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https://www.readbyqxmd.com/read/28527718/rotenone-decreases-ischemia-induced-injury-by-inhibiting-mitochondrial-permeability-transition-in-mature-brains
#1
Evelina Rekuviene, Laima Ivanoviene, Vilmante Borutaite, Ramune Morkuniene
The mitochondrial permeability transition pore (mPTP) is thought to be implicated in brain ischemia-induced cell death. Here we sought to determine whether complex I (CI) of the mitochondrial electron transfer system may be involved in regulation of mPTP opening during ischemia and whether a specific inhibitor of this complex - rotenone can protect against ischemia-induced cell death in an experimental model of total ischemia in adult rat brains. Anesthetized Wistar rats were administered a single injection of rotenone (0...
May 17, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28526935/diabetes-induced-abnormalities-of-mitochondrial-function-in-rat-brain-cortex-the-effect-of-n-3-fatty-acid-diet
#2
Maria Chomova, Maria Balazova, Jana Muchova
Diabetic encephalopathy, a proven complication of diabetes is associated with gradually developing end-organ damage in the CNS increasing the risk of stroke, cognitive dysfunction or Alzheimer's disease. This study investigated the response of rat cortical mitochondria to streptozotocin-induced diabetes and the potential for fish oil emulsion (FOE) to modulate mitochondrial function. Diabetes-induced deregulation of the respiratory chain function as a result of diminished complex I activity (CI) and cytochrome c oxidase hyperactivity was associated with attenuation of antioxidant defense of isolated cortical mitochondria, monitored by SOD activity, the thiol content, the dityrosine and protein-lipid peroxidation adduct formation...
May 19, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28526448/the-catechol-o-methyltransferase-inhibitors-tolcapone-and-entacapone-uncouple-and-inhibit-the-mitochondrial-respiratory-chain-in-heparg-cells
#3
David Grünig, Andrea Felser, Jamal Bouitbir, Stephan Krähenbühl
The catechol-O-methyltransferase inhibitor tolcapone causes hepatotoxicity and mitochondrial damage in animal models. We studied the interaction of tolcapone with mitochondrial respiration in comparison to entacapone in different experimental models. In HepaRG cells (human cell-line), tolcapone decreased the ATP content (estimated IC50 100±15μM) and was cytotoxic (estimated IC50 333±45μM), whereas entacapone caused no cytotoxicity and no ATP depletion up to 200μM. Cytochrome P450 induction did not increase the toxicity of the compounds...
May 16, 2017: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/28526246/impaired-mitophagy-facilitates-mitochondrial-damage-in-danon-disease
#4
Sherin I Hashem, Anne N Murphy, Ajit S Divakaruni, Matthew L Klos, Bradley C Nelson, Emily C Gault, Teisha J Rowland, Cynthia N Perry, Yusu Gu, Nancy D Dalton, William H Bradford, Eric J Devaney, Kirk L Peterson, Kenneth L Jones, Matthew R G Taylor, Ju Chen, Neil C Chi, Eric D Adler
RATIONALE: Lysosomal associated membrane protein type-2 (LAMP-2) is a highly conserved, ubiquitous protein that is critical for autophagic flux. Loss of function mutations in the LAMP-2 gene cause Danon disease, a rare X-linked disorder characterized by developmental delay, skeletal muscle weakness, and severe cardiomyopathy. We previously found that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from Danon patients exhibited significant mitochondrial oxidative stress and apoptosis...
May 16, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28524859/mesenchymal-stem-cells-sense-mitochondria-released-from-damaged-cells-as-danger-signals-to-activate-their-rescue-properties
#5
Meriem Mahrouf-Yorgov, Lionel Augeul, Claire Crola Da Silva, Maud Jourdan, Muriel Rigolet, Sylvie Manin, René Ferrera, Michel Ovize, Adeline Henry, Aurélie Guguin, Jean-Paul Meningaud, Jean-Luc Dubois-Randé, Roberto Motterlini, Roberta Foresti, Anne-Marie Rodriguez
Mesenchymal stem cells (MSCs) protect tissues against cell death induced by ischemia/reperfusion insults. This therapeutic effect seems to be controlled by physiological cues released by the local microenvironment following injury. Recent lines of evidence indicate that MSC can communicate with their microenvironment through bidirectional exchanges of mitochondria. In particular, in vitro and in vivo studies report that MSCs rescue injured cells through delivery of their own mitochondria. However, the role of mitochondria conveyed from somatic cells to MSC remains unknown...
