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https://www.readbyqxmd.com/read/28631341/evaluation-of-flubendiamide-induced-mitochondrial-dysfunction-and-metabolic-changes-in-helicoverpa-armigera-hubner
#1
Bharat Nareshkumar, Shaik Mohammad Akbar, Hari Chand Sharma, Senigala K Jayalakshmi, Kuruba Sreeramulu
Phthalic acid diamide insecticides are the most effective insecticides used against most of the lepidopteran pests including Helicoverpa armigera, a polyphagous pest posing threat to several crops worldwide. The present studies were undertaken to understand different target sites and their interaction with insect ryanodine receptors (RyR). Bioassays indicated that flubendiamide inhibited the larval growth in dose-dependent manner with LD50 value of 0.72 μM, and at 0.8 μM larval growth decreased by about 88%...
June 20, 2017: Archives of Insect Biochemistry and Physiology
https://www.readbyqxmd.com/read/28630339/ucp1-deficiency-causes-brown-fat-respiratory-chain-depletion-and-sensitizes-mitochondria-to-calcium-overload-induced-dysfunction
#2
Lawrence Kazak, Edward T Chouchani, Irina G Stavrovskaya, Gina Z Lu, Mark P Jedrychowski, Daniel F Egan, Manju Kumari, Xingxing Kong, Brian K Erickson, John Szpyt, Evan D Rosen, Michael P Murphy, Bruce S Kristal, Steven P Gygi, Bruce M Spiegelman
Brown adipose tissue (BAT) mitochondria exhibit high oxidative capacity and abundant expression of both electron transport chain components and uncoupling protein 1 (UCP1). UCP1 dissipates the mitochondrial proton motive force (Δp) generated by the respiratory chain and increases thermogenesis. Here we find that in mice genetically lacking UCP1, cold-induced activation of metabolism triggers innate immune signaling and markers of cell death in BAT. Moreover, global proteomic analysis reveals that this cascade induced by UCP1 deletion is associated with a dramatic reduction in electron transport chain abundance...
June 19, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28628841/mitochondrial-dysfunction-in-autism-spectrum-disorder-clinical-features-and-perspectives
#3
REVIEW
Fiona Hollis, Alexandros K Kanellopoulos, Claudia Bagni
Autism Spectrum Disorder (ASD) is a prototypic pervasive developmental disorder characterized by social interaction, and communication deficits, repetitive, stereotypic patterns of behavior, and impairments in language and development. Clinical studies have identified mitochondrial disturbances at the levels of DNA, activity, complexes, oxidative stress, and metabolites in blood and urine of ASD patients. However, these observations from postmortem brains or peripheral tissues do not provide a direct link between autism and mitochondria...
June 16, 2017: Current Opinion in Neurobiology
https://www.readbyqxmd.com/read/28626500/mitophagy-transcriptome-mechanistic-insights-into-polyphenol-mediated-mitophagy
#4
REVIEW
Sijie Tan, Esther Wong
Mitochondria are important bioenergetic and signalling hubs critical for myriad cellular functions and homeostasis. Dysfunction in mitochondria is a central theme in aging and diseases. Mitophagy, a process whereby damaged mitochondria are selectively removed by autophagy, plays a key homeostatic role in mitochondrial quality control. Upregulation of mitophagy has shown to mitigate superfluous mitochondrial accumulation and toxicity to safeguard mitochondrial fitness. Hence, mitophagy is a viable target to promote longevity and prevent age-related pathologies...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28626071/nlrx1-dampens-oxidative-stress-and-apoptosis-in-tissue-injury-via-control-of-mitochondrial-activity
#5
Geurt Stokman, Lotte Kors, Pieter J Bakker, Elena Rampanelli, Nike Claessen, Gwendoline J D Teske, Loes Butter, Harmen van Andel, Marius A van den Bergh Weerman, Per W B Larsen, Mark C Dessing, Coert J Zuurbier, Stephen E Girardin, Sandrine Florquin, Jaklien C Leemans
Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and chronic kidney disease. NLRX1 is a receptor of the innate immune system that is ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress-dependent fashion...
