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Mitochondria play an important role in cell energy metabolism due to the main function of producing biologically available energy in the form of adenosine triphosphate (ATP), through biochemical processes such as oxidative phosphorylation, beta oxidation of fatty acids and the Krebs cycle. Acute respiratory distress syndrome is a severe lung disease characterized by the appearance of diffuse alveolar infiltrates, dysregulated immune response and alveolocapillary injury that limits gas exchange. Alveolar cells maintain an oxygen tension of 5% and mitochondria consume oxygen through the cytochrome c oxidase enzyme in the electron transport chain, allowing ATP production. The reduction in oxygen consumption is crucial in mitochondrial damage, as mitochondria are sensitive to hypoxemia, affecting the transfer of molecules in the electron transport chain that disrupt the Krebs cycle. Hypoxia due to hypoxemia affects mitochondrial fusion and fission, while OXPHOS remodels, mainly in complex I, to maintain mitochondrial integrity. Lack of oxygen activates hypoxia-inducible factors, generating oxidative stress, acidosis and cell damage; therefore, this review aims to describe mitochondrial adaptations in acute respiratory distress syndrome. [ABSTRACT FROM AUTHOR]

For years, it was considered that the most important function of mitochondria was to provide the cell with energy in the form of ATP or even to function as a buffer of the cytosolic calcium concentration. However, it has been shown that mitochondria are a key part of signaling cascades or either, they establish shared functions with intra- and extracellular structures, allowing to maintain homeostasis and cell function. In addition, there are several reports showing that healthy cells are capable of transferring mitochondria to the bloodstream or to damaged cells with the aim of providing protection or to improve their bioenergetic condition under specific conditions. The signaling mechanisms for the recognition of marker molecules are decisive to establish the transfer of mitochondria between cells through vesicular structures or tunnels (TNT), among other systems. Currently, it has been developed strategies for mitochondrial isolation, which in turn, are injected into the tissues allowing their functional recovery, opening the door to what has been called "mitochondrial medicine" or "mitocure". Although these findings suggest that mitochondria could be a new prophylactic method for diseases or metabolic disorders, it is also necessary to analyze mitochondrial transfer may not always be positive for the organism in certain ailments. [ABSTRACT FROM AUTHOR]

: Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated in GC tissues and several GC cell lines. Yet, the underlying mechanism remains to be investigated. Here, we aim to investigate the role and mechanism of gastrin in GC proliferation. Gastrin-overexpressing GC cell model was constructed using SGC7901 cells. Then the differentially expressed proteins were identified by iTRAQ analysis. Next, we use flow cytometry and immunofluorescence to study the effect of gastrin on the mitochondrial potential and mitochondria-derived ROS production. Finally, we studied the underlying mechanism of gastrin regulating mitochondrial function using Co-IP, mass spectrometry and immunofluorescence. Overexpression of gastrin promoted GC cell proliferation in vitro and in vivo. A total of 173 proteins were expressed differently between the controls and gastrinoverexpression cells and most of these proteins were involved in tumorigenesis and cell proliferation. Among them, Cox17, Cox5B and ATP5J that were all localized to the mitochondrial respiratory chain were down-regulated in gastrin-overexpression cells. Furthermore, gastrin overexpression led to mitochondrial potential decrease and mitochondria-derived ROS increase. Additionally, gastrin-induced ROS generation resulted in the inhibition of cell apoptosis via activating NF-κB, inhibiting Bax expression and promoting Bcl-2 expression. Finally, we found gastrin interacted with mitochondrial membrane protein Annexin A2 using Co-IP and mass spectrometry. Overexpr ession of gastrin inhibits GC cell apoptosis by inducing mitochondrial dysfunction through interacting with mitochondrial protein Annexin A2, then up-regulating ROS production to activate NF-κB and further leading to Bax/Bcl-2 ratio decrease. [ABSTRACT FROM AUTHOR]

Background: At present, the etiology and pathogenesis of Moyamoya disease (MMD) are not completely clear. Patients are usually diagnosed after cerebrovascular events. Therefore, it is of great clinical significance to explore the predictive factors of MMD. Objective: This study aimed to investigate the serum level of CoQ10B, the amount of endothelial progenitor cells (EPCs), and mitochondrial function of EPCs in MMD patients. Methods: Forty-one MMD patients and 20 healthy controls were recruited in this study. Patients with MMD were divided into two groups: Ischemic type (n=23) and hemorrhagic type (n=18). Blood samples were collected from the antecubital vein and analyzed by CoQ10B ELISA and flow cytometry. Measures of mitochondrial function of EPCs include oxygen consumption rate (OCR), mitochondrial membrane potential, Ca2+ concentration, adenosine triphosphatases activity and ROS level. Results: The serum CoQ10B level in MMD patients was significantly lower than that in healthy controls (p<0.001). The relative number of EPCs in MMD patients was significantly higher than that in healthy controls (p<0.001). Moreover, the OCR, mitochondrial membrane potential and ATPase activity were decreased and the Ca2+ and reactive oxygen species levels were increased in MMD patients (p<0.001). Conclusions: Our results showed obviously decreased serum CoQ10B level and increased EPCs number in patients with MMD compared with healthy patients, and the mitochondria function of EPCs in MMD patients was abnormal. [ABSTRACT FROM AUTHOR]

Copyright of Revista Cientifica de la Facultade de Veterinaria is the property of Universidad del Zulia, Facultad de Ciencias Veterinarias 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 Revista de la Academia Colombiana de Ciencias Exactas, Físicas y Naturales is the property of Academia Colombiana de Ciencias Exactas, Fisicas y Naturales 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.)