May 19, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28522880/immunolocalization-of-glutathione-peroxidase-gpx1-in-the-rat-adrenal-cortex-correlation-between-steroidogenesis-and-lipid-peroxidation
#6
Masanori Murakoshi, Robert Yoshiyuki Osamura
In order to confirm the relationship between glutathione-peroxidase (GPx1) and biological significance on steroidogenesis, we have studied the immunocytochemical localization of GPx1 in the rat adrenal cortical cells. GPx1 was observed not only in cytoplasm (cytosol GPx1) but in mitochondria (mitochondrial GPx1). The staining intensity was altered by the functional state of the adrenal cortical cells. Furthermore, cytosol- and mitochondrial-GPx1 was modified by lipoperoxidative damage in the adrenal cortical cells...
April 27, 2017: Acta Histochemica et Cytochemica
https://www.readbyqxmd.com/read/28515764/the-effect-of-epicatechin-on-oxidative-stress-and-mitochondrial-damage-induced-by-homocycteine-using-isolated-rat-hippocampus-mitochondria
#7
Fatemeh Shaki, Yaghoub Shayeste, Mohammad Karami, Esmaeil Akbari, Mahdi Rezaei, Ramin Ataee
Oxidative stress and mitochondrial dysfunction are the main suggested mechanisms for neurodegenerative diseases. In this study, we have evaluated the effects of epicatechin (EC) on mitochondrial damage induced by homocycteine (Hcy) using isolated rat hippocampus mitochondria in vivo. EC (50 mg/kg) was gavaged daily for a period of 10 days, starting 5 days prior to Hcy (0.5 μmol/μL) intra hippocampus injection in rats. Mitochondria were isolated from brain by different centrifuge techniques. Mitochondrial function was assayed by MTT test...
April 2017: Research in Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28515082/parkin-independent-mitophagy-fkbp8-takes-the-stage
#8
Grace Gy Lim, Kah-Leong Lim
Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the selective clearance of mitochondria in the absence of Parkin. In this issue, Bhujabal et al expand the repertoire of Parkin-independent mitophagy receptors to include the anti-apoptotic protein, FKBP8. The authors demonstrate that FKBP8 interacts preferentially with LC3A via its LIR motif to destroy damaged mitochondria...
May 17, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28513781/mitochondria-rich-cells-changes-induced-by-nitrite-exposure-in-tambaqui-colossoma-macropomum-cuvier-1818
#9
Oscar T F DA Costa, Cleverson A Ramos, Wallice P Duncan, Juliana L V Lameiras, Marisa N Fernandes
The gill mitochondria-rich cells of the juvenile Amazonian fish Colossoma macropomum were analyzed using light and scanning and transmission electron microscopy after 96 h exposure to 0.04 and 0.2 mM nitrite. Although the number of mitochondria-rich cells decreased significantly in the lamellar epithelium, no decrease was found in the interlamellar region of the gill filament. Nitrite exposure caused significant reduction on the apical surface area of individual mitochondria-rich cells (p < 0.05), with a resulting reduction of the fractional area of these cells in both the lamellar and filament epithelium...
May 15, 2017: Anais da Academia Brasileira de Ciências
https://www.readbyqxmd.com/read/28510423/phycocyanin-functionalized-selenium-nanoparticles-reverse-palmitic-acid-induced-pancreatic-beta-cells-apoptosis-by-enhancing-cellular-uptake-and-blocking-ros-mediated-mitochondria-dysfunction
#10
Chang Liu, Yuanting Fu, Chang-E Li, Tianfeng Chen, Xiaoling Li
Accumulation of palmitic acid (PA) in human bodies could cause damage to pancreatic beta cells and lead to chronic diseases by generation of reactive oxygen species (ROS). Therefore, it is of great significance to search for nutrition available agents with antioxidant activity to protect pancreatic islet cells against PA-induced damage. Phycocyanin (PC) and selenium (Se) have been reported to have excellent antioxidant activity. In this study, PC-functionalized selenium nanoparticles (PC-SeNPs) were synthesized to investigate the in vitro protective effects on INS-1E rat insulinoma beta cells against PA-induced cell death...