June 16, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28624784/mitochondrial-pyruvate-carrier-function-determines-cell-stemness-and-metabolic-reprogramming-in-cancer-cells
#6
Xiaoli Li, Gaoyang Han, Xiaoran Li, Quancheng Kan, Zhirui Fan, Yaqing Li, Yasai Ji, Jing Zhao, Mingzhi Zhang, Mantas Grigalavicius, Viktor Berge, Mariusz Adam Goscinski, Jahn M Nesland, Zhenhe Suo
One of the remarkable features of cancer cells is aerobic glycolysis, a phenomenon known as the "Warburg Effect", in which cells rely preferentially on glycolysis instead of oxidative phosphorylation (OXPHOS) as the main energy source even in the presence of high oxygen tension. Cells with dysfunctional mitochondria are unable to generate sufficient ATP from mitochondrial OXPHOS, and then are forced to rely on glycolysis for ATP generation. Here we report our results in a prostate cancer cell line in which the mitochondrial pyruvate carrier 1 (MPC1) gene was knockout...
May 25, 2017: Oncotarget
https://www.readbyqxmd.com/read/28624767/effects-of-nrf1-on-steroidogenesis-and-apoptosis-in-goat-luteinized-granulosa-cells
#7
Guo-Min Zhang, Ming-Tian Deng, Zhi-Hai Lei, Yong-Jie Wan, Hai-Tao Nie, Zi-Yu Wang, Yi-Xuan Fan, Feng Wang, Yan-Li Zhang
During goat follicular development, abnormal expression of nuclear respiratory factor 1 (NRF1) in granulosa cells may drive follicular atresia with unknown regulatory mechanisms. In this study, we investigated the effects of NRF1 on steroidogenesis and cell apoptosis by overexpressing or silencing it in goat luteinized granulosa cells (LGCs). Results showed that knockdown of NRF1 expression significantly inhibited the expression of STAR and CYP19A1, which are involved in sex steroid hormones synthesis, and led to lower estrogen levels...
August 2017: Reproduction: the Official Journal of the Society for the Study of Fertility
https://www.readbyqxmd.com/read/28624657/adiponectin-improves-the-osteointegration-of-titanium-implant-under-diabetic-conditions-by-reversing-mitochondrial-dysfunction-via-the-ampk-pathway-in-vivo-and-in-vitro
#8
Xiao-Fan Hu, Lin Wang, Yi-Zhao Lu, Geng Xiang, Zi-Xiang Wu, Ya-Bo Yan, Yang Zhang, Xiong Zhao, Yuan Zang, Lei Shi, Wei Lei, Ya-Fei Feng
Diabetes-induced reactive oxygen species (ROS) overproduction would result in compromised osteointegration of titanium implant (TI) and high rate of implant failure, yet the underlying mechanisms remain elusive. Adiponectin (APN) is a fat-derived adipocytokine with strong antioxidant, mitochondrial-protective and anti-diabetic efficacies. We hypothesized that mitochondrial dysfunction under diabetes may account for the oxidative stress in osteoblasts and titanium-bone interface (TBI) instability, which could be ameliorated by APN...
June 14, 2017: Acta Biomaterialia
https://www.readbyqxmd.com/read/28624490/bioenergetics-dysfunction-mitochondrial-permeability-transition-pore-opening-and-lipid-peroxidation-induced-by-hydrogen-sulfide-as-relevant-pathomechanisms-underlying-the-neurological-dysfunction-characteristic-of-ethylmalonic-encephalopathy
#9
Gabriela Miranda Fernandez Cardoso, Julia Tauana Pletsch, Belisa Parmeggiani, Mateus Grings, Nícolas Manzke Glanzel, Larissa Daniele Bobermin, Alexandre Umpierrez Amaral, Moacir Wajner, Guilhian Leipnitz
Hydrogen sulfide (sulfide) accumulates at high levels in the brains of patients with ethylmalonic encephalopathy (EE). In the present study, we evaluated whether sulfide could disturb energy and redox homeostasis, and induce mitochondrial permeability transition (mPT) pore opening in rat brain aiming to better clarify the neuropathophysiology of EE. Sulfide decreased the activities of citrate synthase and aconitase in rat cerebral cortex mitochondria, and of creatine kinase (CK) in rat cerebral cortex, striatum and hippocampus supernatants...