La placenta humana requiere de colesterol para sintetizar la progesterona que mantiene la relación entre el feto y la madre, lo que le permite concluir de manera exitosa el embarazo. La placenta incorpora el colesterol principalmente a través de las lipoproteínas de baja densidad (LDL) que se obtienen del torrente circulatorio materno por un mecanismo de endocitosis. A los endosomas que se generan en este proceso se les unen varias proteínas conformando los endosomas tardíos, que degradan las LDL y liberan el colesterol a las mitocondrias del sinciciotrofoblasto que lo transforman en pregnenolona y posteriormente en progesterona. Las proteínas de fusión de membranas denominados complejos SNARE participan en la liberación del colesterol en sitios de contacto específicos en donde se localizan las proteínas mitocondriales responsables de la esteroidogénesis.

The world population is going through an obesity epidemic that has severe consequences for the health system. This study focused on studying hepatic mitochondria in obese animals induced by a high-fat (HF) diet and used the model-based stereology in electron micrographs for the quantitative study. Besides, the gene expressions of molecular markers of mitochondrial biogenesis carnitine palmitoyltransferase 1a (Cpt 1a), mitochondrial transcription factor a (Tfam), uncoupling protein 3 (Ucp 3), and nuclear respiratory factor 1 (Nrf 1) were analyzed. The HF diet caused a weight gain of +1820 % comparing the control group (C) with the HF group (from 0.32±0.31 g to 5.5±0.39 g, P<0.001). The HF group showed fat droplets in the hepatocyte cytoplasm (steatosis) and less dense and large mitochondria in transmission electron microscopy. The mitochondria size (cross-section) did not show a significant difference between the groups C and HF. However, the mitochondria numerical density per area was 30 % less, the mitochondrial surface density (outer membrane) was 20 % less, and the mitochondrial volume density was 22 % less in the HF group than the C group. The gene expressions of molecular markers of mitochondrial biogenesis Cpt 1a, Tfam, Ucp 3, and Nrf 1 decreased in the HF group compared to the C group. The quantitative results match perfectly with the molecular ones of mitochondrial biogenesis markers. In the future, it will be crucial to verify if and how these data recover with the reduction of obesity, which would be of significant interest given the current obesity epidemic that affects the world population. [ABSTRACT FROM AUTHOR]

Este artigo é uma revisão do efeito do estresse oxidativo (EO) no Transtorno Bipolar (TB). Esta doença é caracterizada como sendo crônica, grave, com alta morbidade, mortalidade e altas taxas de suicídio. É uma doença progressiva, com episódios cada vez mais curtos e frequentes ao longo do tempo. Modificações ocorrem no cérebro, como alterações na neuroplasticidade, neurotransmissão, falhas na apoptose, ativação no processo imunoinflamatório, com alterações na via de sinalização do cálcio, e mais recentemente, sobre o EO. Esses eventos envolvem uma reorganização patológica no cérebro e, portanto, estão associados a alterações morfológicas, como; redução do volume do córtex pré-frontal, do hipocampo e da amígdala aumentada. Essas alterações estruturais e bioquímicas são conhecidas como neuroprogressão, e apresentam diferenças entre o estágio inicial e final do TB. Neurônios e células da glia têm uma das mais altas demandas de energia, onde estas alterações bioquímicas e anatômicas afetam essas células e principalmente organelas, como as mitocôndrias. A mitocôndria é uma organela especializada que gera trifosfato de adenosina (ATP) sendo considerada a principal fonte de espécies reativas de oxigênio (EROs) e espécies reativas de nitrogênio (ERNs), produzidas pela cadeia de transporte de elétrons (CTE), levando assim ao EO. O papel do EO na fisiopatologia da TB tem sido investigado em vários estudos relatando mudanças nos níveis das enzimas antioxidantes, na peroxidação lipídica e do óxido nítrico (NO). Os mecanismos fisiopatológicos do TB contribuem para uma melhor compreensão da atividade da doença e podem revelar possíveis soluções para o diagnóstico e prognóstico.

