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https://www.readbyqxmd.com/read/28106766/the-anti-oxidant-defense-system-of-the-marine-polar-ciliate-euplotes-nobilii-characterization-of-the-msrb-gene-family
#1
Francesca Ricci, Federico M Lauro, Joseph J Grzymski, Robert Read, Rigers Bakiu, Gianfranco Santovito, Pierangelo Luporini, Adriana Vallesi
Organisms living in polar waters must cope with an extremely stressful environment dominated by freezing temperatures, high oxygen concentrations and UV radiation. To shed light on the genetic mechanisms on which the polar marine ciliate, Euplotes nobilii, relies to effectively cope with the oxidative stress, attention was focused on methionine sulfoxide reductases which repair proteins with oxidized methionines. A family of four structurally distinct MsrB genes, encoding enzymes specific for the reduction of the methionine-sulfoxide R-forms, were identified from a draft of the E...
January 18, 2017: Biology
https://www.readbyqxmd.com/read/28104750/gene-networks-in-skeletal-muscle-following-endurance-exercise-are-co-expressed-in-blood-neutrophils-and-linked-with-blood-inflammation-markers
#2
James A Broadbent, Dayle Sampson, Surendran Sabapathy, Luke J Haseler, Karl-Heinz Wagner, Andrew Cameron Bulmer, Jonathan M Peake, Oliver Neubauer
It remains incompletely understood whether there is an association between the transcriptome profiles of skeletal muscle and blood leukocytes in response to exercise or other physiological stressors. We have previously analyzed the changes in the muscle and blood neutrophil transcriptome in eight trained men before and 3 h, 48 h and 96 h after 2 h cycling and running. Because we collected muscle and blood in the same individuals and under the same conditions, we were able to directly compare gene expression between the muscle and blood neutrophils...
January 19, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28104397/pink1-alleviates-myocardial-hypoxia-reoxygenation-injury-by-ameliorating-mitochondrial-dysfunction
#3
Yang Li, Liangxian Qiu, Xiping Liu, Zhiwen Hou, Bo Yu
PTEN inducible kinase-1 (PINK1) mutant induces mitochondrial dysfunction of cells, resulting in an inherited form of Parkinson's disease. However its exact role in the cardiomyocytes is unclear. The present study examined the function of PINK1 in hypoxia-reoxygenation (H/R) induced H9c2 cell damage and its potential mechanism. The H/R model in H9c2 cells was established by 6 h of hypoxia and 12 h of reoxygenation. The CCK8 and LDH assay indicated that the cell viability was obviously reduced after H/R. The expression of PINK1 was decreased in H/R-induced H9c2 cells compared with control group...
January 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28104376/lipidomic-profile-of-gm95-cell-death-induced-by-clostridium-perfringens-alpha-toxin
#4
Marco M Manni, Juan G Valero, Miriam Pérez-Cormenzana, Ainara Cano, Cristina Alonso, Félix M Goñi
Clostridium perfringens alpha-toxin (ATX) is considered as a prototype of cytotoxic bacterial phospholipases C, and is the major virulence factor in C. perfringens-induced gas gangrene. It is known that, depending on the dose, ATX causes membrane disruption and cytolysis or only limited hydrolysis of its substrates. In the latter case, toxin activity leads to the unregulated generation of bioactive lipids that can ultimately induce cell death. We have characterized apoptosis and necrosis in highly ATX-sensitive, ganglioside-deficient cells exposed to different concentrations of ATX and we have studied the lipidomic profile of cells treated with ATX as compared to native cells to detect the main changes in the lipidomic profile and the possible involvement of lipid signals in cell death...
January 16, 2017: Chemistry and Physics of Lipids
https://www.readbyqxmd.com/read/28103798/selenium-suppresses-glutamate-induced-cell-death-and-prevents-mitochondrial-morphological-dynamic-alterations-in-hippocampal-ht22-neuronal-cells
#5
Yan-Mei Ma, Gordon Ibeanu, Li-Yao Wang, Jian-Zhong Zhang, Yue Chang, Jian-Da Dong, P Andy Li, Li Jing
BACKGROUND: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage...