May 16, 2017: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/28508041/mitochondrial-protein-linked-dna-breaks-perturb-mitochondrial-gene-transcription-and-trigger-free-radical-induced-dna-damage
#11
Shih-Chieh Chiang, Martin Meagher, Nick Kassouf, Majid Hafezparast, Peter J McKinnon, Rachel Haywood, Sherif F El-Khamisy
Breakage of one strand of DNA is the most common form of DNA damage. Most damaged DNA termini require end-processing in preparation for ligation. The importance of this step is highlighted by the association of defects in the 3'-end processing enzyme tyrosyl DNA phosphodiesterase 1 (TDP1) and neurodegeneration and by the cytotoxic induction of protein-linked DNA breaks (PDBs) and oxidized nucleic acid intermediates during chemotherapy and radiotherapy. Although much is known about the repair of PDBs in the nucleus, little is known about this process in the mitochondria...
April 2017: Science Advances
https://www.readbyqxmd.com/read/28507507/pink1-parkin-dependent-mitochondrial-surveillance-from-pleiotropy-to-parkinson-s-disease
#12
REVIEW
Francois Mouton-Liger, Maxime Jacoupy, Jean-Christophe Corvol, Olga Corti
Parkinson's disease (PD) is one of the most frequent neurodegenerative disease caused by the preferential, progressive degeneration of the dopaminergic (DA) neurons of the substantia nigra (SN) pars compacta. PD is characterized by a multifaceted pathological process involving protein misfolding, mitochondrial dysfunction, neuroinflammation and metabolism deregulation. The molecular mechanisms governing the complex interplay between the different facets of this process are still unknown. PARK2/Parkin and PARK6/PINK1, two genes responsible for familial forms of PD, act as a ubiquitous core signaling pathway, coupling mitochondrial stress to mitochondrial surveillance, by regulating mitochondrial dynamics, the removal of damaged mitochondrial components by mitochondria-derived vesicles, mitophagy, and mitochondrial biogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28504722/thyroid-hormone-protects-hepatocytes-from-hbx-induced-carcinogenesis-by-enhancing-mitochondrial-turnover
#13
H-C Chi, S-L Chen, S-L Lin, C-Y Tsai, W-Y Chuang, Y-H Lin, Y-H Huang, M-M Tsai, C-T Yeh, K-H Lin
Infection by hepatitis B virus (HBV) accounts for 50-80% of hepatocellular carcinoma (HCC) development worldwide, in which the HBV-encoded X protein (HBx) has critical role in the induction of carcinogenesis. Several studies have shown that thyroid hormone (TH) suppresses HCC development and protects hepatocytes from HBx-induced damage, thus it is of interest to examine whether TH can protect hepatocytes from HBx-induced carcinogenesis. By treating HBx- transgenic mice with or without TH, we confirmed the protective effects of TH on HBx-induced hepatocarcinogenesis, which was achieved via reduction of reactive oxygen species (ROS) inflicted DNA damage...
May 15, 2017: Oncogene
https://www.readbyqxmd.com/read/28504653/metabolic-shifts-in-residual-breast-cancer-drive-tumor-recurrence
#14
Kristina M Havas, Vladislava Milchevskaya, Ksenija Radic, Ashna Alladin, Eleni Kafkia, Marta Garcia, Jens Stolte, Bernd Klaus, Nicole Rotmensz, Toby J Gibson, Barbara Burwinkel, Andreas Schneeweiss, Giancarlo Pruneri, Kiran R Patil, Rocio Sotillo, Martin Jechlinger
Tumor recurrence is the leading cause of breast cancer-related death. Recurrences are largely driven by cancer cells that survive therapeutic intervention. This poorly understood population is referred to as minimal residual disease. Here, using mouse models that faithfully recapitulate human disease together with organoid cultures, we have demonstrated that residual cells acquire a transcriptionally distinct state from normal epithelium and primary tumors. Gene expression changes and functional characterization revealed altered lipid metabolism and elevated ROS as hallmarks of the cells that survive tumor regression...
May 15, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28502921/umbilical-cord-mscs-reverse-d-galactose-induced-hepatic-mitochondrial-dysfunction-via-activation-of-nrf2-ho-1-pathway
#15
Weihong Yan, Dong Li, Tong Chen, Guiying Tian, Panpan Zhou, Xiuli Ju
Mitochondria are the central hubs for cellular bioenergetics and are crucial to cell survival. It is well accepted that compromised mitochondrial function is linked with hepatocytes injury and contribute to progression of liver diseases. Despite the therapeutic potential of mesenchymal stem cells (MSCs) transplantation on hepatic disorders have been extensively investigated, the effects of MSCs on mitochondrial function in liver injury models remain unknown. Here we investigated the effects of treatment with umbilical cord (UC) MSC in a rat model of D-Gal induced liver injury, characterized by organ damage, oxidative stress and mitochondrial dysfunction...
