mature oocytes, which is desirable. Mature oocytes had a higher percentage of dispersed mitochondria in the cytoplasm and immature oocytes in the periphery, regardless of the experimental group (low and high CFA). In immature oocytes, there was no difference (p = 0.1542) in the location of mitochondria between the low and high CFA groups. However, the oocytes of the low CFA group, after maturation, presented smaller number of oocytes with mitochondria in the periphery compared to the high CFA (p = 0.0355), indicating for this parameter a better competence of these oocytes for PIVE. [ABSTRACT FROM AUTHOR]

The brain is one of the main organs affected by hypoxia and reoxygenation in the neonatal period and one of the most vulnerable to oxidative stress. Hypoxia/ischemia and reoxygenation leads to impairment of neurogenesis, disruption of cortical migration, mitochondrial damage and neuroinflammation. The extent of the injury depends on the clinical manifestation in the affected regions. Preterm newborns are highly vulnerable, and they exhibit severe clinical manifestations such as intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP) and diffuse white matter injury (DWMI) among others. In the neonatal period, the accumulation of high levels of reactive oxygen species exacerbated by the immature antioxidant defense systems in represents cellular threats that, if they exceed or bypass physiological counteracting mechanisms, are responsible of significant neuronal damage. Several experimental models in mice mimic the consequences of perinatal asphyxia and the use of oxygen in the reanimation process that produce brain injury. The aim of this review is to highlight brain damage associated with oxidative stress in different murine models of hypoxia/ischemia and reoxygenation. Image 1 • Brain damage produced by hypoxia/ischemia and hyperoxia in premature newborns, leads to deleterious consequences for the development of the newborn. • Study of mechanisms in murine animals' models subjected to hypoxic/ischemia and ischemic complications during the pre- and perinatal periods has been relevant to decipher key steps of human brain development. • The understanding of physiological and molecular mechanisms which are altered during hypoxia/ischemia and hyperoxia insults is essential to envisage the development of new therapeutic targets or treatments which will be beneficial clinically for premature children. [ABSTRACT FROM AUTHOR]

Las miopatías metabólicas son un grupo de trastornos genéticos que disminuyen la capacidad del músculo esquelético para utilizar sustratos energéticos y sintetizar ATP. Estas alteraciones pueden clasificarse en tres tipos fundamentalmente: i) trastornos del metabolismo de los carbohidratos (del glucógeno y de la glucosa), ii) defectos del metabolismo lipídico, y iii) alteraciones de la fosforilación oxidativa –OXPHOS-. Las dos primeras se deben a deficiencias enzimáticas de las rutas metabólicas de degradación y síntesis de glúcidos y lípidos y muestran diversas manifestaciones clínicas, pero una buena parte de ellas cursan con intolerancia al ejercicio. Aunque un buen número de pacientes con estos trastornos musculares presentan síntomas en la infancia, el diagnóstico normalmente se retrasa hasta la segunda y tercera década de la vida. Por tanto, reconocer las características clínicas de estas deficiencias conduce a un diagnóstico precoz y a un mejor tratamiento. Las enfermedades mitocondriales son un grupo de trastornos originados por una deficiencia en la síntesis de ATP a través del sistema de fosforilación oxidativa. Este sistema está formado por proteínas codificadas en los dos genomas de la célula (nuclear y mitocondrial) y, por tanto, pueden presentar un modelo de herencia mendeliano o materno. En esta revisión se describirán las características especiales del sistema genético mitocondrial y las principales mutaciones que causan enfermedades en humanos.

El artículo propone estudiar la propagación de los campos electromagnéticos a través de la mitocondria. Se presenta un modelo simplifica - do de la mitocondria como un sistema periódico de multicapas de índices de refracción alternantes. Mediante el método de transferencia matricial se calcula la dependencia, la reflectancia y transmitancia en función de la longitud de onda del campo electromagnético incidente. Se observa la existencia de una región de longitudes de onda (o frecuencia prohibidas) en la cual no existe propagación de los campos a través del sistema, esto corresponde a una reflectancia máxima R=1.

