Navegando por Palavras-chave "mitocôndrias"
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- ItemAcesso aberto (Open Access)Calcium and cell death signaling in neurodegeneration and aging(Academia Brasileira de Ciências, 2009-09-01) Smaili, Soraya Soubhi [UNIFESP]; Hirata, Hanako [UNIFESP]; Ureshino, Rodrigo Portes [UNIFESP]; Monteforte, Priscila T. [UNIFESP]; Morales, Ana P. [UNIFESP]; Muler, Mari Luminosa [UNIFESP]; Terashima, Juliana [UNIFESP]; Oseki, Karen Tubono [UNIFESP]; Rosenstock, Tatiana R. [UNIFESP]; Lopes, Guiomar Silva [UNIFESP]; Bincoletto, Claudia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)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.
- ItemSomente MetadadadosO impacto da obesidade sobre a qualidade funcional dos espermatozoides e os mecanismos proteômicos do sêmen(Universidade Federal de São Paulo (UNIFESP), 2015-11-30) Ferigolo, Paola Cristine [UNIFESP]; Fraietta, Renato Fraietta [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Purpose: To evaluate the effect of obesity on the sperm function and seminal plasma proteome. Methods: A prospective study was performed including 47 male volunteers, of which 27 participated in the obese group (BMI ? 30 kg / m2) and 20 in the control group (? 18.5 and BMI <25 kg / m2). After semen retrieval by masturbation, an aliquot was used for semen analysis and another for evaluation of the main functional characteristics of sperm. Mitochondrial activity was determined by a colorimetric stain (3,3?-diaminobenzidine - DAB) and classified as DAB I (all mitochondria active) to DAB IV (all mitochondria inactive); acrosome integrity was determined by a fluorescent probe (PNA-FITC) and assessed by fluorescent microscopy; and sperm DNA fragmentation was assessed by an alkaline Comet assay, in which sperm were classified as high DNA integrity (class I) to high DNA fragmentation (class IV). The remaining semen volume was centrifuged and the supernatant seminal plasma was utilized for proteomic analysis by LC-MS/MS. Groups were compared by an unpaired Student?s t test. Differentially expressed proteins were subsequently used for functional enrichment analysis of Gene Ontology categories using the online platform PantherDB. Results: Significant diferences were observed in sperm non-progressive motility (p = 0.018), morphology (p = 0.028), PNA-FITC (p <0.0001), DAB I (p = 0.0001), DAB III (p = 0 , 0017), IV DAB (0.026), DAB (p = 0.0003), Comet III (p = 0.001), and Comet (p = 0.003). In proteomics analysis, a total of 489 proteins were quantified and identified, in which 73 are differentially expressed between the two groups and 416 proteins are conserved. Among the differentially expressed proteins, 1 protein was absent, 19 were down-regulated, 49 were up-regulated and 4 were exclusive in the study group. The main functions enriched in the obesity group were negative regulation of the intrinsic pathway of apoptosis, regulation of phagocytosis, endocytosis regulation, regulation of proteolysis, endopeptidase inhibitory activity, activation of immune and inflammatory and antioxidant activity. The functions depleted in the obesity group were the following: regulation of metabolic process, regulation of response to stimulus and regulation of cellular process. Conclusions: Based on our findings, obesity may affect semen quality and sperm function. There is a significant change in the proteome of the seminal plasma of men with excess weight that elucidates some processes involved in infertility of these men, such as excessive production of reactive oxygen species, endocrine disorders, testicular hyperthermia, exacerbated immune response, inflammatory response, inhibiting phospholipase and changes in apoptotic pathway.
- ItemAcesso aberto (Open Access)Mitochondrial DNA damage associated with lipid peroxidation of the mitochondrial membrane induced by Fe2+-citrate(Academia Brasileira de Ciências, 2006-09-01) Almeida, Andréa M.; Bertoncini, Clelia Rejane Antonio [UNIFESP]; Borecký, Jiri; Souza-Pinto, Nadja C.; Vercesi, Aníbal E.; Universidade Estadual de Campinas (UNICAMP); Universidade Federal de São Paulo (UNIFESP); Universidade Federal de Viçosa Departamento de Biologia Vegetal; National Institute on Aging Laboratory of Molecular GerontologyIron 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.