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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]

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]

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]

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]