Los fibroblastos son células constituyentes de los tejidos conectivo. Los fibroblastos gingivales (FGs), células responsables de la síntesis de la matriz extracelular (MEC) en el tejido conectivo gingival, participan en la regulación de los procesos de cicatrización y de reparación de la encía. Debido a su potencial regenerativo, los FGs podrían ser células capaces de contribuir a mejorar los procesos de cicatrización, a nivel local y sistémico e, incluso, ser utilizadas como un modelo celular útil en la comprensión de los aspectos fisiopatológicos de la cavidad oral. El objetivo del presente trabajo fue describir el impacto de la concentración del suero fetal bovino (SFB), en la supervivencia, el crecimiento y la expresión de marcadores celulares en los FGs. Cultivos celulares de FGs fueron realizados durante 7 días, utilizando medio de cultivo DMEM (Dulbecco’s Modified Eagle’s médium), en ausencia y presencia de 10% de SFB. Análisis morfológicos e inmunohistoquímicos de la actina, mitocondrias, lisosomas y retículo endoplasmático (RE) fueron usados para evaluar el impacto de la concentración del SFB sobre los FGs. Los resultados indican que los FGs cultivados en presencia de 10% de SFB tuvieron una tasa de crecimiento más elevada en comparación con los FGs, cultivados en ausencia de SFB. El marcaje de los elementos celulares indica la ausencia de alteraciones en las organelas celulares de los FGs, cuando son cultivados en ausencia de SFB. En conclusión, los FGs son capaces de sobrevivir, proliferar y conservar sus características morfológicas, cuando son cultivados en presencia y ausencia de SFB.

Objetivo. Describir la influencia del Suero Fetal Bovino (SFB) en la supervivencia, crecimiento y expresión de organelas celulares en las células epiteliales dentales de rata. Materiales y métodos. Cultivos de células epiteliales dentales de rata fueron llevados a cabo a 37°C en una atmosfera húmeda, en ausencia y a una concentración de 10% de SFB. Se realizó una evaluación morfológica durante la proliferación y confluencia de las células en cultivo. Dobles marcajes por inmunofluorescencia fueron efectuados haciendo uso de anticuerpos anti-actina, anti-TOMM20 y anti-LAMP1. Resultados. Se evidenciaron células epiteliales dentales circulares u ovoides con núcleos voluminosos durante la proliferación y confluencias de manera similar en las células cultivas en presencia y ausencia de SFB. La carencia de SFB impactó negativamente la proliferación de las células epiteliales. No fueron observadas alteraciones en la localización de los inmunomarcajes anti-actina, anti-TOMM20 y anti-LAMP1 en las dos condiciones de cultivos experimentales. Conclusiones. La supresión del SFB en el cultivo de células epiteliales dentales de rata disminuyó la supervivencia, proliferación y sugiere no tener un impacto sobre las organelas evaluadas.

The spectacled bear (Ursidae: Tremarctos ornatus) is an emblematic umbrella species and one of the top carnivores in the Andean mountains. It is also listed as vulnerable by IUCN and as endangered by CITES. We analyzed the genetic structure of this species in nine geographical regions representing the three Andean Cordilleras in Colombia. We sequenced six mitochondrial genes in 115 spectacled bears; a subset of these specimens (n = 61) were genotyped at seven nuclear microsatellites. We addressed three objectives: 1) determine the genetic diversity and historical demographic changes of the spectacled bear in Colombia; 2) determine phylogeographic patterns of genetic divergence among spectacled bear populations in Colombia; and 3) estimate the levels of gene flow among different regions of Colombia. Our analyses show evidence of high mitochondrial genetic diversity in spectacled bears, both in Colombia as well as in each of the nine regions, most particularly Norte de Santander, Nariño, and Antioquia-Córdoba. In addition, we detected population expansion in Colombia that occurred around 24,000 years ago, followed by a population decrease during the last 7,000 years, and a sudden expansion in the last 300 years. Phylogenetic analyses showed few well-supported clades, with some haplotypes detected in all the departments and Colombian Andean Cordilleras, and other haplotypes restricted to certain geographical areas (Antioquia, Norte de Santander, Cundinamarca, and Nariño). We detected significant genetic heterogeneity among some departments and among the three Colombian Andean Cordilleras for both mitochondrial and nuclear genes. Nevertheless, the moderate levels of gene flow estimated from F ST statistics suggest that geographical barriers have not been definitive obstacles to the dispersion of the spectacled bear throughout Colombia. Despite these gene flow estimates, significant spatial autocorrelation was detected for spectacled bear in Colombia, where two kinds of spatial patterns were discovered: genetic patches of 144 km of diameter, and isolation by distance among bears separated from 578 to 800 km. The two most northern spectacled bear populations of Colombia (Norte de Santander and Antioquia) also were the two most differentiated. Their distinctiveness may qualify them as distinct Management Units (MUs) in the context of conservation policies for the spectacled bear in Colombia. [ABSTRACT FROM AUTHOR]