Antecedentes: El linalool (2,6-dimetil-2,7-octadien-6-ol) es un monoterpeno presente en más de 200 tipos de plantas, y constituye el componente mayoritario de varios aceites esenciales. El linalool posee una amplia variedad de potenciales propiedades farmacológicas; que van desde propiedades antisépticas, ansiolíticas, anti-inflamatorias, antifúngicas, antimicrobianas y proapotóticas en diferentes líneas de células tumorales. Sin embargo, su principal uso está relacionado como una molécula odorante o fragancia en productos de uso tópico en productos cosméticos y en la industria del perfume. Objetivo: En este estudio se evaluó el efecto del linalool sobre la bioenergética de mitocondrias aisladas de hígado de rata. Métodos: El linalool en concentraciones entre (5-100μg/mL) fue evaluado en mitocondrias aisladas de ratas machos albinas raza Wistar, de acuerdo al método descrito por Voss et al (1961). Inicialmente, se determinó el consumo de oxígeno en mitocondrias intactas mediante un método polarográfico por medio de un oxígrafo. Posteriormente, se determinó el efecto del compuesto sobre las enzimas de la cadena respiratoria mitocondrial usando métodos polarográficos y espectrofotométricos. Resultados: Los resultados obtenidos indican que el linalool en las concentraciones de 5, 10, 50 y 100μg/mL, afecta la velocidad de consumo de oxígeno en el estado 3 y 4 de mitocondrias energizadas con glutamato-malato y succinato. Sin embargo, el efecto inhibitorio es mayor al usar glutamato-malato como sustrato. Por su parte, el análisis de la actividad de las enzimas de la cadena respiratoria mitocondrial mostró que el linalool (50μg/mL) inhibe los complejos I, III y la actividad ATPasa. Conclusiones: El linalool inhibe el complejo I, complejo III y la ATPasa, esta inhibición podría aumentar la generación de especies reactivas de oxígeno.

The evaluation of seed deterioration is very important to control the quality of the seeds stored. This study aimed to investigate the potential of fast ethanol assay for seed quality assessment of maize stored under different conditions. The first experiment was to determine the incubating temperature, incubating time, and amount of seed used in the assay. The results showed that the best protocol for the detection of headspace ethanol was incubation of 3 g of maize seed with 20% moisture content (wet basis) in a 20 mL gas chromatography vial at 70 °C for 1.5 h. The assay induced approximately 200-700 µg.L-1 of headspace ethanol, which was sufficient to identify seeds with different vigour levels. In the second experiment, the optimal conditions were used for quality assessment in aged maize seed stored for 12 months under different storage conditions. The increase in the ethanol production of stored maize seed under the controlled conditions (15 °C and 20% RH in the hermetic seal) was lower than under ambient conditions. The ethanol production levels of maize seed samples at the start of storage was significantly lesser than at six months storage (p < 0.05). The test limitations in deteriorated seed with different cultivars and ages will be discussed. [ABSTRACT FROM AUTHOR]

The loss of functional capacities, aging and death are inherent to all living matter due to metabolism and other factors causing the formation of substances which damage irreversibly cell structure components. With the objective of updating about the last findings which explain the role of oxidative stress on cell aging, a bibliographic review is done. It is concluded that oxygen which is necessary for cell viability and other exogenous substances show toxicity since they lead to the formation of free radicals whose action is the main cause of aging. In addition, the administration of anti- oxidants is very important to prevent aging and improve the population´s quality of life. [ABSTRACT FROM AUTHOR]

En este artículo de revisión, examinamos el papel de la mitocondria en el buen funcionamiento del corazón, y en la generación de diversas afecciones cardíacas, las cuales están caracterizadas por una baja producción de energía por parte de las mitocondrias y, por ende, hay un aumento en la pérdida de cardiomiocitos que conlleva al mal funcionamiento del corazón. Se ha determinado, que ciertas disfunciones mitocondriales asociadas a trastornos cardíacos se relacionan con alteraciones del sistema de fosforilación oxidativa, así como, con la disminución de ciertos componentes estructurales como la cardiolipina y la formación de supercomplejos. Se estima que cerca del 2.3% de la población colombiana puede presentar una prevalencia a la falla cardíaca. La presente revisión tiene como objetivo dar a conocer los avances investigativos relacionados con enfermedades cardíacas ocasionadas por disfunción mitocondrial, así como, la identificación de diferentes investigaciones dirigidas en la creación de alternativas de tratamiento para dichas patologías, todo esto con el fin de contribuir a la construcción de líneas de trabajo que tomen a la mitocondria como blanco terapéutico.