June 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28623559/ifn-%C3%AE-induced-reactive-oxygen-species-and-mitochondrial-damage-contribute-to-muscle-impairment-and-inflammation-maintenance-in-dermatomyositis
#10
Alain Meyer, Gilles Laverny, Yves Allenbach, Elise Grelet, Vanessa Ueberschlag, Andoni Echaniz-Laguna, Béatrice Lannes, Ghada Alsaleh, Anne Laure Charles, François Singh, Joffrey Zoll, Evelyne Lonsdorfer, François Maurier, Olivier Boyer, Jacques-Eric Gottenberg, Anne Sophie Nicot, Jocelyn Laporte, Olivier Benveniste, Daniel Metzger, Jean Sibilia, Bernard Geny
Dermatomyositis (DM) is an autoimmune disease associated with enhanced type I interferon (IFN) signalling in skeletal muscle, but the mechanisms underlying muscle dysfunction and inflammation perpetuation remain unknown. Transcriptomic analysis of early untreated DM muscles revealed that the main cluster of down-regulated genes was mitochondria-related. Histochemical, electron microscopy, and in situ oxygraphy analysis showed mitochondrial abnormalities, including increased reactive oxygen species (ROS) production and decreased respiration, which was correlated with low exercise capacities and a type I IFN signature...
June 16, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28619690/metformin-the-aspirin-of-the-21-st-century-its-role-in-gestational-diabetes-prevention-of-preeclampsia-and-cancer-and-the-promotion-of-longevity
#11
REVIEW
Roberto Romero, Offer Erez, Maik Hüttemann, Eli Maymon, Bogdan Panaitescu, Agustin Conde-Agudelo, Percy Pacora, Bo Hyun Yoon, Lawrence I Grossman
Metformin is everywhere. Originally introduced in clinical practice as an anti-diabetic agent, its role as a therapeutic agent is expanding to include treatment of pre-diabetes, gestational diabetes, polycystic ovarian disease, and more recently, experimental studies, as well as observations in randomized clinical trials, suggest that metformin could have a place in the treatment or prevention of preeclampsia. This article provides a brief overview of the history of metformin in the treatment of diabetes, reviews the results of meta-analyses of metformin in gestational diabetes, and the treatment of obese non-diabetic pregnant women to prevent macrosomia...
June 12, 2017: American Journal of Obstetrics and Gynecology
https://www.readbyqxmd.com/read/28619506/near-infra-red-light-attenuates-corneal-endothelial-cell-dysfunction-in-situ-and-in%C3%A2-vitro
#12
Claudia Núñez-Álvarez, Susana Del Olmo-Aguado, Jesús Merayo-Lloves, Neville N Osborne
In the present study mechanical damage to the corneal endothelium was induced by elevation of intraocular pressure (IOP, 140 mmHg, 60 min) to one eye of rats, delivered either in complete darkness or in the presence of red light (16.5 W/m(2), 3000 lx, 625-635 nm). IOP raised in the dark revealed the endothelium to be damaged as staining for the gap junction protein ZO-1 was irregular in appearance with some cells displaced in position or lost to leave gaps or holes. This damage was clearly attenuated when red light was focused through the pupil during the insult of raised IOP...
June 13, 2017: Experimental Eye Research
https://www.readbyqxmd.com/read/28618992/modulating-mitophagy-in-mitochondrial-disease
#13
Eszter Dombi, Heather Mortiboys, Joanna Poulton
Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28615325/calcium-calmodulin-dependent-protein-kinase-regulates-the-pink1-parkin-and-dj-1-pathways-of-mitophagy-during-sepsis
#14
Xianghong Zhang, Du Yuan, Qian Sun, Li Xu, Emma Lee, Anthony J Lewis, Brian S Zuckerbraun, Matthew R Rosengart
During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (ΔΨ) and mitophagy has not been identified. Mitochondria also buffer Ca(2+), and their buffering capacity is dependent on ΔΨ...
June 14, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28615314/mitochondria-and-reactive-oxygen-species-contribute-to-neurogenic-hypertension
#15
REVIEW
Samuel H H Chan, Julie Y H Chan
Beyond its primary role as fuel generators, mitochondria are engaged in a variety of cellular processes, including redox homeostasis. Mitochondrial dysfunction, therefore, may have a profound impact on high-energy-demanding organs such as the brain. Here, we review the roles of mitochondrial biogenesis and bioenergetics, and their associated signaling in cellular redox homeostasis, and illustrate their contributions to the oxidative stress-related neural mechanism of hypertension, focusing on specific brain areas that are involved in the generation or modulation of sympathetic outflows to the cardiovascular system...