Introduction. Gingival fibroblasts (GF) are cells of gingival connective tissue that have taken promising relevance in recent years due to their probable use in cell therapy, given their multipotencial and self-renewal capabilities. Objective. To know and to describe the impact of the absence of Fetal Bovine Serum (FBS supplementation on the survival of gingival fibroblasts in cultures. Materials and methods. Gingival fibroblasts were isolated from gingival tissue of healthy patients and cultured in DMEM (Dulbecco's Modified of Eagle Medium) culture media in absence and supplemented with 0.2% FBS at 37 ° C in a humid atmosphere with 5% CO2. A morphological evaluation, survival and proliferation of GF were carried out, as well as the identification by the immunofluorescence technique of cellular cytoskeleton markers such as actin and mitochondria. Results. The GF grown in the absence and with supplementation of 0.2% FBS showed a fusiform shape, with oval nuclei and numerous cytoplasmic extensions during the culture time. A slight increase in the proliferation of GF was observed in those cells in contact with the DMEM medium +0.2% FBS compared to the medium where the supplementation was absent. Immunostaining of actin and mitochondria showed that the absence and supplementation to 0.2% of FBS did not affect its location in the evaluated. Conclusion. Gingival fibroblasts survive and proliferate in the absence of FBS, preserving their cellular morphological characteristics. [ABSTRACT FROM AUTHOR]

Objective. Describe the influence of Fetal bovine serum (FBS) on the survival, growth and expression of cellular organelles in rat dental epithelial cells. Material and methods. Cell cultures of rat dental epithelial cells were carried out at 37°C in a humid atmosphere, in the absence and at a concentration of 10% FBS. Morphological evaluation was performed during the proliferation and confluence of cell in culture. Double immunofluorescence labels were made using anti-Actin, anti-TOMM20A, and anti-LAMP1 antibodies. Results. Circular or ovoid dental epithelial cells with bulky nuclei were evidenced during proliferation and confluences in a similar manner in culturing cells in the presence and absence of FBS. The lack of FBS negatively impacts the proliferation of epithelial cells. No alterations were observed in the localization of the anti-actin, anti-TOMM20 and anti-LAMP1 immunomarkers in both conditions of experimental cultures. Conclusion. FBS suppression in rat dental epithelial cells decreased survival, proliferation and suggests not having an impact on the organelles evaluated. [ABSTRACT FROM AUTHOR]

The venom of the black rattlesnake, Crotalus pifanorum, contains proteolytic enzymes, peptidases, proteinases, phospholipases and neurotoxins resulting in cytotoxic and neurotoxic effects. In addition, the venom similarly acts on adrenal glands of mice, as it was observed in the present study. The basic structures of the cortex cells from the glands are typical of steroid-producing cells. It has little rough endoplasmic reticulum, but abundant smooth endoplasmic reticulum, where numerous lipid inclusions and mitochondria usually rounded with tubular cristae were observed. From 3 until 24 h after the venom injection, mitochondria, smooth endoplasmic reticulum, nuclear structure and microvasculature damages could be observed. This venom is highly toxic for the adrenal glands. The present results will help the physicians in evaluating the function of these glands in order to avoid fatal outcomes due to an acute suprarenal insufficiency. To our knowledge, this is the first report of adrenal gland damage in mice caused by the injection of C. pifanorum venom. Our results advise that adrenal cortex lesions may be significant in the envenoming etiopathogenesis caused by this venom. [ABSTRACT FROM AUTHOR]

The human placenta requires cholesterol to synthesize the progesterone that maintains the relationship between the fetus and the mother, which allows it to successfully conclude pregnancy. The placenta incorporates cholesterol through the LDL obtained from the maternal blood stream by a mechanism of endocytosis. Endosomes formed by this process degrade the LDL, bind several proteins forming the late endosomes and releasing the cholesterol to syncytiotrophoblast mitochondria to transform it into pregnenolone and then, into progesterone. The soluble attachment proteins denominated SNARE participates in the transport of cholesterol in specific contact sites where the mitochondrial proteins responsible for steroidogenesis are located. [ABSTRACT FROM AUTHOR]

A criopreservação de sêmen de Curimba (Prochilodus lineatus) é de importância ecológica e comercial. O objetivo deste estudo foi avaliar o efeito de diferentes concentrações (2, 5, 8 e 11%) de dimetilsulfóxido (DMSO) diluído em Betsville Thawing Solution (BTS) sobre a qualidade do sêmen de Curimba pós-descongelamento. Foram analisadas a taxa e período de motilidade, viabilidade espermática, integridade da membrana plasmática e do DNA, funcionalidade mitocondrial, e taxa de fertilização e eclosão. A membrana plasmática e a integridade do DNA a uma concentração de DMSO de 11% obtiveram melhores resultados que na concentração de 5% (p .