January 19, 2017: BMC Neuroscience
https://www.readbyqxmd.com/read/28103389/the-use-of-antioxidants-in-the-treatment-of-traumatic-brain-injury
#6
Whitney Venegoni, Qiuhua Shen, Amanda R Thimmesch, Meredith Bell, John B Hiebert, Janet D Pierce
AIMS: To discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. BACKGROUND: One of the leading causes of death in young adults internationally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life...
January 19, 2017: Journal of Advanced Nursing
https://www.readbyqxmd.com/read/28102324/antiproliferative-and-apoptosis-inducing-effect-of-exo-protoporphyrin-ix-based-sonodynamic-therapy-on-human-oral-squamous-cell-carcinoma
#7
Yanhong Lv, Jinhua Zheng, Qi Zhou, Limin Jia, Chunying Wang, Nian Liu, Hong Zhao, Hang Ji, Baoxin Li, Wenwu Cao
Sonodynamic therapy (SDT) is an innovative modality for cancer treatment. But the biological effect of SDT on oral squamous cell carcinoma has not been studied. Our previous study has shown that endo-Protoporphyrin IX based SDT (ALA-SDT) could induce apoptosis in human tongue squamous carcinoma SAS cells through mitochondrial pathway. Herein, we investigated the effect of exo- Protoporphyrin based SDT (PpIX-SDT) on SAS cells in vitro and in vivo. We demonstrated that PpIX-SDT increased the ratio of cells in the G2/M phase and induced 3-4 times more cell apoptosis compared to sonocation alone...
January 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28101642/late-sodium-current-and-intracellular-ionic-homeostasis-in-acute-ischemia
#8
Carlotta Ronchi, Eleonora Torre, Riccardo Rizzetto, Joyce Bernardi, Marcella Rocchetti, Antonio Zaza
Blockade of the late Na(+) current (I NaL) protects from ischemia/reperfusion damage; nevertheless, information on changes in I NaL during acute ischemia and their effect on intracellular milieu is missing. I NaL, cytosolic Na(+) and Ca(2+) activities (Nacyt, Cacyt) were measured in isolated rat ventricular myocytes during 7 min of simulated ischemia (ISC); in all the conditions tested, effects consistently exerted by ranolazine (RAN) and tetrodotoxin (TTX) were interpreted as due to I NaL blockade. The results indicate that I NaL was enhanced during ISC in spite of changes in action potential (AP) contour; I NaL significantly contributed to Nacyt rise, but only marginally to Cacyt rise...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28101459/venlafaxine-induced-cytotoxicity-towards-isolated-rat-hepatocytes-involves-oxidative-stress-and-mitochondrial-lysosomal-dysfunction
#9
Elham Ahmadian, Hossein Babaei, Alireza Mohajjel Nayebi, Aziz Eftekhari, Mohammad Ali Eghbal
Purpose: Depression is a public disorder worldwide. Despite the widespread use of venlafaxine in the treatment of depression, it has been associated with the incidence of toxicities. Hence, the goal of the current investigation was to evaluate the mechanisms of venlafaxine-induced cell death in the model of the freshly isolated rat hepatocytes. Methods: Collagenase-perfused rat hepatocytes were treated with venlafaxine and other agents. Cell damage, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial membrane potential decline, lysosomal damage, glutathione (GSH) level were analyzed...
December 2016: Advanced Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28100347/-salvianolate-protects-h9c2-cells-from-hypoxia-reoxygenation-injury-induced-apoptosis-by-attenuating-mitochondrial-dna-oxidative-damage
#10
R C Yue, X L Yang, R Y Zhang, S Liu, J Liu, J Zeng, H Liang, W Wang, H X Hu, C Y Zeng
Objective: To investigate the possible mechanism related to the protective effects of salvianolate in H9c2 cells underwent hypoxia/reoxygenation (H/R)-injury. Methods: H9c2 cells were divided into four groups: control group, salvianolate group (S group), H/R group, and salvianolate+ H/R group(S+ H/R group), in which the H9c2 cells were pretreated with salvianolate before H/R-treatment.Apoptotic cells were detected by Tunel assays and AnnexinⅤ-FITC apoptosis detection kit.The intracellular ATP level, the change of mitochondrial membrane potential and the mitochondrial DNA oxidative damage were also determined in these groups...