May 13, 2017: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28502703/cell-death-induced-by-mitochondrial-complex-i-inhibition-is-mediated-by-iron-regulatory-protein-1
#16
Pamela J Urrutia, Pabla Aguirre, Victoria Tapia, Carlos M Carrasco, Natalia P Mena, Marco T Núñez
Mitochondrial dysfunction and oxidative damage, often accompanied by elevated intracellular iron levels, are pathophysiological features in a number of neurodegenerative processes. The question arises as to whether iron dyshomeostasis is a consequence of mitochondrial dysfunction. Here we have evaluated the role of Iron Regulatory Protein 1 (IRP1) in the death of SH-SY5Y dopaminergic neuroblastoma cells subjected to mitochondria complex I inhibition. We found that complex I inhibition was associated with increased levels of transferrin receptor 1 (TfR1) and iron uptake transporter divalent metal transporter 1 (DMT1), and decreased levels of iron efflux transporter Ferroportin 1 (FPN1), together with increased (55)Fe uptake activity and an increased cytoplasmic labile iron pool...
May 11, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28501614/shaping-mitochondrial-dynamics-the-role-of-camp-signalling
#17
Giulietta Di Benedetto, Andrea Gerbino, Konstantinos Lefkimmiatis
In recent years, our idea of mitochondria evolved from "mere" energy and metabolite producers to key regulators of many cellular functions. In order to preserve and protect their functional status, these organelles engage a number of dynamic processes that allow them to decrease accumulated burden and maintain their homeostasis. Indeed, mitochondria can unite (fusion), divide (fission), position themselves strategically in the cell (motility/trafficking) and if irreversibly damaged or dysfunctional eliminated (mitophagy)...
May 10, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28500761/melatonin-ameliorates-myocardial-ischemia-reperfusion-injury-through-sirt3-dependent-regulation-of-oxidative-stress-and-apoptosis
#18
Mengen Zhai, Buying Li, Weixun Duan, Lin Jing, Bin Zhang, Meng Zhang, Liming Yu, Zhenhua Liu, Bo Yu, Kai Ren, Erhe Gao, Yang Yang, Hongliang Liang, Zhenxiao Jin, Shiqiang Yu
Sirtuins are a family of highly evolutionarily conserved nicotinamide adenine nucleotide-dependent histone deacetylases. Sirtuin-3 (SIRT3) is a member of the sirtuin family that is localized primarily to the mitochondria and protects against oxidative stress-related diseases, including myocardial ischemia/reperfusion (MI/R) injury. Melatonin has a favorable effect in ameliorating MI/R injury. We hypothesized that melatonin protects against MI/R injury by activating the SIRT3 signaling pathway. In this study, mice were pre-treated with or without a selective SIRT3 inhibitor and then subjected to MI/R operation...
May 13, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28499983/photostimulation-of-mitochondria-as-a-treatment-for-retinal-neurodegeneration
#19
Kathy Beirne, Malgorzata Rozanowska, Marcela Votruba
Absorption of photon energy by neuronal mitochondria leads to numerous downstream neuroprotective effects. Red and near infrared (NIR) light are associated with significantly less safety concerns than light of shorter wavelengths and they are therefore, the optimal choice for irradiating the retina. Potent neuroprotective effects have been demonstrated in various models of retinal damage, by red/NIR light, with limited data from human studies showing its ability to improve visual function. Improved neuronal mitochondrial function, increased blood flow to neural tissue, upregulation of cell survival mediators and restoration of normal microglial function have all been proposed as potential underlying mechanisms of red/NIR light...
May 9, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28499253/the-role-of-sodium-hydrosulfide-in-attenuating-the-aging-process-via-pi3k-akt-and-camkk%C3%AE-ampk-pathways
#20
Xubo Chen, Xueyan Zhao, Hua Cai, Haiying Sun, Yujuan Hu, Xiang Huang, Wen Kong, Weijia Kong
Age-related dysfunction of the central auditory system, known as central presbycusis, is characterized by defects in speech perception and sound localization. It is important to determine the pathogenesis of central presbycusis in order to explore a feasible and effective intervention method. Recent work has provided fascinating insight into the beneficial function of H2S on oxidative stress and stress-related disease. In this study, we investigated the pathogenesis of central presbycusis and tried to explore the mechanism of H2S action on different aspects of aging by utilizing a mimetic aging rat and senescent cellular model...
April 25, 2017: Redox Biology
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