Comparados com outras espécies animais, a capacidade para a resistência de seres humanos é notável. A tese dos fatores limitantes e determinantes da resistência considera variáveis como consumo máximo de oxigênio (VO2max), limiares metabólicos e economia de movimento as mais importantes para a efetivação de exercícios físicos de longa duração. Como o oxigênio (O2) e produtos do metabolismo de substratos (glicose e ácidos graxos) são utilizados no interior de mitocôndrias do tecido muscular para obtenção de energia por processos oxidativos durante esse tipo de exercício físico, esta é outra variável importante a ser considerada. O objetivo deste texto é demonstrar que a incidência de fadiga em exercícios físicos prolongados intensos pode estar relacionada com modificações negativas ocorridas no potencial oxidativo mitocondrial. A funcionalidade mitocondrial encontra-se situada entre limites extremos que correspondem aos estados 4 (repouso) e 3 (VO2max). A tese desse texto é a de que quando essa variável aproxima-se do estado 3 durante o exercício físico prolongado intenso, o organismo esgota suas possibilidades de produção de energia pela fosforilação oxidativa, com consequente modificações nos valores de limiares metabólicos e no percentual do VO2max utilizado durante o esforço físico. Portanto, mitocôndrias funcionam como um termostato bioenergético celular durante situações como as que envolvem o exercício físico intenso prolongado.

Myoclonic epilepsy associated with ragged red fibers (MERRF) is a rare mitochondrial disorder. Diagnostic criteria for MERRF include typical manifestations of the disease: myoclonus, generalized epilepsy, cerebellar ataxia and ragged red fibers (RRF) on muscle biopsy. Clinical features of MERRF are not necessarily uniform in the early stages of the disease, and correlations between clinical manifestations and physiopathology have not been fully elucidated. It is estimated that point mutations in the tRNALys gene of the DNAmt, mainly A8344G, are responsible for almost 90% of MERRF cases. Morphological changes seen upon muscle biopsy in MERRF include a substantive proportion of RRF, muscle fibers showing a deficient activity of cytochrome c oxidase (COX) and the presence of vessels with a strong reaction for succinate dehydrogenase and COX deficiency. In this review, we discuss mainly clinical and laboratory manifestations, brain images, electrophysiological patterns, histology and molecular findings as well as some differential diagnoses and treatments.

Con el fin de contribuir al conocimiento de su actividad a nivel celular, se evaluó el mecanismo de acción del aceite esencial de Eucalyptus citriodora (Fam. Myrtaceae) sobre la bioenergética mitocondrial, su efecto sobre la velocidad de consumo de oxígeno de mitocondrias energizadas (estados 3 y 4) y su coeficiente de control respiratorio (CCR). Además, se analizó la actividad de los complejos de la cadena respiratoria usando técnicas espectrofotométricas. Los resultados obtenidos indican que el aceite esencial de E. citriodora aumenta la velocidad del consumo de oxígeno en los estados 3 y 4, disminuye el CCR, desacopla la fosforilación oxidativa, aumenta la actividad de la citocromo c oxidasa y aumenta la actividad ATPasa en mitocondrias íntegras, a partir de la concentración de 10 μg/mL. Estos resultados sugieren que el aceite esencial o sus metabolitos afectan el funcionamiento normal del transporte de electrones de la cadena respiratoria y la síntesis de ATP.

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Antecedents: focal cerebral ischemia (FCI) causes mitochondrial injure. Due to its participation in ATP production and in cell death processes, it is important to characterize the damage. Objetive: To show the tissue injures and mitochondrial proteomic profile changes in striatum and hippocampus in FCI. Material and methods: Fifteen min and 1h of FCI with and without 24h of sanguineous reperfusion (rpf) was induced in Male Wistar rats. Neurological evaluation, histological assessment and mitochondrial proteomic analysis was done. Results: Neurological deficit was observed from the 15 min of FCI. Tissue damage was observed with H&E stain; TTC stain show macroscopic cellular death at 1h-FCI/24h rpf. By proteomic strategy, 20 protein spots were initially found to be differentially expressed; 6 spots in striatum and 4 spots in hippocampus show qualitative differences, of these spots, two protein spots show evident changes from 15 min of FCI, in both cerebral regions. Conclusion: focal cerebral ischemia induces mitochondrial protein expression changes from the first minutes of the ischemic insult, as were observed by proteomic strategy. The subsequent identification and characterization of these proteins will allow studying the biochemical processes that take place in FCI, and will contribute to broaden the knowledge of the sequence of events that occur in response to ischemia. [ABSTRACT FROM AUTHOR]