January 25, 2017: Zhonghua Xin Xue Guan Bing za Zhi
https://www.readbyqxmd.com/read/28098432/a-multi-mitochondrial-anticancer-agent-that-selectively-kills-cancer-cells-and-overcomes-drug-resistance
#11
Yong Bo Peng, Zi Long Zhao, Teng Liu, Guo Jian Xie, Cheng Jin, Tang Gang Deng, Yang Sun, Xiong Li, Xiao Xiao Hu, Xiao Bing Zhang, Mao Ye, Wei Hong Tan
Mitochondria are double-membrane-bound organelles involved mainly in supplying cellular energy, but also play roles in signaling, cell differentiation, and cell death. Mitochondria are implicated in carcinogenesis, and therefore dozens of lethal signal transduction pathways converge on these organelles. Accordingly, mitochondria provide an alternative target for cancer management. In this study, F16, a drug that targets mitochondria, and chlorambucil (CBL), which is indicated for the treatment of selected human neoplastic diseases, were covalently linked, resulting in the synthesis of a multi-mitochondrial anticancer agent, FCBL...
January 18, 2017: ChemMedChem
https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#12
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/28095073/preclinical-and-potential-applications-of-common-western-herbal-supplements-as-complementary-treatment-in-parkinson-s-disease
#13
Luke A Morgan, Oliver Grundmann
Parkinson's disease (PD) is a neurological disorder with a complex pathological etiology, which is not fully understood. Progression of PD may be the result of a buildup of iron in the substantia nigra, microglia-mediated neuroinflammation, dysfunctional mitochondria, or abnormal protein handling. Dopamine is the main neurotransmitter affected, but as the disease progresses, a decrease in all the brain's biogenic amines occurs. Current medication used in the treatment of PD aims to prevent the breakdown of dopamine or increase dopaminergic neurotransmission in the central nervous system...
January 17, 2017: Journal of Dietary Supplements
https://www.readbyqxmd.com/read/28094012/mammalian-mitochondria-and-aging-an-update
#14
REVIEW
Timo E S Kauppila, Johanna H K Kauppila, Nils-Göran Larsson
Mitochondria were first postulated to contribute to aging more than 40 years ago. During the following decades, multiple lines of evidence in model organisms and humans showed that impaired mitochondrial function can contribute to age-associated disease phenotypes and aging. However, in contrast to the original theory favoring oxidative damage as a cause for mtDNA mutations, there are now strong data arguing that most mammalian mtDNA mutations originate as replication errors made by the mtDNA polymerase. Currently, a substantial amount of mitochondrial research is focused on finding ways to either remove or counteract the effects of mtDNA mutations with the hope of extending the human health- and lifespan...
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28093935/new-methods-for-monitoring-mitochondrial-biogenesis-and-mitophagy-in%C3%A2-vitro-and-in%C3%A2-vivo
#15
Jessica A Williams, Katrina Zhao, Shengkan Jin, Wen-Xing Ding
Removal of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. Increasing evidence implicates mitophagy in red blood cell differentiation, neurodegeneration, macrophage-mediated inflammation, ischemia, adipogenesis, drug-induced tissue injury, and cancer. Considerable progress has been made toward understanding the biochemical mechanisms involved in mitophagy regulation. However, few reliable assays to monitor and quantify mitophagy have been developed, particularly in vivo...