July 2017: Physiology
https://www.readbyqxmd.com/read/28614042/bnip3l-nix-dependent-mitophagy-regulates-cell-differentiation-via-metabolic-reprogramming
#16
Lorena Esteban-Martínez, Patricia Boya
Macroautophagy/autophagy is the process by which cellular components are degraded and recycled within the lysosome. These components include mitochondria, the selective degradation of which is known as mitophagy. Mitochondria are dynamic organelles that constantly adapt their morphology, function, and number to accommodate the metabolic needs of the cell. Extensive metabolic reconfiguration occurs during cell differentiation, when mitochondrial activity increases in most cell types. However, our data demonstrate that during physiological retinal ganglion cell (RGC) development, mitophagy-dependent metabolic reprogramming towards glycolysis regulates numbers of RGCs, which are the first neurons to differentiate in the retina and whose axons form the optic nerve...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28613105/rug3-is-a-negative-regulator-of-plant-responses-to-aba-in-arabidopsis-thaliana
#17
Chao Su, Jinhong Yuan, Hongtao Zhao, Yankun Zhao, Hongtao Ji, Youning Wang, Xia Li
Mitochondria is a main target of various stressors. Dysfunction of mitochondria stimulates overproduction of reactive oxygen species (ROS), which can cause oxidative damage to mitochondria and DNA. Recently, we demonstrated that RCC1/UVR8/GEF-like 3 (RUG3), a member of the Regulator of Chromatin Condensation 1 (RCC1) protein family, can directly interact with ataxia telangiectasia mutated (ATM), a key regulator of the DNA damage response (DDR), and synergistically regulates the alternative splicing of mitochondrial nad2...
June 14, 2017: Plant Signaling & Behavior
https://www.readbyqxmd.com/read/28611662/an-antifungal-mechanism-of-protolichesterinic-acid-from-the-lichen-usnea-albopunctata-lies-in-the-accumulation-of-intracellular-ros-and-mitochondria-mediated-cell-death-due-to-apoptosis-in-candida-tropicalis
#18
S N Kumar, C Mohandas
Candida species causes superficial and life-threatening systemic infections and are difficult to treat due to the resistance of these organism to various clinically used drugs. Protolichesterinic acid is a well-known lichen compound. Although the antibacterial activity of protolichesterinic acid has been reported earlier, the antifungal property and its mechanism of action are still largely unidentified. The goal of the present investigation is to explore the anticandidal activity and mechanism of action of protolichesterinic acid, especially against Candida tropicalis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28611589/mitochondrial-effects-of-pgc-1alpha-silencing-in-mpp-treated-human-sh-sy5y-neuroblastoma-cells
#19
Qinyong Ye, Chun Chen, Erwang Si, Yousheng Cai, Juhua Wang, Wanling Huang, Dongzhu Li, Yingqing Wang, Xiaochun Chen
The dopaminergic neuron degeneration and loss that occurs in Parkinson's disease (PD) has been tightly linked to mitochondrial dysfunction. Although the aged-related cause of the mitochondrial defect observed in PD patients remains unclear, nuclear genes are of potential importance to mitochondrial function. Human peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) is a multi-functional transcription factor that tightly regulates mitochondrial biogenesis and oxidative capacity. The goal of the present study was to explore the potential pathogenic effects of interference by the PGC-1α gene on N-methyl-4-phenylpyridinium ion (MPP(+))-induced SH-SY5Y cells...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28608850/cellular-senescence-drives-age-dependent-hepatic-steatosis
#20
Mikolaj Ogrodnik, Satomi Miwa, Tamar Tchkonia, Dina Tiniakos, Caroline L Wilson, Albert Lahat, Christoper P Day, Alastair Burt, Allyson Palmer, Quentin M Anstee, Sushma Nagaraja Grellscheid, Jan H J Hoeijmakers, Sander Barnhoorn, Derek A Mann, Thomas G Bird, Wilbert P Vermeij, James L Kirkland, João F Passos, Thomas von Zglinicki, Diana Jurk
The incidence of non-alcoholic fatty liver disease (NAFLD) increases with age. Cellular senescence refers to a state of irreversible cell-cycle arrest combined with the secretion of proinflammatory cytokines and mitochondrial dysfunction. Senescent cells contribute to age-related tissue degeneration. Here we show that the accumulation of senescent cells promotes hepatic fat accumulation and steatosis. We report a close correlation between hepatic fat accumulation and markers of hepatocyte senescence. The elimination of senescent cells by suicide gene-meditated ablation of p16(Ink4a)-expressing senescent cells in INK-ATTAC mice or by treatment with a combination of the senolytic drugs dasatinib and quercetin (D+Q) reduces overall hepatic steatosis...
June 13, 2017: Nature Communications
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