PURPOSE: To investigate the effect of lovastatin on renal ischemia followed by reperfusion. METHODS: Thirty one Wistar rats submitted to left renal ischemia for 60 minutes followed by contralateral nephrectomy were divided into two groups: A (n =17, control, no treatment), and B (n=14, lovastatin 15 mg/kg/day p.o. ten days before ischemia). The animals were sacrificed at the end of ischemia, after 24 hours and at seven days after reperfusion. Survival, serum urea and creatinine levels and renal mitochondrial function were evaluated. RESULTS: Mortality was 29.4% in group A and 0.7% in group B. Urea and creatinine levels were increased in both groups, but the values were significantly lower in group B. Mitochondrial function showed decoupling in 83.4% of group A, as opposed to 38.4/% of group B. CONCLUSIONS: The result shows a protective action of renal function by lovastatin administered before ischemia/reperfusion. Since most of the mitochondrial fraction presented membranes with the ability to maintain ATP production in group B, stabilization of the mitochondrial membrane should be considered as part of the protective action of lovastatin on renal function in ischemia/reperfusion.OBJETIVO: Investigar a ação da lovastatina na isquemia renal seguida de reperfusão. MÉTODOS: Trinta e um ratos Wistar submetidos à isquemia renal esquerda durante 60 minutos, seguida da nefrectomia contralateral, foram distribuídos em dois grupos: A (n=17, controle, sem tratamento) e B (n=14, recebendo 15 mg/Kg/dia de lovastatina via oral), durante os dez dias que antecederam a isquemia. Os animais foram mortos ao final da isquemia, e com 24 horas e sete dias após a reperfusão. Foram avaliadas a sobrevida, os valores séricos de uréia e creatinina e a função mitocondrial renal. RESULTADOS: A mortalidade foi 29,4% no grupo A e 0,7% no grupo B. Os níveis de uréia e creatinina elevaram-se nos dois grupos, mas foram significativamente menores no grupo B. No grupo A a função mitocondrial renal ficou desacoplada em 83,4% dos ensaios, enquanto que no grupo B isto ocorreu em apenas 38,4% dos ensaios. CONCLUSÕES: Os resultados mostram que a administração de lovastatina antes do episódio de isquemia protege a função renal. No grupo B, como a maior parte da fração mitocondrial isolada apresentou função acoplada à produção de ATP, deve-se também considerar a estabilização da membrana mitocondrial como parte da ação protetora da lovastatina na função renal durante isquemia e reperfusão.

OBJETIVO: Um amplo corpo de evidência oriundo de estudos experimentais indica que a sepse se associa com um aumento da produção de espécies de oxigênio reativo, depleção de antioxidantes, e acúmulo de marcadores de estresse oxidativo. Além disto, a disfunção mitocondrial foi implicada na patogênese da síndrome de disfunção de múltiplos órgãos. A citrato sintase é uma enzima que se localiza no interior das células, na matriz mitocondrial, sendo uma etapa importante do ciclo de Krebs; esta enzima foi utilizada como um marcador enzimático quantitativo da presença de mitocôndrias intactas. Assim, investigamos a atividade da citrato sintase no cérebro de ratos submetidos ao modelo sepse com de ligadura e punção do ceco. MÉTODOS: Em diferentes horários (3, 6, 12, 24 e 48 horas) após cirurgia de ligadura e punção do ceco, seis ratos foram sacrificados por decapitação, sendo seus cérebros removidos e dissecados o hipocampo, estriato, cerebelo, córtex cerebral e córtex pré-frontal, e utilizados para determinação da atividade de citrato sintase. RESULTADOS: Verificamos que a atividade de citrato sintase no córtex pré-frontal estava inibida após 12, 24 e 48 horas da ligadura e punção do ceco. No córtex cerebral, esta atividade estava inibida após 3, 12, 24 e 48 horas da ligadura e punção do ceco. Por outro lado a citrato sintase não foi afetada no hipocampo, estriato e cerebelo até 48 horas após a ligadura e punção do ceco. CONCLUSÃO: Considerando-se que é bem descrito o comprometimento da energia decorrente da disfunção mitocondrial na sepse, e que o estresse oxidativo desempenha um papel essencial no desenvolvimento da sepse, acreditamos que o comprometimento da energia pode também estar evolvido nestes processos. Se a inibição da citrato sintase também ocorre em um modelo de sepse, é tentador especular que a redução do metabolismo cerebral pode provavelmente estar relacionada com a fisiopatologia desta doença.OBJECTIVE: An extensive body of evidence from experimental studies indicates that sepsis is associated with increased reactive oxygen species production, depletion of antioxidants, and accumulation of markers of oxidative stress. Moreover, mitochondrial dysfunction has been implicated in the pathogenesis of multiple organ dysfunction syndrome (MODS). Citrate synthase is an enzyme localized in the mitochondrial matrix and an important component of the Krebs cycle; consequently, citrate synthase has been used as a quantitative enzyme marker for the presence of intact mitochondria. Thus, we investigated citrate synthase activity in the brains of rats submitted to a cecal ligation puncture model of sepsis. METHODS: At several times points (3, 6, 12, 24 and 48 hours) after the cecal ligation puncture operation, six rats were killed by decapitation. Their brains were removed, and the hippocampus, striatum, cerebellum, cerebral cortex and prefrontal cortex were dissected and used to determine citrate synthase activity. RESULTS: We found that citrate synthase activity in the prefrontal cortex was inhibited 12, 24 and 48 hours after cecal ligation puncture. In the cerebral cortex, citrate synthase activity was inhibited 3, 12, 24 and 48 hours after cecal ligation puncture. Citrate synthase was not affected in the hippocampus, striatum or cerebellum up to 48 hours after cecal ligation puncture. CONCLUSION: Considering that energy impairment due to mitochondrial dysfunction in sepsis has been well described and that oxidative stress plays a crucial role in sepsis development, we believe that energy impairment may also be involved in these processes. If citrate synthase inhibition also occurs in a sepsis model, it is tempting to speculate that a reduction in brain metabolism may be related to the pathophysiology of this disease.

Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Ca m2+) are essential elements in the control of many physiological processes. However, sustained increases in Ca c2+ and Ca m2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Ca m2+, including regulation and activation of a number of Ca2+ dependent enzymes, such as phospholipases, proteases and nucleases. Mitochondria and endoplasmic reticulum (ER) play pivotal roles in the maintenance of intracellular Ca2+ homeostasis and regulation of cell death. Several lines of evidence have shown that, in the presence of some apoptotic stimuli, the activation of mitochondrial processes maylead to the release of cytochrome c followed by the activation of caspases, nuclear fragmentation and apoptotic cell death. The aim of this review was to show how changes in calcium signaling can be related to the apoptotic cell death induction. Calcium homeostasis was also shown to be an important mechanism involved in neurodegenerative and aging processes.Aumentos transientes no cálcio citosólico (Ca c2+) e mitocondrial (Ca m2+) são elementos essenciais no controle de muitos processos fisiológicos. No entanto, aumentos sustentados do Ca c2+ e do Ca m2+ podem contribuir para o estresse oxidativo ea morte celular. Muitos eventos estão relacionados ao aumentono Ca c2+, incluindo a regulação e ativação de várias enzimas dependentes de Ca2+ como as fosfolipases, proteases e nucleases. A mitocôndria e o retículo endoplasmático têm um papel central na manutenção da homeostase intracellular de Ca c2+ e na regulação da morte celular. Várias evidências mostraram que, na presença de certos estímulos apoptóticos, a ativação dos processos mitocondriais pode promover a liberação de citocromo c, seguida da ativação de caspases, fragmentação nuclear e morte celular por apoptose. O objetivo desta revisão é mostrar como aumentos na sinalização de Ca2+ podem estar relacionados aos eventos de indução da morte celular apoptótica. Além disso, evidenciar como a homeostase de Ca2+ pode ser importante e está envolvida nos mecanismos presentes nos processos de neurodegeneração e envelhecimento.

Antecedentes: La adquisición del fenotipo metastático es el resultado de la potente acción generada por on-cogenes transformantes sobre una célula normal los cuales con la consiguiente expresión de oncoproteínas determinan drásticos cambios tanto en la morfología como en los volúmenes de los componentes celulares, generando una célula con diferente funcionalidad. Este mecanismo corresponde a la transformación celular. Objetivo: Precisar las modificaciones que caracterizan al mecanismo transformante en células de epitelio mamario transfectado con el oncogén ras (HC11 ras) en comparación con su tipo celular normal (HC11GM). Método: Se estudió con microscopia electrónica de transmisión aplicando técnicas morfométricas a estos tipos celulares con énfasis en las mitocondrias, cuantificando variaciones del organelo generador de energía. Resultados: Todos los parámetros mitocondriales evaluados en el tipo celular transformado presentan diferencias significativas con respecto a la célula normal. Conclusión: Las drásticas modificaciones experimentadas por las mitocondrias se reflejan en la adquisición de nuevos requerimientos energéticos y metabólicos en la célula transformada.Background: The acquisition of the metastatic phenotype is the result of the transforming oncogene powerful action over a normal cell which with the subsequent oncoprotein expression leads to drastic changes in mor-phology as well as in cell components volumes, generating a cell with a different function. This mechanism relates to the cell transformation. Objective: To specify the modifications that characterize the transforming mechanism in mammary epithelial cells transfected with the ras oncogene comparing them with its normal cell type. Method: Transmission electronic microscopy using morphometric techniques was applied to this cell types, emphasizing mitochondria variations, trying to clarify its role in each cell type metabolism. Results: Everyone mitochondrial parameters examined in transformed cell type present significant differences regar-ding to the normal cells. Conclusión: The drastic changes in mitochondria are reflected in the acquisition of new energy requirements and metabolism in the transformed cell.