January 1, 2017: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28093764/pre-ischemic-mitochondrial-substrate-constraint-by-inhibition-of-malate-aspartate-shuttle-preserves-mitochondrial-function-after-ischemia-reperfusion
#16
Nichlas Riise Jespersen, Takashi Yokota, Nicolaj Brejnholt Støttrup, Andreas Bergdahl, Kim Bolther Paelestik, Jonas Agerlund Povlsen, Flemming Dela, Hans Erik Bøtker
Mitochondrial dysfunction plays a central role in ischemia-reperfusion (IR) injury. The pre-ischemic administration of aminooxyacetate (AOA), an inhibitor of the malate-aspartate shuttle (MAS), provides cardioprotection against IR injury, but the underlying mechanism remains unknown. We hypothesized that a transient inhibition of the MAS during ischemia and early reperfusion could preserve mitochondrial function at later phase of reperfusion in IR-injured heart to the same extent as ischemic preconditioning (IPC), which is a well-validated cardioprotective strategy against IR injury...
January 17, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28093214/the-upr-reduces-glucose-metabolism-via-ire1-signaling
#17
Judith M van der Harg, Jessica C van Heest, Fabian N Bangel, Sanne Patiwael, Jan R T van Weering, Wiep Scheper
Neurons are highly dependent on glucose. A disturbance in glucose homeostasis therefore poses a severe risk that is counteracted by activation of stress responses to limit damage and restore the energy balance. A major stress response that is activated under conditions of glucose deprivation is the unfolded protein response (UPR) that is aimed to restore proteostasis in the endoplasmic reticulum. The key signaling of the UPR involves the transient activation of a transcriptional program and an overall reduction of protein synthesis...
January 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28093052/erk-nrf2-ho-1-pathway-mediated-mitophagy-alleviates-traumatic-brain-injury-induced-intestinal-mucosa-damage-and-epithelial-barrier-dysfunction
#18
Yinlong Liu, Zhongyuan Bao, Xiupeng Xu, Honglu Chao, Chao Lin, Zheng Li, Yan Liu, Xiaoming Wang, Yongping You, Ning Liu, Jing Ji
Gastrointestinal dysfunction is one of several physiologic complications in patients with traumatic brain injury (TBI). TBI can result in increased intestinal permeability due to apoptosis of intestinal epithelial cells, which contain a large number of mitochondria for persisting barrier function. Autophagy of damaged mitochondria (mitophagy) controls the quality of the mitochondria and regulates cellular homeostasis. However, the exact mechanism of mitophagy that underlies the pathological changes induced by TBI is unknown...
January 16, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28087840/vibrio-cholerae-cholix-toxin-induced-hepg2-cell-death-is-enhanced-by-tumor-necrosis-factor-alpha-through-ros-and-intracellular-signal-regulated-kinases
#19
Kohei Ogura, Yasuhiro Terasaki, Tohru Miyoshi-Akiyama, Mika Terasaki, Joel Moss, Masatoshi Noda, Kinnosuke Yahiro
Cholix toxin (Cholix) from Vibrio cholerae is a potent virulence factor exhibiting ADP-ribosyltransferase activity on eukaryotic elongation factor 2 (eEF2) of host cells, resulting in inhibition of protein synthesis. Administration of Cholix or its homologue Pseudomonas exotoxin A (PEA) to mice causes lethal hepatocyte damage. In this study, we demonstrate cytotoxicity of Cholix on immortalized human hepatocytes in the presence of tumor necrosis factor α (TNF-α), which has been reported to play a fatal role in PEA administered to mice...
January 13, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28086886/biochemical-mechanism-underlying-hypertriglyceridemia-and-hepatic-steatosis-hepatomegaly-induced-by-acute-schisandrin-b-treatment-in-mice
#20
Yi Zhang, Jing Zhao, Shu-Feng Zhou, Zhi-Ling Yu, Xiao-Yan Wang, Pei-Li Zhu, Zhu-Sheng Chu, Si-Yuan Pan, Ming Xie, Kam-Ming Ko
BACKGROUND: It has been demonstrated that acute oral administration of schisandrin B (Sch B), an active dibenzocyclooctadiene isolated from Schisandrae Fructus (a commonly used traditional Chinese herb), increased serum and hepatic triglyceride (TG) levels and hepatic mass in mice. The present study aimed to investigate the biochemical mechanism underlying the Sch B-induced hypertriglyceridemia, hepatic steatosis and hepatomegaly. METHODS: Male ICR mice were given a single oral dose of Sch B (0...
January 13, 2017: Lipids in Health and Disease
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