El proceso de diferenciación representa un complejo mecanismo mediante el cual las células, variando notablemente su morfología, adquieren una forma determinada, tamaño específico, cierta polaridad y constancia de constituyentes celulares, producto de la activación génica que permiten que dicha célula diferenciada cumpla con una función en forma óptima. Estas modificaciones pueden ser precisadas utilizando técnicas morfométricas que dan cuenta de las variaciones que caracterizan el mecanismo. Células normales de epitelio mamario de rata en cultivo, estimuladas a proliferar con el factor de crecimiento epidérmico (EGF) origina la célula HC11 GM. Ellas son inducidas a diferenciarse con inducciones hormonales de dexametasona, insulina y prolactina, generándose la célula HC11 IM. Se estudió con microscopía electrónica de transmisión estos tipos celulares con énfasis en las mitocondrias, determinando variaciones del organelo generador de energía, en lo relacionado a variables tanto cuantitativas como morfológicas, precisando así su rol en la actividad metabólica de cada tipo celularThe cell differentiation process represents a complex mechanism through which, cells, change remarkably their morphology due to gene activation, acquire certain form, size, polarity and maintain their cellular components, which allows that this differentiated cell fulfils an optimal function. These changes can be measured by morphometric techniques that take account of variations that characterize this mechanism. Cultured normal rat epithelial cell, stimulated to proliferate by epidermic growth factor (EGF), give rise to HC11 GM cell group. These cells are induced to differentiate by hormonal inducers like dexamethasone, insulin and prolactine, originating HC11 IM cell. These cell types, emphasizing mitochondria, were studied by transmition electronic microscopy that showed variation in this energy generator organelle, about its morphologic as well as quantitative variables, demonstrating mitochondrial function in metabolic activity in each cell type

Iron imbalance/accumulation has been implicated in oxidative injury associated with many degenerative diseases such as hereditary hemochromatosis, beta-thalassemia, and Friedreich's ataxia. Mitochondria are particularly sensitive to iron-induced oxidative stress - high loads of iron cause extensive lipid peroxidation and membrane permeabilization in isolated mitochondria. Here we detected and characterized mitochondrial DNA damage in isolated rat liver mitochondria exposed to a Fe2+-citrate complex, a small molecular weight complex. Intense DNA fragmentation was induced after the incubation of mitochondria with the iron complex. The detection of 3' phosphoglycolate ends at the mtDNA strand breaks by a 32P-postlabeling assay, suggested the involvement of hydroxyl radical in the DNA fragmentation induced by Fe2+-citrate. Increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine also suggested that Fe2+-citrate-induced oxidative stress causes mitochondrial DNA damage. In conclusion, our results show that iron-mediated lipid peroxidation was associated with intense mtDNA damage derived from the direct attack of reactive oxygen species.Desequilíbrio/acúmulo de ferro tem sido implicado em injúria oxidativa associada a diversas doenças degenerativas tais como, hemocromatose hereditária, beta-talassemia e ataxia de Friedreich. As mitocôndrias são particularmente sensíveis a estresse oxidativo induzido por ferro - um carregamento alto de ferro em mitocôndrias isoladas pode causar uma extensiva peroxidação lipídica e a permeabilização de membrana. Nesse estudo, nós detectamos e caracterizamos danos do DNA mitocondrial em mitocôndrias isoladas de fígado de rato, expostas ao complexo Fe2+-citrato, um dos complexos de baixo peso molecular. A intensa fragmentação do DNA foi induzida após a incubação das mitocôndrias com o complexo de ferro. A detecção de finais 3' de fosfoglicolato nas quebras de fitas de DNA mitocondrial pelo ensaio 32P-postlabeling sugere um envolvimento de radicais hidroxila na fragmentação do DNA induzido por complexo Fe2+-citrato. Os níveis elevados de 8-oxo-7,8-diidro-2'-desoxiguanosina também sugerem que o estresse oxidativo induzido por Fe2+-citrato causa danos no DNA mitocondrial. Em conclusão, nossos resultados mostram que a peroxidação lipídica mediada por ferro esteve associada com severos danos do DNA mitocondrial derivados de ataque direto das espécies reativas de oxigênio.

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Se analizó la ultraestructura de embriones bovinos producidos in vitro durante su desarrollo temprano y tardío, mediante la técnica de microscopia electrónica de transmisión (MET). Los complejos cúmulus-ovocitos fueron aspirados de vacas sacrificadas en mataderos comerciales del estado Zulia y madurados, fecundados y cultivados in vitro. Luego de 24 horas (periodo temprano) y 48 horas (periodo tardío) de post inseminación, los embriones resultantes se fijaron en glutaraldehído y se procesaron para MET. Se observó la presencia de estructuras celulares como el aparato de Golgi, el núcleo, microvellosidades, la zona pelúcida y vacuolas citoplasmáticas de apariencia normal. Sin embargo, a nivel de las mitocondrias se encontró aumento en el porcentaje de mitocondrias vacuoladas y de mitocondrias edematizadas. Estas alteraciones mitocondriales se observaron mayormente en los embriones durante el periodo tardío. Estos hallazgos pudiesen tener relevancia en el retraso del desarrollo de los embriones obtenidos por el método in vitro durante el periodo tardío.

La Insuficiencia Cardiaca Congestiva (ICC), estaría asociada a alteraciones mitocondriales y al aumento de especies reactivas del oxigeno (ROS). Para esclarecer estos aspectos estudiamos la estructura, función mitocondrial como así la presencia de enzima oxido nitrosintasa inducible (iNOS) y la lipoperoxidacion de membranas, mediante el ion peroxidonitrito (ONOO-), en el músculo cardíaco y esquelético de pacientes con ICC. Se incluyeron 25 pacientes que fueron sometidos a cirugía cardiovasculares a los que se realizaron biopsias endomio-cardica y de músculo esquelético. Se los estratificó en: grupo con ICC (n=18) y grupo control (n=7). En dichas biopsias se analizó actividad enzimática del complejo III mitocondrial por espectrofotometría, medida en mM.ubiquinona-1.mg prot, mientras que la morfología mitocondrial se analizo con microscopio electrónico Zeiss. La lipoperoxidacion de membranas se midió por la presencia de ONOO- por inmunohistoquimica. El test estadístico utilizado fue ANOVA. El músculo cardiaco de los pacientes con ICC mostró un área mitocondrial disminuida (78%) con respecto al control (160,37?m2 ±9,87); (936,81?m2±78,48) p

The effects of sublethal concentrations of cadmium (0.64 µ-g/L), iron (0.043 mg/L) and zinc (0.31 mg/L) and a mixture of these metals on succinate dehydrogenase (SD) and alkaline phosphatase (AP) activity and on structural changes in the mitochondria of epithelium cells of the digestive tract were examined in the oligochaete Limnodrillus hoffmeisteri after 96 h of exposure in artificial sediments. SD activity was significantly inhibited, particularly in treatments with Cd alone (92.57%), while AP increased its activity with Cd alone (73.23%). However, when this metal was mixed with Fe and Zn, the inhibition of SD activity was lower (67.82%) than with Cd alone, showing an antagonistic effect and AP increased its activity (73.26%). Mitochondria were structurally damaged by exposure to Cd alone. However, in the metal mixtures, the toxic effects may exert interactive effects eliciting a less structural damage in the mitochondria of epithelium cells of the digestive tract than when Cd is alone. [ABSTRACT FROM AUTHOR]

Genetic mitochondrial disorders are responsible for the most common inborn errors of metabolism, caused by mutations in either nuclear genes or in mitochondrial DNA. This article presents the prokaryotic origin of the organelle and the relation between nuclear and mitochondrial genomes, as well as current evolutionary models for such mechanisms. It also addresses the structure of mitochondrial genes, their expression pattern, clinical features of gene defects, risk of transmission and current techniques to avoid these events in assisted human reproduction. Finally, it discusses the ethical implications of these possibilities. [ABSTRACT FROM AUTHOR]

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Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. 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 Revista Portuguesa de Ciências do Desporto is the property of Universidade do Porto, Faculdade de Desporto 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 Revista Chilena de Obstetricia y Ginecología is the property of Revista Chilena de Obstetricia y Ginecologia 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 Revista Chilena de Obstetricia y Ginecología is the property of Revista Chilena de Obstetricia y Ginecologia 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.)

La nutria gigante de río Pteronura brasiliensises un mamífero carnívoro de la familia Mustelidae, ala cual pertenecen también las tairas y los hurones. La nutria es considerada por el CITES comouna especie vulnerable y por la IUCN como especie en peligro de extinción. Por esta razón, elCentro de Biología Molecular del Gimnasio Campestre inicio un proyecto de genética conser-vacionista que pretende proveer información utilizable para el análisis, tanto de la especieP. brasiliensiscomo de sus familiares mas cercanos, y de esta forma, proponer planes de manejode la especie y su hábitat previniendo su extinción.

ABSTRACT Genetic mitochondrial disorders are responsible for the most common inborn errors of metabolism, caused by mutations in either nuclear genes or in mitochondrial DNA. This article presents the prokaryotic origin of the organelle and the relation between nuclear and mitochondrial genomes, as well as current evolutionary models for such mechanisms. It also addresses the structure of mitochondrial genes, their expression pattern, clinical features of gene defects, risk of transmission and current techniques to avoid these events in assisted human reproduction. Finally, it discusses the ethical implications of these possibilities.

Introduction: Several mitochondrial DNA mutations have been reported to be associated with nonsyndromic hearing loss in several families. However, little is known about the prevalence of these mutations in sporadic patients with nonsyndromic sensorineural hearing loss., Objective: The purpose of our study was to investigate the incidence of these mitochondrial DNA mutations in such population., Methods: A total of 178 sporadic patients with nonsyndromic sensorineural hearing loss were enrolled in this study. Genomic DNA was extracted from the peripheral blood sample. We employed the SNaPshot(®) sequencing method to detect five mitochondrial DNA mutations, including A1555G and A827G in 12S rRNA gene and A7445G, 7472insC, and T7511C in tRNA(Ser(UCN)) gene. Meanwhile, we used polymerase chain reaction and sequenced the products to screen GJB2 gene mutations in patients carrying mitochondrial DNA mutations., Results: We failed to detect the presence of A1555G mutation in 12S rRNA gene, and of A7445G, 7472insC, T7511C mutations in tRNA(Ser(UCN)) gene in our population. However, we found that 6 patients (3.37%) were carriers of a homozygous A827G mutation and one of them also carried homozygous GJB2 235delC mutation., Conclusion: Our findings in the present study indicate that even in sporadic patients with nonsyndromic sensorineural hearing loss, mitochondrial DNA mutations might also contribute to the clinical phenotype., (Copyright © 2015 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier Editora Ltda. All rights reserved.)